{{infobox disease | name	HIV | Image HIV Virion-en.png | Caption Diagram of HIV | Width 190 | ICD10 B20-B24 | ICD9 - | DiseasesDB | MedlinePlus 000602 | eMedicineSubj article | eMedicineTopic 783434 | eMedicine_mult | MeshID D006678 | OMIM 609423 }}

Human immunodeficiency virus (HIV) is a lentivirus (a member of the retrovirus family) that causes ''acquired immunodeficiency syndrome'' (AIDS), a condition in humans in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive. Infection with HIV occurs by the transfer of blood, semen, vaginal fluid, pre-ejaculate, or breast milk. Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells. The four major routes of transmission are unsafe sex, contaminated needles, breast milk, and transmission from an infected mother to her baby at birth (perinatal transmission). Screening of blood products for HIV has largely eliminated transmission through blood transfusions or infected blood products in the developed world.

HIV infection in humans is considered pandemic by the World Health Organization (WHO). Nevertheless, complacency about HIV may play a key role in HIV risk. From its discovery in 1981 to 2006, AIDS killed more than 25 million people. HIV infects about 0.6% of the world's population. In 2009, AIDS claimed an estimated 1.8 million lives, down from a global peak of 2.1 million in 2004. Approximately 260,000 children died of AIDS in 2009. A disproportionate number of AIDS deaths occur in Sub-Saharan Africa, retarding economic growth and exacerbating the burden of poverty. In 2005, it was estimated that HIV would infect 90 million people in Africa, resulting in a minimum estimate of 18 million orphans. Treatment with antiretroviral drugs reduces both the mortality and the morbidity of HIV infection. Although antiretroviral medication is still not universally available, expansion of antiretroviral therapy programs since 2004 has helped to turn the tide of AIDS deaths and new infections in many parts of the world. Intensified awareness and preventive measures, as well as the natural course of the epidemic, have also played a role. Nevertheless, an estimated 2.6 million people were newly infected in 2009.

HIV infects vital cells in the human immune system such as helper T cells (specifically CD4⁺ T cells), macrophages, and dendritic cells. HIV infection leads to low levels of CD4⁺ T cells through three main mechanisms: First, direct viral killing of infected cells; second, increased rates of apoptosis in infected cells; and third, killing of infected CD4⁺ T cells by CD8 cytotoxic lymphocytes that recognize infected cells. When CD4⁺ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections.

Most untreated people infected with HIV-1 eventually develop AIDS. These individuals mostly die from opportunistic infections or malignancies associated with the progressive failure of the immune system. HIV progresses to AIDS at a variable rate affected by viral, host, and environmental factors; most will progress to AIDS within 10 years of HIV infection: some will have progressed much sooner, and some will take much longer. Treatment with anti-retrovirals increases the life expectancy of people infected with HIV. Even after HIV has progressed to diagnosable AIDS, the average survival time with antiretroviral therapy was estimated to be more than 5 years as of 2005. Without antiretroviral therapy, someone who has AIDS typically dies within a year.

Classification

+Comparison of HIV species
Species !! Virulence !! Infectivity !! Prevalence !! Inferred origin
! HIV-1	High	High	Global
HIV-2	Lower	Low	West Africa

HIV is a member of the genus ''Lentivirus'', part of the family of Retroviridae. Lentiviruses have many morphologies and biological properties in common. Many species are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long incubation period. Lentiviruses are transmitted as single-stranded, positive-sense, enveloped RNA viruses. Upon entry into the target cell, the viral RNA genome is converted (reverse transcribed) into double-stranded DNA by a virally encoded reverse transcriptase that is transported along with the viral genome in the virus particle. The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded integrase and host co-factors. Once integrated, the virus may become latent, allowing the virus and its host cell to avoid detection by the immune system. Alternatively, the virus may be transcribed, producing new RNA genomes and viral proteins that are packaged and released from the cell as new virus particles that begin the replication cycle anew.

Two types of HIV have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was initially discovered and termed both LAV and HTLV-III. It is more virulent, more infective, and is the cause of the majority of HIV infections globally. The lower infectivity of HIV-2 compared to HIV-1 implies that fewer of those exposed to HIV-2 will be infected per exposure. Because of its relatively poor capacity for transmission, HIV-2 is largely confined to West Africa.

Signs and symptoms

Infection with HIV-1 is associated with a progressive decrease of the CD4⁺ T cell count and an increase in viral load, the level of HIV in the blood. The stage of infection can be determined by measuring the patient's CD4⁺ T cell count and viral load.

The stages of HIV infection are acute infection (also known as primary infection), latency and AIDS. Acute infection lasts for several weeks and may include symptoms such as fever, lymphadenopathy (swollen lymph nodes), pharyngitis (sore throat), rash, myalgia (muscle pain), malaise, and mouth and esophageal sores. The latency stage involves few or no symptoms and can last anywhere from two weeks to twenty years or more, depending on the individual. AIDS, the final stage of HIV infection, is defined by low CD4+ T cell counts (fewer than 200 per microliter), various opportunistic infections, cancers and other conditions.

A small percentage of HIV-1 infected individuals retain high levels of CD4+ T-cells without antiretroviral therapy. However, most have detectable viral load and will eventually progress to AIDS without treatment, albeit more slowly than others. These individuals are classified as HIV controllers or long-term nonprogressors (LTNP). People who maintain CD4+ T cell counts and also have low or clinically undetectable viral load without anti-retroviral treatment are known as elite controllers or elite suppressors (ES).

Acute infection

Infection with HIV generally occurs by introduction of bodily fluids from an infected person into the body of an uninfected person. A period of rapid viral replication ensues, leading to an abundance of virus in the peripheral blood. During primary infection, the level of HIV may reach several million virus particles per milliliter of blood.

This response is accompanied by a marked drop in the numbers of circulating CD4⁺ T cells. This acute viremia is associated in virtually all patients with the activation of CD8⁺ T cells, which kill HIV-infected cells, and subsequently with antibody production, or seroconversion. The CD8⁺ T cell response is thought to be important in controlling virus levels, which peak and then decline, as the CD4⁺ T cell counts rebound. A good CD8⁺ T cell response has been linked to slower disease progression and a better prognosis, though it does not eliminate the virus.

During this period (usually 2–4 weeks post-exposure) most individuals (80 to 90%) develop an influenza or mononucleosis-like illness called acute HIV infection, the most common symptoms of which may include fever, lymphadenopathy, pharyngitis, rash, myalgia, malaise, mouth and esophageal sores, and may also include, but less commonly, headache, nausea and vomiting, enlarged liver/spleen, weight loss, thrush, and neurological symptoms. Infected individuals may experience all, some, or none of these symptoms. The duration of symptoms varies, averaging 28 days and usually lasting at least a week.

Because of the nonspecific nature of these symptoms, they are often not recognized as signs of HIV infection. Even if patients go to their doctors or a hospital, they will often be misdiagnosed as having one of the more common infectious diseases with the same symptoms. As a consequence, these primary symptoms are not used to diagnose HIV infection, as they do not develop in all cases and because many are caused by other more common diseases. However, recognizing the syndrome can be important because the patient is much more infectious during this period.

Chronic infection

A strong immune defense reduces the number of viral particles in the blood stream, marking the start of secondary or chronic HIV infection. The secondary stage of HIV infection can vary between two weeks and 20 years. During this phase of infection, HIV is active within lymph nodes, which typically become persistently swollen, in response to large amounts of virus that become trapped in the follicular dendritic cells (FDC) network. The surrounding tissues that are rich in CD4⁺ T cells may also become infected, and viral particles accumulate both in infected cells and as free virus. Individuals who are in this phase are still infectious. During this time, CD4⁺ CD45RO⁺ T cells carry most of the proviral load.

During this stage of infection early initiation of antiretroviral therapy significantly improves survival, as compared with deferred therapy.

AIDS

:''For more details on this topic, see AIDS Diagnosis, AIDS Symptoms and WHO Disease Staging System for HIV Infection and Disease'' When CD4⁺ T cell numbers decline below a critical level of 200 cells per µL, cell-mediated immunity is lost, and infections with a variety of opportunistic microbes appear. The first symptoms often include moderate and unexplained weight loss, recurring respiratory tract infections (such as sinusitis, bronchitis, otitis media, pharyngitis), prostatitis, skin rashes, and oral ulcerations.

Common opportunistic infections and tumors, most of which are normally controlled by robust CD4⁺ T cell-mediated immunity then start to affect the patient. Typically, resistance is lost early on to oral Candida species and to ''Mycobacterium tuberculosis'', which leads to an increased susceptibility to oral candidiasis (thrush) and tuberculosis. Later, reactivation of latent herpes viruses may cause worsening recurrences of herpes simplex eruptions, shingles, Epstein-Barr virus-induced B-cell lymphomas, or Kaposi's sarcoma.

Pneumonia caused by the fungus ''Pneumocystis jirovecii'' is common and often fatal. In the final stages of AIDS, infection with cytomegalovirus (another herpes virus) or Mycobacterium avium complex is more prominent. Not all patients with AIDS get all these infections or tumors, and there are other tumors and infections that are less prominent but still significant.

Transmission

+ Estimated per-act risk for acquisition of HIV by exposure route
Exposure Route	Estimated infections per 10,000 exposures to an infected source
	9,000 (90%)
	2,500 (25%)
	100-200 (1%-2%)
	67 (.67%)
	30 (.30%)
	170 (1.7%)‡ [30–890] / 143 [48-285]
	50 (.5%)
	62 (.62%)a [7-168]
	11 (.11%)a [2–24]
	6.5(.065%)
	38 (.38%)‡ [13–110]
	30 (.3%)‡ [14–63]
	10 (.1%)
	5 (.05%)
style="text-align:left"	1 (.01%)†b
	0.5 (.005%)†b
	The data shown represents transmission without the use of condoms. Risk increases substantially in the presence of genital ulcers, mucosal lacerations, concurrent sexually transmitted infections, or a partner with a high viral load of HIV. Commercial sex exposure and national income levels may also impact risk.

Three main transmission routes for HIV have been identified. HIV-2 is transmitted much less frequently by the mother-to-child and sexual route than HIV-1.

Sexual

The majority of HIV infections are acquired through unprotected sexual relations. Complacency about HIV plays a key role in HIV risk. Sexual transmission can occur when infected sexual secretions of one partner come into contact with the genital, oral, or rectal mucous membranes of another. In high-income countries, the risk of female-to-male transmission is 0.04% per act and male-to-female transmission is 0.08% per act. For various reasons, these rates are 4 to 10 times higher in low-income countries. The rate for receptive anal intercourse is much higher, 1.7% per act.

A 1999 meta-analysis of studies of condom use showed that the consistent use of latex condoms reduces the risk of sexual transmission of HIV by about 85%. However, spermicide may actually increase the transmission rate.

Randomized, controlled trials in which uncircumcised men were randomly assigned to be medically circumcised in sterile conditions and given counseling and other men were not circumcised have been conducted in South Africa, Kenya, and Uganda showing reductions in female-to-male sexual HIV transmission of 60%, 53%, and 51%, respectively. As a result, a panel of experts convened by WHO and the UNAIDS Secretariat has "recommended that male circumcision now be recognized as an additional important intervention to reduce the risk of heterosexually acquired HIV infection in men." Among men who have sex with men, there is insufficient evidence that male circumcision protects against HIV infection or other Sexually Transmitted Infections.

Studies of HIV among women having undergone female genital cutting (FGC) have reported mixed results, but with some evidence of increased risk of transmission. Programmes that aim to encourage sexual abstinence while also encouraging and teaching safer sex strategies for those who are sexually active can reduce short- and long-term HIV risk behaviour among young people in high-income countries, according to a 2007 Cochrane Review of studies.

Blood products

In general, if infected blood comes into contact with any open wound, HIV may be transmitted. This transmission route can account for infections in intravenous drug users, hemophiliacs, and recipients of blood transfusions (though most transfusions are checked for HIV in the developed world) and blood products. It is also of concern for persons receiving medical care in regions where there is prevalent substandard hygiene in the use of injection equipment, such as the reuse of needles in Third World countries. Health care workers such as nurses, laboratory workers, and doctors have also been infected, although this occurs more rarely. Since transmission of HIV by blood became known medical personnel are required to protect themselves from contact with blood by the use of universal precautions. People giving and receiving tattoos, piercings, and scarification procedures can also be at risk of infection.

HIV has been found at low concentrations in the saliva, tears, and urine of infected individuals, but there are no recorded cases of infection by these secretions and the potential risk of transmission is negligible. It is not possible for mosquitoes to transmit HIV.

Mother-to-child

The transmission of the virus from the mother to the child can occur ''in utero'' (during pregnancy), ''intrapartum'' (at childbirth), or via breast feeding. In the absence of treatment, the transmission rate up to birth between the mother and child is around 25%. However, where combination antiretroviral drug treatment and Cesarian section are available, this risk can be reduced to as low as one percent. Postnatal mother-to-child transmission may be largely prevented by complete avoidance of breast feeding; however, this has significant associated morbidity. Exclusive breast feeding and the provision of extended antiretroviral prophylaxis to the infant are also efficacious in avoiding transmission. UNAIDS estimate that 430,000 children were infected worldwide in 2008 (19% of all new infections), primarily by this route, and that a further 65,000 infections were averted through the provision of antiretroviral prophylaxis to HIV-positive women.

Multiple infection

Unlike some other viruses, infection with HIV does not provide immunity against additional infections, in particular, in the case of more genetically distant viruses. Both inter- and intra-clade multiple infections have been reported, and even associated with more rapid disease progression. Multiple infections are divided into two categories depending on the timing of the acquisition of the second strain. ''Coinfection'' refers to two strains that appear to have been acquired at the same time (or too close to distinguish). Reinfection (or superinfection) is infection with a second strain at a measurable time after the first. Both forms of dual infection have been reported for HIV in both acute and chronic infection around the world.

Prevention

There is currently no publicly available vaccine for HIV or AIDS. However, a vaccine that is a combination of two previously unsuccessful vaccine candidates (ALVAC-HIV and AIDSVAX) was reported in September 2009 to have resulted in a 30% reduction in infections in a trial conducted in Thailand. Further trials of the vaccine are ongoing. Additionally, a course of antiretroviral treatment administered immediately after exposure, referred to as post-exposure prophylaxis, is believed to reduce the risk of infection if begun as quickly as possible. In July 2010, a vaginal gel containing tenofovir, a reverse transcriptase inhibitor, was shown to reduce HIV infection rates by 39 percent in a trial conducted in South Africa.

Early treatment of HIV-infected people with antiretrovirals protected 96% of partners from infection.

Virology

Structure and genome

HIV is different in structure from other retroviruses. It is roughly spherical with a diameter of about 120 nm, around 60 times smaller than a red blood cell, yet large for a virus. It is composed of two copies of positive single-stranded RNA that codes for the virus's nine genes enclosed by a conical capsid composed of 2,000 copies of the viral protein p24. The single-stranded RNA is tightly bound to nucleocapsid proteins, p7, and enzymes needed for the development of the virion such as reverse transcriptase, proteases, ribonuclease and integrase. A matrix composed of the viral protein p17 surrounds the capsid ensuring the integrity of the virion particle.

This is, in turn, surrounded by the viral envelope that is composed of two layers of fatty molecules called phospholipids taken from the membrane of a human cell when a newly formed virus particle buds from the cell. Embedded in the viral envelope are proteins from the host cell and about 70 copies of a complex HIV protein that protrudes through the surface of the virus particle. This protein, known as Env, consists of a cap made of three molecules called glycoprotein (gp) 120, and a stem consisting of three gp41 molecules that anchor the structure into the viral envelope. This glycoprotein complex enables the virus to attach to and fuse with target cells to initiate the infectious cycle. Both these surface proteins, especially gp120, have been considered as targets of future treatments or vaccines against HIV.

The RNA genome consists of at least seven structural landmarks (LTR, TAR, RRE, PE, SLIP, CRS, and INS), and nine genes (''gag'', ''pol'', and ''env'', ''tat'', ''rev'', ''nef'', ''vif'', ''vpr'', ''vpu'', and sometimes a tenth ''tev'', which is a fusion of tat env and rev), encoding 19 proteins. Three of these genes, ''gag'', ''pol'', and ''env'', contain information needed to make the structural proteins for new virus particles. For example, ''env'' codes for a protein called gp160 that is broken down by a viral enzyme to form gp120 and gp41. The six remaining genes, ''tat'', ''rev'', ''nef'', ''vif'', ''vpr'', and ''vpu'' (or ''vpx'' in the case of HIV-2), are regulatory genes for proteins that control the ability of HIV to infect cells, produce new copies of virus (replicate), or cause disease.

The two Tat proteins (p16 and p14) are transcriptional transactivators for the LTR promoter acting by binding the TAR RNA element. The TAR may also be processed into microRNAs that regulate the apoptosis genes ERCC1 and IER3. The Rev protein (p19) is involved in shuttling RNAs from the nucleus and the cytoplasm by binding to the RRE RNA element. The Vif protein (p23) prevents the action of APOBEC3G (a cell protein that deaminates DNA:RNA hybrids and/or interferes with the Pol protein). The Vpr protein (p14) arrests cell division at G2/M. The Nef protein (p27) down-regulates CD4 (the major viral receptor), as well as the MHC class I and class II molecules.

Nef also interacts with SH3 domains. The Vpu protein (p16) influences the release of new virus particles from infected cells. The ends of each strand of HIV RNA contain an RNA sequence called the long terminal repeat (LTR). Regions in the LTR act as switches to control production of new viruses and can be triggered by proteins from either HIV or the host cell. The Psi element is involved in viral genome packaging and recognized by Gag and Rev proteins. The SLIP element (TTTTTT) is involved in the frameshift in the Gag-Pol reading frame required to make functional Pol.

Tropism

The term viral tropism refers to which cell types HIV infects. HIV can infect a variety of immune cells such as CD4⁺ T cells, macrophages, and microglial cells. HIV-1 entry to macrophages and CD4⁺ T cells is mediated through interaction of the virion envelope glycoproteins (gp120) with the CD4 molecule on the target cells and also with chemokine coreceptors.

Macrophage (M-tropic) strains of HIV-1, or non-syncitia-inducing strains (NSI) use the ''β''-chemokine receptor CCR5 for entry and are, thus, able to replicate in macrophages and CD4⁺ T cells. This CCR5 coreceptor is used by almost all primary HIV-1 isolates regardless of viral genetic subtype. Indeed, macrophages play a key role in several critical aspects of HIV infection. They appear to be the first cells infected by HIV and perhaps the source of HIV production when CD4⁺ cells become depleted in the patient. Macrophages and microglial cells are the cells infected by HIV in the central nervous system. In tonsils and adenoids of HIV-infected patients, macrophages fuse into multinucleated giant cells that produce huge amounts of virus.

T-tropic isolates, or syncitia-inducing (SI) strains replicate in primary CD4⁺ T cells as well as in macrophages and use the ''α''-chemokine receptor, CXCR4, for entry. Dual-tropic HIV-1 strains are thought to be transitional strains of HIV-1 and thus are able to use both CCR5 and CXCR4 as co-receptors for viral entry.

The ''α''-chemokine SDF-1, a ligand for CXCR4, suppresses replication of T-tropic HIV-1 isolates. It does this by down-regulating the expression of CXCR4 on the surface of these cells. HIV that use only the CCR5 receptor are termed R5; those that use only CXCR4 are termed X4, and those that use both, X4R5. However, the use of coreceptor alone does not explain viral tropism, as not all R5 viruses are able to use CCR5 on macrophages for a productive infection and HIV can also infect a subtype of myeloid dendritic cells, which probably constitute a reservoir that maintains infection when CD4⁺ T cell numbers have declined to extremely low levels.

Some people are resistant to certain strains of HIV. For example, people with the CCR5-Δ32 mutation are resistant to infection with R5 virus, as the mutation stops HIV from binding to this coreceptor, reducing its ability to infect target cells.

Sexual intercourse is the major mode of HIV transmission. Both X4 and R5 HIV are present in the seminal fluid, which is passed from a male to his sexual partner. The virions can then infect numerous cellular targets and disseminate into the whole organism. However, a selection process leads to a predominant transmission of the R5 virus through this pathway. How this selective process works is still under investigation, but one model is that spermatozoa may selectively carry R5 HIV as they possess both CCR3 and CCR5 but not CXCR4 on their surface and that genital epithelial cells preferentially sequester X4 virus. In patients infected with subtype B HIV-1, there is often a co-receptor switch in late-stage disease and T-tropic variants appear that can infect a variety of T cells through CXCR4. These variants then replicate more aggressively with heightened virulence that causes rapid T cell depletion, immune system collapse, and opportunistic infections that mark the advent of AIDS. Thus, during the course of infection, viral adaptation to the use of CXCR4 instead of CCR5 may be a key step in the progression to AIDS. A number of studies with subtype B-infected individuals have determined that between 40 and 50% of AIDS patients can harbour viruses of the SI and, it is presumed, the X4 phenotypes.

HIV-2 is much less pathogenic than HIV-1 and is restricted in its worldwide distribution. The adoption of "accessory genes" by HIV-2 and its more promiscuous pattern of coreceptor usage (including CD4-independence) may assist the virus in its adaptation to avoid innate restriction factors present in host cells. Adaptation to use normal cellular machinery to enable transmission and productive infection has also aided the establishment of HIV-2 replication in humans. A survival strategy for any infectious agent is not to kill its host but ultimately become a commensal organism. Having achieved a low pathogenicity, over time, variants more successful at transmission will be selected.

Replication cycle

Entry to the cell

HIV enters macrophages and CD4⁺ T cells by the adsorption of glycoproteins on its surface to receptors on the target cell followed by fusion of the viral envelope with the cell membrane and the release of the HIV capsid into the cell.

Entry to the cell begins through interaction of the trimeric envelope complex (gp160 spike) and both CD4 and a chemokine receptor (generally either CCR5 or CXCR4, but others are known to interact) on the cell surface. gp120 binds to integrin α₄β₇ activating LFA-1 the central integrin involved in the establishment of virological synapses, which facilitate efficient cell-to-cell spreading of HIV-1. The gp160 spike contains binding domains for both CD4 and chemokine receptors.

The first step in fusion involves the high-affinity attachment of the CD4 binding domains of gp120 to CD4. Once gp120 is bound with the CD4 protein, the envelope complex undergoes a structural change, exposing the chemokine binding domains of gp120 and allowing them to interact with the target chemokine receptor. This allows for a more stable two-pronged attachment, which allows the N-terminal fusion peptide gp41 to penetrate the cell membrane. Repeat sequences in gp41, HR1, and HR2 then interact, causing the collapse of the extracellular portion of gp41 into a hairpin. This loop structure brings the virus and cell membranes close together, allowing fusion of the membranes and subsequent entry of the viral capsid.

After HIV has bound to the target cell, the HIV RNA and various enzymes, including reverse transcriptase, integrase, ribonuclease, and protease, are injected into the cell. During the microtubule-based transport to the nucleus, the viral single-strand RNA genome is transcribed into double-strand DNA, which is then integrated into a host chromosome.

HIV can infect dendritic cells (DCs) by this CD4-CCR5 route, but another route using mannose-specific C-type lectin receptors such as DC-SIGN can also be used. DCs are one of the first cells encountered by the virus during sexual transmission. They are currently thought to play an important role by transmitting HIV to T-cells when the virus is captured in the mucosa by DCs. The presence of FEZ-1, which occurs naturally in neurons, is believed to prevent the infection of cells by HIV.

Replication and transcription

Shortly after the viral capsid enters the cell, an enzyme called ''reverse transcriptase'' liberates the single-stranded (+)RNA genome from the attached viral proteins and copies it into a complementary DNA (cDNA) molecule. The process of reverse transcription is extremely error-prone, and the resulting mutations may cause drug resistance or allow the virus to evade the body's immune system. The reverse transcriptase also has ribonuclease activity that degrades the viral RNA during the synthesis of cDNA, as well as DNA-dependent DNA polymerase activity that creates a sense DNA from the ''antisense'' cDNA. Together, the cDNA and its complement form a double-stranded viral DNA that is then transported into the cell nucleus. The integration of the viral DNA into the host cell's genome is carried out by another viral enzyme called ''integrase''. This integrated viral DNA may then lie dormant, in the latent stage of HIV infection. To actively produce the virus, certain cellular transcription factors need to be present, the most important of which is NF-''κ''B (NF kappa B), which is upregulated when T-cells become activated. This means that those cells most likely to be killed by HIV are those currently fighting infection.

During viral replication, the integrated DNA provirus is transcribed into mRNA, which is then spliced into smaller pieces. These small pieces are exported from the nucleus into the cytoplasm, where they are translated into the regulatory proteins Tat (which encourages new virus production) and Rev. As the newly produced Rev protein accumulates in the nucleus, it binds to viral mRNAs and allows unspliced RNAs to leave the nucleus, where they are otherwise retained until spliced. At this stage, the structural proteins Gag and Env are produced from the full-length mRNA. The full-length RNA is actually the virus genome; it binds to the Gag protein and is packaged into new virus particles.

HIV-1 and HIV-2 appear to package their RNA differently; HIV-1 will bind to any appropriate RNA, whereas HIV-2 will preferentially bind to the mRNA that was used to create the Gag protein itself. This may mean that HIV-1 is better able to mutate (HIV-1 infection progresses to AIDS faster than HIV-2 infection and is responsible for the majority of global infections).

Assembly and release

The final step of the viral cycle, assembly of new HIV-1 virons, begins at the plasma membrane of the host cell. The Env polyprotein (gp160) goes through the endoplasmic reticulum and is transported to the Golgi complex where it is cleaved by protease and processed into the two HIV envelope glycoproteins gp41 and gp120. These are transported to the plasma membrane of the host cell where gp41 anchors the gp120 to the membrane of the infected cell. The Gag (p55) and Gag-Pol (p160) polyproteins also associate with the inner surface of the plasma membrane along with the HIV genomic RNA as the forming virion begins to bud from the host cell. Maturation occurs either in the forming bud or in the immature virion after it buds from the host cell. During maturation, HIV proteases cleave the polyproteins into individual functional HIV proteins and enzymes. The various structural components then assemble to produce a mature HIV virion. This cleavage step can be inhibited by protease inhibitors. The mature virus is then able to infect another cell.

Genetic variability

HIV differs from many viruses in that it has very high genetic variability. This diversity is a result of its fast replication cycle, with the generation of about 10¹⁰ virions every day, coupled with a high mutation rate of approximately 3 x 10⁻⁵ per nucleotide base per cycle of replication and recombinogenic properties of reverse transcriptase.

This complex scenario leads to the generation of many variants of HIV in a single infected patient in the course of one day. This variability is compounded when a single cell is simultaneously infected by two or more different strains of HIV. When simultaneous infection occurs, the genome of progeny virions may be composed of RNA strands from two different strains. This hybrid virion then infects a new cell where it undergoes replication. As this happens, the reverse transcriptase, by jumping back and forth between the two different RNA templates, will generate a newly synthesized retroviral DNA sequence that is a recombinant between the two parental genomes. This recombination is most obvious when it occurs between subtypes.

The closely related simian immunodeficiency virus (SIV) has evolved into many strains, classified by the natural host species. SIV strains of the African green monkey (SIVagm) and sooty mangabey (SIVsmm) are thought to have a long evolutionary history with their hosts. These hosts have adapted to the presence of the virus, which is present at high levels in the host's blood but evokes only a mild immune response, does not cause the development of simian AIDS, and does not undergo the extensive mutation and recombination typical of HIV infection in humans.

In contrast, when these strains infect species that have not adapted to SIV ("heterologous" hosts such as rhesus or cynomologus macaques), the animals develop AIDS and the virus generates genetic diversity similar to what is seen in human HIV infection. Chimpanzee SIV (SIVcpz), the closest genetic relative of HIV-1, is associated with increased mortality and AIDS-like symptoms in its natural host. SIVcpz appears to have been transmitted relatively recently to chimpanzee and human populations, so their hosts have not yet adapted to the virus. This virus has also lost a function of the Nef gene that is present in most SIVs; without this function, T cell depletion is more likely, leading to immunodeficiency.

Three groups of HIV-1 have been identified on the basis of differences in the envelope (''env'') region: M, N, and O. Group M is the most prevalent and is subdivided into eight subtypes (or clades), based on the whole genome, which are geographically distinct. The most prevalent are subtypes B (found mainly in North America and Europe), A and D (found mainly in Africa), and C (found mainly in Africa and Asia); these subtypes form branches in the phylogenetic tree representing the lineage of the M group of HIV-1. Coinfection with distinct subtypes gives rise to circulating recombinant forms (CRFs). In 2000, the last year in which an analysis of global subtype prevalence was made, 47.2% of infections worldwide were of subtype C, 26.7% were of subtype A/CRF02_AG, 12.3% were of subtype B, 5.3% were of subtype D, 3.2% were of CRF_AE, and the remaining 5.3% were composed of other subtypes and CRFs. Most HIV-1 research is focused on subtype B; few laboratories focus on the other subtypes. The existence of a fourth group, "P", has been hypothesised based on a virus isolated in 2009. The strain is apparently derived from gorilla SIV (SIVgor), first isolated from western lowland gorillas in 2006.

The genetic sequence of HIV-2 is only partially homologous to HIV-1 and more closely resembles that of SIVsmm.

Diagnosis

Many HIV-positive people are unaware that they are infected with the virus. For example, less than 1% of the sexually active urban population in Africa have been tested and this proportion is even lower in rural populations. Furthermore, only 0.5% of pregnant women attending urban health facilities are counselled, tested or receive their test results. Again, this proportion is even lower in rural health facilities. Since donors may therefore be unaware of their infection, donor blood and blood products used in medicine and medical research are routinely screened for HIV.

HIV-1 testing consists of initial screening with an enzyme-linked immunosorbent assay (ELISA) to detect antibodies to HIV-1. Specimens with a nonreactive result from the initial ELISA are considered HIV-negative unless new exposure to an infected partner or partner of unknown HIV status has occurred. Specimens with a reactive ELISA result are retested in duplicate. If the result of either duplicate test is reactive, the specimen is reported as repeatedly reactive and undergoes confirmatory testing with a more specific supplemental test (e.g., Western blot or, less commonly, an immunofluorescence assay (IFA)). Only specimens that are repeatedly reactive by ELISA and positive by IFA or reactive by Western blot are considered HIV-positive and indicative of HIV infection. Specimens that are repeatedly ELISA-reactive occasionally provide an indeterminate Western blot result, which may be either an incomplete antibody response to HIV in an infected person or nonspecific reactions in an uninfected person.

Although IFA can be used to confirm infection in these ambiguous cases, this assay is not widely used. In general, a second specimen should be collected more than a month later and retested for persons with indeterminate Western blot results. Although much less commonly available, nucleic acid testing (e.g., viral RNA or proviral DNA amplification method) can also help diagnosis in certain situations. In addition, a few tested specimens might provide inconclusive results because of a low quantity specimen. In these situations, a second specimen is collected and tested for HIV infection.

Modern HIV testing is extremely accurate. The chance of a false-positive result in the two-step testing protocol is estimated to be 0.0004% to 0.0007% in the general U.S. population.

Screening at schools

The South African government announced a plan to start HIV testing in secondary schools by March 2011 but this plan was eventually scrapped because doing so would invade pupil's privacy at schools, schools typicaly don't have the facilities to securely store such information, and schools generally do not have the capacity to provide counselling for HIV positive pupils. In South Africa, anyone over the age of 12 may request an HIV test without parental knowledge or consent. Some 80 000 pupils in three provinces were tested under this programme before it was cancelled.

Treatment

There is currently no cure for HIV infection. Treatment consists of highly active antiretroviral therapy, or HAART. This has been highly beneficial to many HIV-infected individuals since its introduction in 1996, when the protease inhibitor-based HAART initially became available. Current HAART options are combinations (or "cocktails") consisting of at least three drugs belonging to at least two types, or "classes," of antiretroviral agents. Typically, these classes are two nucleoside analogue reverse transcriptase inhibitors (NARTIs or NRTIs) plus either a protease inhibitor or a non-nucleoside reverse transcriptase inhibitor (NNRTI).

There is no empirical evidence for withholding treatment at any stage of HIV infection, and death rates are almost twice as high when therapy is deferred (until the CD4 count falls below 500) compared to starting therapy when the CD4 count is above 500. However, the timing for starting HIV treatment is still subject to debate.

The United States Panel on Antiretroviral Guidelines for Adults and Adolescents in 2009 recommended that antiretroviral therapy should be initiated in all patients with a CD4 count less than 350, with treatment also recommended for patients with CD4 counts between 350 and 500. However, for patients with CD4 counts over 500, the expert Panel was evenly divided, with 50% in favor of starting antiretroviral therapy at this stage of HIV disease, and 50% viewing initiating therapy at this stage as optional. They noted that "Patients initiating antiretroviral therapy should be willing and able to commit to lifelong treatment and should understand the benefits and risks of therapy and the importance of adherence".

New classes of drugs such as entry inhibitors provide treatment options for patients infected with viruses already resistant to common therapies, although they are not widely available and not typically accessible in resource-limited settings. Because AIDS progression in children is more rapid and less predictable than in adults, in particular, in young infants, more aggressive treatment is recommended for children than adults. In developed countries where HAART is available, doctors assess their patients thoroughly: measuring the viral load, how fast CD4 declines, and patient readiness. They then decide when to recommend starting treatment.

HAART neither cures the patient nor uniformly removes all symptoms; high levels of HIV-1, often HAART-resistant, return if treatment is stopped. Moreover, it would take more than a lifetime for HIV infection to be cleared using HAART. Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to a large reduction in HIV-associated morbidity and mortality in the developed world. One study suggests the average life expectancy of an HIV infected individual is 32 years from the time of infection if treatment is started when the CD4 count is 350/µL. Life expectancy is further enhanced if antiretroviral therapy is initiated before the CD4 count falls below 500/µL.

In the absence of HAART, progression from HIV infection to AIDS has been observed to occur at a median of between nine to ten years and the median survival time after developing AIDS is only 9.2 months. However, HAART sometimes achieves far less than optimal results, in some circumstances being effective in less than fifty percent of patients. This is due to a variety of reasons such as medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. However, non-adherence and non-persistence with antiretroviral therapy is the major reason most individuals fail to benefit from HAART.

The reasons for non-adherence and non-persistence with HAART are varied and overlapping. Major psychosocial issues, such as poor access to medical care, inadequate social supports, psychiatric disease and drug abuse contribute to non-adherence. The complexity of these HAART regimens, whether due to pill number, dosing frequency, meal restrictions or other issues along with side effects that create intentional non-adherence also contribute to this problem. The side effects include lipodystrophy, dyslipidemia, insulin resistance, an increase in cardiovascular risks, and birth defects.

Anti-retroviral drugs are expensive, and the majority of the world's infected individuals do not have access to medications and treatments for HIV and AIDS. Research to improve current treatments includes decreasing side effects of current drugs, further simplifying drug regimens to improve adherence, and determining the best sequence of regimens to manage drug resistance. Unfortunately, only a vaccine is thought to be able to halt the pandemic. This is because a vaccine would cost less, thus being affordable for developing countries, and would not require daily treatment. However, after over 20 years of research, HIV-1 remains a difficult target for a vaccine.

HIV latent reservoir

Despite the success of highly active antiretroviral therapy (HAART) in controlling HIV infection and reducing HIV-associated mortality, current drug regimens are unable to completely eradicate HIV infection. Many people on HAART achieve suppression of HIV to levels below the limit of detection of standard clinical assays for many years. However, upon withdrawal of HAART, HIV viral loads rebound quickly with a concomitant decline in CD4+ T-Cells, which, in most cases, without a resumption of treatment, leads to AIDS.

To successfully reproduce itself, HIV must convert its RNA genome to DNA, which is then imported into the host cell's nucleus and inserted into the host genome through the action of HIV integrase. Because HIV's primary cellular target, CD4+ T-Cells, function as the memory cells of the immune system, integrated HIV can remain dormant for the duration of these cells' lifetime. Memory T-Cells may survive for many years and possibly for decades. The latent HIV reservoir can be measured by co-culturing CD4+ T-Cells from infected patients with CD4+ T-Cells from uninfected donors and measuring HIV protein or RNA.

The failure of vaccine candidates to protect against HIV infection and progression to AIDS has led to a renewed focus on the biological mechanisms responsible for HIV latency. A limited period of therapy combining anti-retrovirals with drugs targeting the latent reservoir may one day allow for total eradication of HIV infection.

Prognosis

Without treatment, the net median survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype, and the median survival rate after diagnosis of AIDS in resource-limited settings where treatment is not available ranges between 6 and 19 months, depending on the study. In areas where it is widely available, the development of HAART as effective therapy for HIV infection and AIDS reduced the death rate from this disease by 80%, and raised the life expectancy for a newly diagnosed HIV-infected person to 20–50 years.

As new treatments continue to be developed and because HIV continues to evolve resistance to treatments, estimates of survival time are likely to continue to change. Without antiretroviral therapy, death normally occurs within a year after the individual progresses to AIDS. Most patients die from opportunistic infections or malignancies associated with the progressive failure of the immune system. The rate of clinical disease progression varies widely between individuals and has been shown to be affected by many factors such as host susceptibility and immune function health care and co-infections, as well as which particular strain of the virus is involved.

Epidemiology

thumb|Numbers of people living with, newly infected with, and killed by HIV (1990–2008)

UNAIDS and the WHO estimated that AIDS killed more than 25 million people between 1981, when it was first recognized, and 2005, making it one of the most destructive pandemics in recorded history. Despite improved access to antiretroviral treatment and care in many regions of the world, the AIDS pandemic claimed an estimated 2.8 million (between 2.4 and 3.3 million) lives in 2005 of which more than half a million (570,000) were children.

UNAIDS estimated that 33.3 million people were living with HIV at the end of 2009, up from 26.2 million people in 1999. They also estimated AIDS-related deaths in 2009 at 1.8 million people, down from a peak of 2.1 million in 2004, new infections at 2.6 million, down from a peak of 3.2 million in 1997, and the number of people in low- or middle-income countries receiving antiretroviral therapy in 2009 at 5.2 million, up from 4.0 million in 2008.

Sub-Saharan Africa remains by far the worst-affected region, with an estimated 22.5  million people currently living with HIV (67% of the global total), 1.3 million deaths (72% of the global total) and 1.8 million new infections (69% of the global total). However, the number of new infections declined by 19% across the region between 2001 and 2009, and by more than 25% in 22 sub-Saharan African countries during this period. Asia is the second-worst affected region, with 4.9 million people living with HIV (15% of the global total).

The latest evaluation report of the World Bank's Operations Evaluation Department assesses the development effectiveness of the World Bank's country-level HIV/AIDS assistance defined as policy dialogue, analytic work, and lending with the explicit objective of reducing the scope or impact of the AIDS epidemic. This is the first comprehensive evaluation of the World Bank's HIV/AIDS support to countries, from the beginning of the epidemic through mid-2004. Because the Bank aims to assist in implementation of national government programmes, their experience provides important insights on how national AIDS programmes can be made more effective.

The development of HAART as effective therapy for HIV infection has substantially reduced the death rate from this disease in those areas where these drugs are widely available. As the life expectancy of persons with HIV has increased in countries where HAART is widely used, the continuing spread of the disease has caused the number of persons living with HIV to increase substantially.

In Africa, the number of mother-to-child-transmission (MTCT) cases and the prevalence of AIDS is beginning to reverse decades of steady progress in child survival. Countries such as Uganda are attempting to curb the MTCT epidemic by offering VCT (voluntary counselling and testing), PMTCT (prevention of mother-to-child transmission) and ANC (ante-natal care) services, which include the distribution of antiretroviral therapy.

History

Origins

:''See History of known cases and spread for early cases of HIV / AIDS'' HIV is thought to have originated in non-human primates in sub-Saharan Africa and was transferred to humans late in the 19th or early in the 20th century. The first paper recognizing a pattern of opportunistic infections characteristic of AIDS was published in 1981.

Both HIV-1 and HIV-2 are believed to have originated in West-Central Africa and to have jumped species (a process known as zoonosis) from non-human primates to humans. HIV-1 appears to have originated in southern Cameroon through the evolution of SIV(cpz), a simian immunodeficiency virus (SIV) that infects wild chimpanzees (HIV-1 descends from the SIVcpz endemic in the chimpanzee subspecies ''Pan troglodytes troglodytes''). The closest relative of HIV-2 is SIV(smm), a virus of the sooty mangabey (''Cercocebus atys atys''), an Old World monkey living in litoral West Africa (from southern Senegal to western Ivory Coast. New World monkeys such as the owl monkey are resistant to HIV-1 infection, possibly because of a genomic fusion of two viral resistance genes. HIV-1 is thought to have jumped the species barrier on at least three separate occasions, giving rise to the three groups of the virus, M, N, and O.

There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV. However, SIV is a weak virus, it is typically suppressed by the human immune system within weeks of infection. It is thought that several transmissions of the virus from individual to individual in quick succession are necessary to allow it enough time to mutate into HIV. Furthermore, due to its relatively low person-to-person transmission rate, it can only spread throughout the population in the presence of one or more of high-risk transmission channels, which are thought to have been absent in Africa prior to the 20h century.

Specific proposed high-risk transmission channels, allowing the virus to adapt to humans and spread throughout the society, depend on the proposed timing of the animal-to-human crossing. Genetic studies of the virus suggest that the most recent common ancestor of the HIV-1 M group dates back to circa 1910. Proponents of this dating link the HIV epidemic with the emergence of colonialism and growth of large colonial African cities, leading to social changes, including a higher degree of sexual promiscuity, the spread of prostitution, and the concomitant high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities. There is evidence that transmission rates of HIV during vaginal intercourse, while quite low under regular circumstances, may be increased tens, if not hundreds of times, if one of the partners suffers from a STD resulting in genital ulcers. Early 1900's colonial cities were notable due to their high prevalence of prostitution and genital ulcer STD's, to the degree that, as of 1928, as many as 45% of female residents of eastern Kinshasa were thought to have been prostitutes, and, as of 1933, around 15% of all residents of the same city were infected by one of the forms of syphilis.

An alternative view holds that unsafe medical practices in Africa during years following World War II, such as unsterile reuse of single use syringes during mass vaccination, antibiotic and anti-malaria treatment campaigns, were the initial vector that allowed the virus to adapt to humans and spread.

The earliest well documented case of HIV in a human dates back to 1959. The virus may have been present in the United States as early as 1966, but the vast majority of infections occurring outside sub-Saharan Africa (including the U.S.) can be traced back to a single unknown individual who got infected with HIV in Haiti and then brought the infection to the United States some time around 1969. The epidemic then rapidly spread among high-risk groups (initially, sexually promiscuous gay men). By 1978, the prevalence of HIV-1 among gay male residents of New York and San Francisco was estimated at 5%, suggesting that several thousand individuals in the country had been infected by then.

Discovery

AIDS was first clinically observed between late 1980 and early 1981. Injection drug users and gay men with no known cause of impaired immunity showed symptoms of ''Pneumocystis carinii'' pneumonia (PCP), a rare opportunistic infection that was known to present itself in people with very compromised immune systems. Soon thereafter, additional gay men developed a previously-rare skin cancer called Kaposi’s sarcoma (KS). Many more cases of PCP and KS quickly emerged, alerting U.S. Centers for Disease Control and Prevention (CDC). A CDC task force was formed to monitor the outbreak. After recognizing a pattern of anomalous symptoms presenting themselves in patients, the task force named the condition acquired immune deficiency syndrome (AIDS).

In 1983, two separate research groups led by Robert Gallo and Luc Montagnier independently declared that a novel retrovirus may have been infecting AIDS patients, and published their findings in the same issue of the journal ''Science''. Gallo claimed that a virus his group had isolated from an AIDS patient was strikingly similar in shape to other human T-lymphotropic viruses (HTLVs) his group had been the first to isolate. Gallo's group called their newly isolated virus HTLV-III. At the same time, Montagnier's group isolated a virus from a patient presenting lymphadenopathy (swelling of the lymph nodes) of the neck and physical weakness, two classic symptoms of AIDS. Contradicting the report from Gallo's group, Montagnier and his colleagues showed that core proteins of this virus were immunologically different from those of HTLV-I. Montagnier's group named their isolated virus lymphadenopathy-associated virus (LAV). HIV was chosen as a compromise between the two claims (LAV and HTLV-III).

Whether Gallo or Montagnier deserve more credit for the discovery of the virus that causes AIDS has been a matter of considerable controversy. Together with his colleague Françoise Barré-Sinoussi, Montagnier was awarded one half of the 2008 Nobel Prize in Physiology or Medicine for his "discovery of human immunodeficiency virus". Harald zur Hausen also shared the Prize for his discovery that human papilloma virus leads to cervical cancer, but Gallo was left out. Gallo said that it was "a disappointment" that he was not named a co-recipient. Montagnier said he was "surprised" Gallo was not recognized by the Nobel Committee: "It was important to prove that HIV was the cause of AIDS, and Gallo had a very important role in that. I'm very sorry for Robert Gallo."

AIDS denialism

A small group of individuals continue to dispute the connection between HIV and AIDS, the existence of HIV itself, or the validity of HIV testing and treatment methods. These claims, known as AIDS denialism, have been examined and rejected by the scientific community. However, they have had a significant political impact, particularly in South Africa, where the government's official embrace of AIDS denialism was responsible for its ineffective response to that country's AIDS epidemic, and has been blamed for hundreds of thousands of avoidable deaths and HIV infections.

Research

Stem cell transplantation

In 2007, a 40-year-old HIV-positive man was given a stem cell transplant as part of his treatment for acute myelogenous leukemia (AML). A second transplant was made a year later after a relapse. The donor was chosen not only for genetic compatibility but also for being homozygous for a CCR5-Δ32 mutation that confers resistance to HIV infection. After 20 months without antiretroviral drug treatment, it was reported that HIV levels in the recipient's blood, bone marrow, and bowel were below the limit of detection. Virus remained undetectable over three years after the first transplant. Although the researchers and some commentators have characterized this result as a cure, others suggest that the virus may remain hidden in tissues such as the brain (a viral reservoir). Stem cell treatment remains investigational because of its anecdotal nature, the disease and mortality risk associated with stem cell transplants, and the difficulty of finding suitable donors.

Immunomodulatory agents

Complementing efforts to control viral replication, immunotherapies that may assist in the recovery of the immune system have been explored in past and ongoing trials, including IL-2 and IL-7.

References

External links

Category:HIV/AIDS Category:Lentiviruses Category:Sexually transmitted diseases and infections Category:Discovery and invention controversies Category:Initialisms Category:Causes of death

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Name	Earvin "Magic" Johnson
Width	200
Position	Point guard / Forward
Number	32
Birth date	August 14, 1959
Birth place	Lansing, Michigan
Height ft	6
Height in	9
Height footnote
Weight lbs	255
Weight footnote
Career start	1979
Career end	1996
Draftyear	1979
Draftround	1
Draftpick	1
Draftteam	Los Angeles Lakers
High school	Everett (Lansing, Michigan)
College	Michigan State (1977–1979)
Years1	–, |team1 Los Angeles Lakers
Stat1label	Points
Stat1value	17,707 (19.5 ppg)
Stat2label	Rebounds
Stat2value	6,559 (7.2 rpg)
Stat3label	Assists
Stat3value	10,141 (11.2 apg)
Bbr	johnsma02
Letter	j
Highlights	5× NBA Champion (, , , –) 3× NBA Most Valuable Player (, –) 12× NBA All-Star (, –) 3× NBA Finals MVP (, , ) 9× All-NBA First Team (–) All-NBA Second Team () NBA All-Rookie First Team () 2× NBA All-Star Game MVP (, ) NBA's 50th Anniversary All-Time Team NCAA Champion (1979) #32 Retired by Los Angeles Lakers
Hof player	earvin-magic-johnson }}

Earvin "Magic" Johnson Jr. (born August 14, 1959) is a retired American professional basketball player who played point guard for the Los Angeles Lakers of the National Basketball Association (NBA). After winning championships in high school and college, Johnson was selected first overall in the 1979 NBA Draft by the Lakers. He won a championship and an NBA Finals Most Valuable Player Award in his rookie season, and won four more championships with the Lakers during the 1980s. Johnson retired abruptly in 1991 after announcing that he had contracted HIV, but returned to play in the 1992 All-Star Game, winning the All-Star MVP Award. After protests from his fellow players, he retired again for four years, but returned in 1996, at age 37, to play 32 games for the Lakers before retiring for the third and final time.

Johnson's career achievements include three NBA MVP Awards, nine NBA Finals appearances, twelve All-Star games, and ten All-NBA First and Second Team nominations. He led the league in regular-season assists four times, and is the NBA's all-time leader in assists per game, with an average of 11.2. Johnson was a member of the "Dream Team", the U.S. basketball team that won the Olympic gold medal in 1992.

Johnson was honored as one of the 50 Greatest Players in NBA History in 1996, and enshrined in the Basketball Hall of Fame in 2002. He was rated the greatest NBA point guard of all time by ESPN in 2007. His friendship and rivalry with Boston Celtics star Larry Bird, whom he faced in the 1979 NCAA finals and three NBA championship series, were well documented. Since his retirement, Johnson has been an advocate for HIV/AIDS prevention and safe sex, as well as an entrepreneur, philanthropist and motivational speaker.

Amateur career

Early years

Earvin Johnson Jr. was born to Earvin Sr., a General Motors assembly worker, and Christine, a school custodian. Johnson grew up in Lansing, Michigan, and came to love basketball as a youngster, idolizing players such as Earl Monroe and Marques Haynes, and practicing "all day".

Johnson was first dubbed "Magic" as a 15-year-old sophomore playing for Lansing's Everett High School, when he recorded a triple-double of 36 points, 18 rebounds and 16 assists. After the game, Fred Stabley Jr., a sports writer for the ''Lansing State Journal'', gave him the moniker despite the belief of Johnson's mother, a Christian, that the name was sacrilegious. In his final high school season, Johnson led Lansing Everett to a 27–1 win–loss record while averaging 28.8 points and 16.8 rebounds per game, and took his team to an overtime victory in the state championship game.

Michigan State University

Although Johnson was recruited by several top-ranked colleges such as Indiana and UCLA, he decided to play close to home. His college decision came down to the University of Michigan and Michigan State University in East Lansing. He ultimately decided to attend Michigan State when their coach Jud Heathcote told him he could play the point guard position. The talent already on Michigan State's roster also drew him to the program.

Johnson did not initially aspire to play professionally, focusing instead on his communication studies major and on his desire to become a television commentator. Playing with future NBA draftees Greg Kelser, Jay Vincent and Mike Brkovich, Johnson averaged 17.0 points, 7.9 rebounds, and 7.4 assists per game as a freshman, and led the Spartans to a 25–5 record, the Big Ten Conference title, and a berth in the 1978 NCAA Tournament. The Spartans reached the Elite Eight, but lost narrowly to eventual national champion Kentucky.

During the 1978–79 season, Michigan State again qualified for the NCAA Tournament, where they advanced to the championship game and faced Indiana State University, which was led by senior Larry Bird. In what was the most-watched college basketball game ever, Michigan State defeated Indiana State 75–64, and Johnson was voted Most Outstanding Player of the Final Four. After two years in college, during which he averaged 17.1 points, 7.6 rebounds, and 7.9 assists per game, Johnson was drafted in the 1979 NBA Draft.

Professional career

Rookie season in the NBA (1979–80)

Johnson was drafted first overall in 1979 by the Los Angeles Lakers. Johnson said that what was "most amazing" about joining the Lakers was the chance to play alongside Kareem Abdul-Jabbar, the team's 7 ft 2 in (2.18 m) center who became the leading scorer in NBA history. Despite Abdul-Jabbar's dominance, he had failed to win a championship with the Lakers, and Johnson was expected to help them achieve that goal. Johnson averaged 18.0 points, 7.7 rebounds, and 7.3 assists per game for the season, was selected to the NBA All-Rookie Team, and was named an NBA All-Star Game starter.

The Lakers compiled a 60–22 record in the regular season and reached the 1980 NBA Finals, in which they faced the Philadelphia 76ers, who were led by forward Julius Erving. The Lakers took a 3–2 lead in the series, but Abdul-Jabbar, who averaged 33 points a game in the series, sprained his ankle in Game 5 and could not play in Game 6. Paul Westhead decided to start Johnson at center in Game 6; Johnson recorded 42 points, 15 rebounds, seven assists, and three steals in a 123–107 win, while playing guard, forward, and center at different times during the game. Johnson became the only rookie to win the NBA Finals MVP award, and his clutch performance is still regarded as one of the finest in NBA history. He also became one of four players to win NCAA and NBA championships in consecutive years.

Ups and downs (1980–83)

Early in the 1980–81 season, Johnson was sidelined after he suffered torn cartilage in his left knee. He missed 45 games, and said that his rehabilitation was the "most down" he had ever felt. Johnson returned before the start of the 1981 playoffs, but the Lakers' then-assistant and future head coach Pat Riley later said Johnson's much-anticipated return made the Lakers a "divided team". The 54-win Lakers faced the 40–42 Houston Rockets in the first round of playoffs, where Houston upset the Lakers 2–1 after Johnson airballed a last-second shot in Game 3.

During the off-season, Johnson signed a 25-year, $25 million contract with the Lakers, which was the highest-paying contract in sports history up to that point. At the beginning of the 1981–82 season, Johnson had a heated dispute with Westhead, who Johnson said made the Lakers "slow" and "predictable". After Johnson demanded to be traded, Lakers owner Jerry Buss fired Westhead and replaced him with Riley. Although Johnson denied responsibility for Westhead's firing, he was booed across the league, even by Lakers' fans. Despite his off-court troubles, Johnson averaged 18.6 points, 9.6 rebounds, 9.5 assists, and a league-high 2.7 steals per game, and was voted a member of the All-NBA Second Team. He also joined Wilt Chamberlain and Oscar Robertson as the only NBA players to tally at least 700 points, 700 rebounds, and 700 assists in the same season. The Lakers advanced through the 1982 playoffs and faced Philadelphia for the second time in three years in the 1982 NBA Finals. After a triple-double from Johnson in Game 6, the Lakers defeated the Sixers 4–2, as Johnson won his second NBA Finals MVP award. During the championship series against the Sixers, Johnson averaged 16.2 points on .533 shooting, 10.8 rebounds, 8.0 assists, and 2.5 steals per game. Johnson later said that his third season was when the Lakers first became a great team, and he credited their success to Riley.

During the 1982–83 NBA season, Johnson averaged 16.8 points, 10.5 assists, and 8.6 rebounds per game and earned his first All-NBA First Team nomination. The Lakers again reached the Finals, and for a third time faced the Sixers, who featured center Moses Malone as well as Erving. With Johnson's teammates Norm Nixon, James Worthy and Bob McAdoo all hobbled by injuries, the Lakers were swept by the Sixers, and Malone was crowned the Finals MVP. In a losing effort against Philadelphia, Johnson averaged 19.0 points on .403 shooting, 12.5 assists, and 7.8 rebounds per game.

Battles against the Celtics (1983–87)

In Johnson's fifth season, he averaged a double-double of 17.6 points and 13.1 assists, as well as 7.3 rebounds per game. The Lakers reached the Finals for the third year in a row, where Johnson's Lakers and Bird's Celtics met for the first time in the post-season. The Lakers won the first game, and led by two points in Game 2 with 18 seconds to go, but after a layup by Gerald Henderson, Johnson failed to get a shot off before the final buzzer sounded, and the Lakers lost 124–121 in overtime. In Game 3, Johnson responded with 21 assists in a 137–104 win, but in Game 4, he again made several crucial errors late in the contest. In the final minute of the game, Johnson had the ball stolen by Celtics center Robert Parish, and then missed two free throws that could have won the game. The Celtics won Game 4 in overtime, and the teams split the next two games. In the decisive Game 7 in Boston, as the Lakers trailed by three points in the final minute, opposing point guard Dennis Johnson stole the ball from Johnson, a play that effectively ended the series. Friends Isiah Thomas and Mark Aguirre consoled him that night, talking until the morning in his Boston hotel room amidst fan celebrations on the street. During the Finals, Johnson averaged 18.0 points on .560 shooting, 13.6 assists, and 7.7 rebounds per game. Johnson later described the series as "the one championship we should have had but didn't get".

In the regular season, Johnson averaged 18.3 points, 12.6 assists, and 6.2 rebounds per game and led the Lakers into the 1985 NBA Finals, where they faced the Celtics again. The series started poorly for the Lakers when they allowed an NBA Finals record 148 points to the Celtics in a 34-point loss in Game 1. However, Abdul-Jabbar, who was now 38 years old, scored 30 points and grabbed 17 rebounds in Game 2, and his 36 points in a Game 5 win were instrumental in establishing a 3–2 lead for Los Angeles. After the Lakers defeated the Celtics in six games, Abdul-Jabbar and Johnson, who averaged 18.3 points on .494 shooting, 14.0 assists, and 6.8 rebounds per game in the championship series, said the Finals win was the highlight of their careers.

Johnson again averaged a double-double in the 1985–86 NBA season, with 18.8 points, 12.6 assists, and 5.9 rebounds per game. The Lakers advanced to the Western Conference Finals, but were unable to defeat the Houston Rockets, who advanced to the Finals in five games. In the next season, Johnson averaged a career-high of 23.9 points, as well as 12.2 assists and 6.3 rebounds per game, and earned his first regular season MVP award. The Lakers met the Celtics for the third time in the NBA Finals, and in Game 4 Johnson hit a last-second hook shot over Celtics big men Parish and Kevin McHale to win the game 107–106. The game-winning shot, which Johnson dubbed his "junior, junior, junior sky-hook", helped Los Angeles defeat Boston in six games. Johnson was awarded his third Finals MVP title after averaging 26.2 points on .541 shooting, 13.0 assists, 8.0 rebounds, and 2.33 steals per game.

Repeat and falling short (1987–91)

Before the 1987–88 NBA season, Lakers coach Pat Riley publicly promised that they would defend the NBA title, even though no team had won consecutive titles since the Celtics did so in the 1969 NBA Finals. Johnson had another productive season with averages of 19.6 points, 11.9 assists, and 6.2 rebounds per game. In the 1988 playoffs, the Lakers survived two 4–3 series against the Utah Jazz and the Dallas Mavericks to reach the Finals and face Thomas and the Detroit Pistons, known as the "Bad Boys" for their physical style of play. Johnson and Thomas greeted each other with a kiss on the cheek before the opening tip of Game 1, which they called a display of brotherly love. After the teams split the first six games, Lakers forward and Finals MVP James Worthy had his first career triple-double of 36 points, 16 rebounds, and 10 assists, and led his team to a 108–105 win. Despite not being named MVP, Johnson had a strong championship series, averaging 21.1 points on .550 shooting, 13.0 assists, and 5.7 rebounds per game.

In the 1988–89 NBA season, Johnson's 22.5 points, 12.8 assists, and 7.9 rebounds per game earned him his second MVP award, and the Lakers reached the 1989 NBA Finals, in which they again faced the Pistons. However, after Johnson went down with a hamstring injury in Game 2, the Lakers were no match for the Pistons, who swept them 4–0.

Playing without the retired Abdul-Jabbar for the first time, Johnson won his third MVP award after a strong 1989–90 NBA season in which he averaged 22.3 points, 11.5 assists, and 6.6 rebounds per game. However, the Lakers bowed out to the Phoenix Suns in the Western Conference semifinals, which was the Lakers' earliest playoffs elimination in nine years. Johnson performed well during the 1990–91 NBA season, with averages of 19.4 points, 12.5 assists, and 7.0 rebounds per game, and the Lakers reached the 1991 NBA Finals. There they faced the Chicago Bulls, led by shooting guard Michael Jordan, a five-time scoring champion regarded as the finest player of his era. Although the series was portrayed as a matchup between Johnson and Jordan, Bulls forward Scottie Pippen defended effectively against Johnson. Despite two triple-doubles from Johnson during the series, finals MVP Jordan led his team to a 4–1 win. In the last championship series of his career, Johnson averaged 18.6 points on .431 shooting, 12.4 assists, and 8.0 rebounds per game.

HIV announcement and Olympics (1991–92)

After a physical before the 1991–92 NBA season, Johnson discovered that he had tested positive for HIV. In a press conference held on November 7, 1991, Johnson made a public announcement that he would retire immediately. He stated that his wife Cookie and their unborn child did not have HIV, and that he would dedicate his life to "battle this deadly disease". Johnson initially said that he did not know how he contracted the disease, but later acknowledged that it was through having multiple sexual partners during his playing career. At the time, only a small percentage of HIV-positive people had contracted it from heterosexual sex, and it was initially rumored that Johnson was gay or bisexual, although he denied both. Johnson later accused Isiah Thomas of spreading the rumors, a claim Thomas denied. Johnson's HIV announcement became a major news story in the United States, and in 2004 was named as ESPN's seventh most memorable moment of the past 25 years. Many articles praised Johnson as a hero, and former U.S. President George H. W. Bush said, "For me, Magic is a hero, a hero for anyone who loves sports."

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Despite his retirement, Johnson was voted by fans as a starter for the 1992 NBA All-Star Game at Orlando Arena, although his former teammates Byron Scott and A. C. Green said that Johnson should not play, and several NBA players, including Utah Jazz forward Karl Malone, argued that they would be at risk of contamination if Johnson suffered an open wound while on court. Johnson led the West to a 153–113 win and was crowned All-Star MVP after recording 25 points, 9 assists, and 5 rebounds. The game ended after he made a last-minute three-pointer, and players from both teams ran onto the court to congratulate Johnson.

Johnson was chosen to compete in the 1992 Summer Olympics for the US basketball team, dubbed the "Dream Team" because of the NBA stars on the roster. During the tournament, which the USA won, Johnson played infrequently because of knee problems, but he received standing ovations from the crowd, and used the opportunity to inspire HIV-positive people.

Post-Olympics and later life

Before the 1992–93 NBA season, Johnson announced his intention to stage an NBA comeback. After practicing and playing in several pre-season games, he returned to retirement before the start of the regular season, citing controversy over his return sparked by opposition from several active players. During his retirement, Johnson has written a book on safer sex, run several businesses, worked for NBC as a commentator, and toured Asia and Australia with a basketball team that comprised former college and NBA players.

He returned to the NBA as coach of the Lakers near the end of the 1993–94 NBA season, replacing Randy Pfund. After losing five of six games, Johnson announced he would resign after the season, choosing instead to purchase a 5% share of the team in June 1994. In the following season, at the age of 36, Johnson attempted another comeback as a player. Playing power forward, he averaged 14.6 points, 6.9 assists, and 5.7 rebounds per game in the last 32 games of the season. After the Lakers lost to the Houston Rockets in the first round of the playoffs, Johnson retired permanently, saying, "I am going out on my terms, something I couldn't say when I aborted a comeback in 1992."

Off the court

Personal life

Johnson first fathered a son in 1981, when Andre Johnson was born to Melissa Mitchell. Although Andre was raised by his mother, he visited Johnson each summer, and as of October 2005 was working for Magic Johnson Enterprises as a marketing director. In 1991, Johnson married Earlitha "Cookie" Kelly in a small wedding in Lansing which included guests Thomas, Aguirre, and Herb Williams. Johnson and Cookie had one son, Earvin III; the couple adopted a daughter, Elisa, in 1995.

Media figure and business interests

In 1998, Johnson hosted a late night talk show on the Fox network called ''The Magic Hour'', but the show was canceled after two months because of low ratings. He runs Magic Johnson Enterprises, a company that has a net worth of $700 million; its subsidiaries include Magic Johnson Productions, a promotional company; Magic Johnson Theaters, a nationwide chain of movie theaters; and Magic Johnson Entertainment, a movie studio. Johnson has also worked as a motivational speaker. Johnson was an NBA commentator for Turner Network Television for seven years, before becoming a studio analyst for ESPN's ''NBA Countdown'' in 2008. In 1994, Johnson became a minority owner of the Lakers, having reportedly paid more than $10 million for part ownership. He also held the title of team vice president. Johnson sold his ownership stake in the Lakers in October 2010. In 2006 Johnson created a contract food service with Sodexo USA called Sodexo-Magic.

Politics

Johnson is a supporter of the Democratic Party—in 2006, he publicly endorsed Phil Angelides for governor of California, and in 2007 he supported Hillary Clinton for president of the United States. In 2010 Johnson endorsed Barbara Boxer in her race for re-election.

HIV activism

After announcing his infection in November 1991, Johnson created the Magic Johnson Foundation to help combat HIV, although he later diversified the foundation to include other charitable goals. In 1992, he joined the National Commission on AIDS, but left after eight months, saying that the commission was not doing enough to combat the disease. He was also the main speaker for the United Nations (UN) World AIDS Day Conference in 1999, and has served as a United Nations Messenger of Peace.

HIV had been associated with drug addicts and homosexuals, but Johnson's campaigns sought to show that the risk of infection was not limited to those groups. Johnson stated that his aim was to "help educate all people about what [HIV] is about" and teach others not to "discriminate against people who have HIV and AIDS". Johnson was later criticized by the AIDS community for his decreased involvement in publicizing the spread of the disease.

To prevent his HIV infection from progressing to AIDS, Johnson takes a daily combination of drugs. He has advertised GlaxoSmithKline's drugs, and partnered with Abbott Laboratories to publicize the fight against AIDS in African American communities.

Career achievements

In 905 NBA games, Johnson scored 17,707 points, 6,559 rebounds, and 10,141 assists, translating to career averages of 19.5 points, 7.2 rebounds, and 11.2 assists per game, the highest assists per game average in NBA history. Johnson shares the single-game playoff record for assists (24), holds the Finals record for assists in a game (21), and has the most playoff assists (2,346). He holds the All-Star Game single-game record for assists (22), and the All-Star Game record for career assists (127). Johnson introduced a fast-paced style of basketball called "Showtime", described as a mix of "no-look passes off the fastbreak, pin-point alley-oops from halfcourt, spinning feeds and overhand bullets under the basket through triple teams." Fellow Lakers guard Michael Cooper said, "There have been times when [Johnson] has thrown passes and I wasn't sure where he was going. Then one of our guys catches the ball and scores, and I run back up the floor convinced that he must've thrown it through somebody." Johnson was exceptional because he played point guard despite being 6 ft 9 in (2.06 m), a size reserved normally for frontcourt players. He combined the size of a power forward, the one-on-one skills of a swingman, and the ball handling talent of a guard, making him one of the most dangerous triple-double threats of all time; his 138 triple-double games are second only to Oscar Robertson's 181.

For his feats, Johnson was voted as one of the 50 Greatest Players of All Time by the NBA in 1996, and was inducted into the Naismith Memorial Basketball Hall of Fame in 2002. ESPN's ''SportsCentury'' ranked Johnson #17 in their "50 Greatest Athletes of the 20th Century" In 2006, ESPN.com rated Johnson the greatest point guard of all time, stating, "It could be argued that he's the one player in NBA history who was better than Michael Jordan." Several of his achievements in individual games have also been named among the top moments in the NBA.

Rivalry with Larry Bird

Johnson and Larry Bird were first linked as rivals after Johnson's Michigan State squad defeated Bird's Indiana State team in the 1979 NCAA finals. The rivalry continued in the NBA, and reached its climax when Boston and Los Angeles met in three out of four NBA Finals from 1984 to 1987. Johnson asserted that for him, the 82-game regular season was composed of 80 normal games, and two Lakers–Celtics games. Similarly, Bird admitted that Johnson's daily box score was the first thing he checked in the morning.

Several journalists hypothesized that the Johnson–Bird rivalry was so appealing because it represented many other contrasts, such as the clash between the Lakers and Celtics, between Hollywood flashiness ("Showtime") and Boston/Indiana blue collar grit ("Celtic Pride"), and between blacks and whites. The rivalry was also significant because it drew national attention to the faltering NBA. Prior to Johnson and Bird's arrival, the NBA had gone through a decade of declining interest and low TV ratings. With the two future Hall of Famers, the league won a whole generation of new fans, drawing both traditionalist adherents of Bird's dirt court Indiana game and those appreciative of Johnson's public park flair. Sports journalist Larry Schwartz of ESPN asserted that Johnson and Bird saved the NBA from bankruptcy.

Despite their on-court rivalry, Johnson and Bird became close friends during the filming of a 1984 Converse shoe advertisement that depicted them as enemies. Johnson appeared at Bird's retirement ceremony in 1992, and described Bird as a "friend forever"; during Johnson's Hall of Fame ceremony, Bird formally inducted his old rival.

Works

Biographies

Johnson's autobiography is Other biographies include: (German) (German) (In ''ESPN SportsCentury'')

Instructional

Updated version of

See also

List of National Basketball Association career assists leaders

List of National Basketball Association career steals leaders

List of National Basketball Association career turnovers leaders

List of National Basketball Association career free throw scoring leaders

List of National Basketball Association career playoff scoring leaders

List of National Basketball Association career playoff rebounding leaders

List of National Basketball Association career playoff assists leaders

List of National Basketball Association career playoff steals leaders

List of National Basketball Association career playoff turnovers leaders

List of National Basketball Association career playoff free throw scoring leaders

List of National Basketball Association players with most assists in a game

List of National Basketball Association players with most steals in a game

References

External links

Magic Johnson Bio, NBA Encyclopedia, Playoff Edition

Magic Johnson Foundation

Magic Johnson Official Website

Category:1959 births Category:Living people Category:African American basketball coaches Category:African American basketball players Category:African American sports executives Category:AIDS activists Category:American health activists Category:American motivational speakers Category:Naismith Memorial Basketball Hall of Fame inductees Category:Basketball players at the 1992 Summer Olympics Category:Basketball players from Michigan Category:California Democrats Category:People with HIV/AIDS Category:Los Angeles Lakers draft picks Category:Los Angeles Lakers players Category:Los Angeles Lakers head coaches Category:McDonald's High School All-Americans Category:Michigan State Spartans men's basketball players Category:National Basketball Association players with retired numbers Category:National Basketball Association executives Category:National Basketball Association head coaches Category:National Basketball Association owners Category:National Collegiate Basketball Hall of Fame inductees Category:NBA Finals MVP Award winners Category:Olympic basketball players of the United States Category:Olympic gold medalists for the United States Category:Parade High School All-Americans (boys' basketball) Category:People from Lansing, Michigan Category:Point guards Category:United States men's national basketball team members Category:Olympic medalists in basketball

ar:ماجيك جونسون zh-min-nan:Magic Johnson bs:Magic Johnson bg:Меджик Джонсън ca:Magic Johnson cs:Magic Johnson da:Magic Johnson de:Magic Johnson et:Magic Johnson es:Magic Johnson eu:Magic Johnson fa:مجیک جانسون fr:Magic Johnson gl:Magic Johnson ko:매직 존슨 hr:Magic Johnson id:Magic Johnson is:Earvin „Magic“ Johnson it:Magic Johnson he:מג'יק ג'ונסון la:Magicus Johnson lv:Maģiskais Džonsons lt:Magic Johnson hu:Magic Johnson nl:Magic Johnson ja:マジック・ジョンソン no:Magic Johnson pl:Magic Johnson pt:Magic Johnson ro:Magic Johnson qu:Magic Johnson ru:Джонсон, Мэджик simple:Magic Johnson sr:Меџик Џонсон fi:Magic Johnson sv:Magic Johnson ta:மேஜிக் ஜான்சன் te:మాజిక్ జాన్సన్ th:แมจิก จอห์นสัน tr:Magic Johnson vec:Magic Johnson war:Magic Johnson yo:Magic Johnson zh:魔术师约翰逊

Sean O'Brien Strub (b. 1958) is the founder of several magazines and websites, including POZ magazine and ''POZ en Español'', (for people impacted by HIV/AIDS), ''Mamm'' (for women impacted by breast cancer), ''Real Health'' (an African-American health magazine) and ''Milford Magazine'' (a regional title distributed in the Delaware River Highlands area of northeast Pennsylvania).

He is a long-term AIDS survivor and activist and has been an outspoken advocate for the self-empowerment movement for people with HIV/AIDS. In 2009 he was president of Cable Positive, the cable and telecommunications' industry's AIDS response.

In 1990, he ran for the U.S. House of Representatives to represent New York's 22nd congressional district. He was the first openly HIV+ candidate for federal office in the U.S. and received 46% of the Democratic primary vote. He was a long-time member of ACT UP New York. Strub produced an off-Broadway play, ''The Night Larry Kramer Kissed Me'', written by and starring David Drake, in 1992.

Strub was a pioneer expert in mass-marketed fundraising for LGBT equality.

He is a co-owner of the Hotel Fauchere, a Relais & Chateaux boutique hotel in Milford, Pennsylvania, where he has been active in a community revitalization effort.

Strub co-authored ''Rating America's Corporate Conscience'' (Addison-Wesley, 1985), a guide to corporate social responsibility, with Steve Lydenberg and Alice Tepper Marlin and ''Cracking the Corporate Closet'' (HarperBusiness, 1995) with Daniel B. Baker and Bill Henning.

Miscellaneous

In 1981 Strub got playwright Tennessee Williams to sign the first fundraising letter for the Human Rights Campaign Fund, a then newly-formed political action committee which grew to become the largest organization in the U.S. advocating for LGBT equality. In 1989 Strub asked pop artist Keith Haring to create a logo and poster to launch National Coming Out Day, now also a part of the Human Rights Campaign. Strub was one of the AIDS activists who put a giant condom over then-US Senator Jesse Helms' suburban Washington home in 1991.

References

Category:1958 births Category:Living people Category:AIDS activists Category:Gay writers Category:People with HIV/AIDS Category:LGBT businesspeople Category:LGBT writers from the United States

The term black people is used in some socially-based systems of racial classification for humans of a dark-skinned phenotype, relative to other racial groups represented in a particular social context.

Different societies apply different criteria regarding who is classified as "black", and often social variables such as class and socio-economic status also play a role, so that relatively dark-skinned people can be classified as white if they fulfill other social criteria of "whiteness" and relatively light-skinned people can be classified as black if they fulfill the social criteria for "blackness" in a particular setting.

As a biological phenotype being "black" is often associated with the very dark skin colors of some people who are classified as "black". But, particularly in the United States, the racial or ethnic classification also refers to people with all possible kinds of skin pigmentation from the darkest through to the very lightest skin colors, including albinos, if they are believed by others to have African ancestry, or to exhibit cultural traits associated with being "African-American". As a result, in the United States the term "black people" is not an indicator of skin color but of socially based racial classification.

Some definitions of the term include only people of relatively recent Sub-Saharan African descent (see African diaspora). Among the members of this group, dark skin is most often accompanied by the expression of natural afro-hair texture. Other definitions of the term "black people" extend to other populations characterized by dark skin, sometimes including people indigenous to Oceania.

Physiological traits

Dark skin

The evolution of dark skin is linked intrinsically to the loss of body hair in humans. By 1.2 million years ago, all people having descendants today had the same receptor protein of today's Africans; their skin was dark, and the intense sun lowered the chance of survival of those with lighter skin that resulted from mutational variation in the receptor protein. This is significantly earlier than the speciation of ''Homo sapiens'' from ''Homo erectus'' some 250,000 years ago.

Skin cancer as a result of ultraviolet light radiation causing mutations in the skin is less common among people with dark skin than it is among those with light skin. Dark skin prevents an essential B vitamin, folate, from being destroyed. In the absence of modern medicine and diet, a person with dark skin in the tropics would live longer, be healthier and more likely to reproduce than a person with light skin. As evidence of this expectation of adverse effects of light skin in the tropics, White South Africans and white Australians have some of the highest rates of skin cancer in the world.

Conversely, as dark skin prevents sunlight from penetrating the skin, it hinders the production of vitamin D₃. When humans migrated to less sun-intensive regions in the north, low vitamin D₃ levels became a problem, and humans with lighter skin were more successful in reproducing. White people of Europe, who have low levels of melanin, naturally have an almost colorless skin pigmentation, especially when untanned. This low level of pigmentation allows the blood vessels to become visible, which gives the characteristic pale pink color of white people. The loss of melanin in white people is thought to have been caused by a mutation in one letter out of 3.1 billion letters of DNA.

The genetic mutations leading to light skin, though different among East Asians and Europeans, suggest the two groups experienced a similar selective pressure due to settlement in northern latitudes.

Black skin pigmentation has been linked to a number of other properties, including tactile characteristics, and slower and less pronounced development of wrinkles.

Hair

The texture of hair in people of Sub-Saharan African ancestry is noticeably different from that of European and Asian populations. Herodotus described the peoples of Libya (the "western Ethiopians") as ''woolly-haired''.

Such "afro-hair" texture is denser than its straight counterparts. Due to this, it is often referred to as "coily", "thick", "nappy", "bushy", or "woolly". For several reasons, possibly including its relatively flat cross section (among other factors), this hair type conveys a dry or matte appearance. It is coarse, and its unique shape renders it prone to breakage when combed or brushed.

The specific characteristics of the natural afro-hair form are unique among all mammals. The texture likely predates the evolution of dark skin. It evolved when, as pre-human australopithecines lost most of their fur to enable perspiration, the need to protect the newly exposed pale skin underneath this body hair was crucial (see in light of Rogers and others., 2004 and Harding and others., 2000). The trait ceased to be essential to survival at the equator upon the evolution of hairless dark skin. Yet it has continued to be expressed vestigially among most Melanesians, Andaman Islanders, and sub-Saharan Africans.

Sub-Saharan Africa

Sub-Saharan Africa is a common, if imprecise term that encompasses African countries located south of the Sahara Desert. It is commonly used to differentiate the region culturally, ecologically, politically and, more controversially, racially, from North Africa, which has historically been considered part of the Mediterranean sphere.

Because the indigenous people of this region are primarily dark-skinned, it is alternatively called "Black Africa". However the terminology Black Africa and Sub-Sahara Africa is considered by some as a pejorative term and a vestige of colonialism, which divided Africa into European terms of homogeneity.Some criticize the use of the term, because, as it has become in many quarters synonymous with ''Black Africa'', people may not realize that there are also indigenous black populations in North Africa. In addition, the Sahara cuts across countries such as Mauritania, Mali, Niger, and Chad, leaving some parts of them in North Africa and some in sub-Saharan Africa.

Some black Africans prefer to be culturally distinguished from those who live in the north of the continent.

Cultural ideas of a black race

South Africa

In South Africa during the apartheid era, the population was classified into four main racial groups: ''Black'', ''White'', ''Asian'' (mostly Indian), and ''Coloured''. The Coloured group included people of mixed Bantu, Khoisan, and European descent (with some Malay ancestry, especially in the Western Cape). The Coloured definition occupied an intermediary position between the Black and White definitions in South Africa.

The apartheid bureaucracy devised complex (and often arbitrary) criteria in the Population Registration Act to determine who belonged in which group. Minor officials administered tests to enforce the classifications. When it was unclear from a person's physical appearance whether a person was to be considered Colored or Black, the "pencil test" was employed. This involved inserting a pencil in a person's hair to determine if the hair was kinky enough for the pencil to get stuck.

During the apartheid era, those classed as "Coloured" were oppressed and discriminated against. But, they had limited rights and overall had slightly better socioeconomic conditions than those classed as "Black".

In the post-apartheid era, the ANC government's laws in support of their affirmative action policies define "Black" people to include "Africans", "Coloureds" and "Asians". Their affirmative action policies have also favored "Africans" over "Coloureds". Some South Africans categorized as "African Black" openly state that "Coloureds" did not suffer as much as they did during apartheid. The popular saying by "Coloured" South Africans to illustrate their dilemma is:

In 2008, the High Court in South Africa ruled that Chinese South Africans who were residents during the apartheid era (and their descendents) are to be reclassified as "Black people" solely for the purposes of accessing affirmative action benefits, because they were also "disadvantaged" by racial discrimination. Chinese people who arrived in the country after the end of apartheid do not qualify.

Other than by appearance, "Coloureds" can usually be distinguished from "Blacks" by language. Most speak Afrikaans or English as a first language, as opposed to Bantu languages such as Zulu or Xhosa. They also tend to have more European-sounding names than Bantu names.

In the Middle East

Near East and North Africa

Black African and Near Eastern peoples have interacted since prehistoric times. Some historians estimate that as many as 14 million black slaves were transported across the Red Sea, Indian Ocean, and Sahara Desert in the Arab slave trade from 650 to 1900 CE. The Moroccan Sultan Moulay Ismail "the Bloodthirsty" (1672–1727) raised a corps of 150,000 black slaves, called his Black Guard, who coerced the country into submission.

In more recent times, about 1000 CE, interactions between black people and Arabs resulted in the incorporation of extensive Arabic vocabulary into Swahili, which became a useful ''lingua franca'' for merchants. Some of this linguistic exchange occurred as part of the slave trade; the history of Islam and slavery shows that the major juristic schools traditionally accepted the institution of slavery. As a result, Arab influence spread along the east coast of Africa and to some extent into the interior (see Swahili people). Timbuktu was a trading outpost that linked West Africa with Berber, Arab, and Jewish traders throughout the Arab World. As a result of these interactions, some female-mediated gene flow into the Middle East from Sub-Saharan Africa can be observed in certain populations.

According to Dr. Carlos Moore, resident scholar at Brazil's University of the state of Bahia, Afro-multiracials in the Arab world self-identify in ways that resemble Latin America. He claims that black-looking Arabs, much like black-looking Latin Americans, consider themselves white because they have some distant white ancestry. Moore also claims that a film about Egyptian President Anwar Sadat had to be canceled when Sadat discovered that an African-American had been cast to play him. In fact, the 1983 television movie ''Sadat'', starring Louis Gossett, Jr., was not canceled. The Egyptian government refused to let the drama air in Egypt, partially on the grounds of the casting of Gossett.

Sadat's mother was a dark-skinned Sudanese woman and his father was a lighter-skinned Egyptian. In response to an advertisement for an acting position he remarked, "I am not white but I am not exactly black either. My blackness is tending to reddish".

Fathia Nkrumah was another Egyptian with ties to Black Africa. She was the late wife of Ghanaian revolutionary Kwame Nkrumah, whose marriage was seen as helping plant the seeds of cooperation between Egypt and other African countries as they struggled for independence from European colonization. This helped advance the formation of the African Union. Because of the patriarchal nature of Arab society, Arab men enslaved more black women than men, and used more black female slaves than males. The men interpreted the Qur'an to permit sexual relations between a male master and his female slave outside of marriage, leading to many mixed-race children. When an enslaved woman became pregnant with her Arab master's child, she became ''umm walad'' or “mother of a child”, a status that granted her privileged rights. The child was allowed to prosper from the wealth of the father and was given rights of inheritance. Because the society was patrilineal, the children took their fathers' status at birth and were born free. Some succeeded their fathers as rulers, as was the case with Sultan Ahmad al-Mansur, who ruled Morocco from 1578 to 1608. His mother was a Fulani concubine of his father.

Such tolerance, however, was not extended to wholly black persons, even when technically "free." Arabs commonly believed that blacks were slaves. The term "abd", (,) "slave," remains a common term for black people in the Middle East, and, depending on the context, usually though not always derogatory.

Turkey

Beginning several centuries ago, a number of sub-Saharan Africans were brought by slave traders during the Ottoman Empire to plantations between Antalya and Istanbul in modern-day Turkey. Some of their descendants remain, mixed with the rest of the population in these areas, and many migrated to larger cities. Some came from the island of Crete following the population exchange between Greece and Turkey in 1923.

Israel

About 150,000 black people live in Israel, amounting to just over 2% of the nation's population. The vast majority of these, some 120,000, are Beta Israel, most of whom came during the 1980s and 1990s from Ethiopia. In addition, Israel is home to over 5,000 members of the African Hebrew Israelites of Jerusalem movement, who reside mainly in a distinct neighborhood in the Negev town of Dimona. Unknown numbers of black converts to Judaism reside in Israel, most of them converts from the UK, Canada, and the United States. Thousands of mixed-race individuals with non-black Jewish relatives also live in Israel.

In the Americas

Approximately 12 million Africans were shipped to the Americas during the Atlantic slave trade from 1492 to 1888. Today their descendants number approximately 150 million, most of whom live in the United States, the Caribbean and Latin America. Most notably Brazil has the largest population in the world, aside from Nigeria, of individuals of at least partial African descent. Many have a multiracial background of African, Amerindian, European and Asian ancestry. The various regions developed complex social conventions with which their multi-ethnic populations were classified.

United States

In the first 200 years that black people were in the United States, they commonly referred to themselves as Africans. In Africa, people primarily identified themselves by ethnic group (closely allied to language) and not by skin color. Individuals would be Ashanti, Igbo, Bakongo or Wolof. But when Africans were brought to the Americas, they were forced to give up their ethnic affiliations when they were combined with other groups from Africa. In areas of the Upper South, different ethnic groups were brought together. This is significant as Africans came from a vast geographic region, the West African coastline stretching from Senegal to Angola and in some cases from the south east coast such as Mozambique. A new identity and culture was born that incorporated elements of the various ethnic groups and of European cultural heritage, resulting in fusions such as the Black church and Black English. This new identity was based on African ancestry and slave status rather than any one ethnic group.

In March 1807, Britain, which largely controlled the Atlantic, declared the trans-atlantic slave trade illegal, as did the United States. (The latter prohibition took effect January 1, 1808, the earliest date on which Congress had the power to do so under Article I, Section 9 of the United States Constitution.)

By that time, the majority of black people were U.S.-born, so use of the term "African" became problematic. Though initially a source of pride, many blacks feared the use of African as an identity would be a hindrance to their fight for full citizenship in the US. They also felt that it would give ammunition to those who were advocating repatriating black people back to Africa. In 1835 black leaders called upon black Americans to remove the title of "African" from their institutions and replace it with "Negro" or "Colored American". A few institutions chose to keep their historic names, such as the African Methodist Episcopal Church. "Negro" and "colored" remained the popular terms until the late 1960s.

The term ''black'' was used throughout but not frequently as it carried a certain stigma. In his 1963 "I Have a Dream" speech, Martin Luther King, Jr. uses the terms ''Negro'' 15 times and ''black'' four times. Each time he uses ''black'' it is in parallel construction with ''white'' (for example,, black men and white men).

With the successes of the civil rights movement, a new term was needed to break from the past and help shed the reminders of legalized discrimination. In place of ''Negro'', activists promoted the use of ''black'' as standing for racial pride, militancy and power. Some of the turning points included the use of the term "Black Power" by Kwame Toure (Stokely Carmichael) and the release of James Brown's song "Say It Loud - I'm Black and I'm Proud". In 1988 Jesse Jackson urged Americans to use the term African American because the term has a historical cultural base. Since then African-American and black have essentially a coequal status. Controversy continues over which term is more appropriate. Some such as Maulana Karenga and Owen Alik Shahadah argue African-American is more appropriate because it accurately articulates geography and historical origin. Others have argued that "black" is a better term because "African" suggests foreignness, despite the long presence of black people in the US. Still others believe the term black is inaccurate because African Americans have a variety of skin tones. Surveys show that the majority of black Americans have no preference for "African American" or "Black," although they have a slight preference for "black" in personal settings and "African-American" in more formal settings. Increases in the number of immigrants to the United States from Africa, the Caribbean and Latin America have brought up questions about who uses the term African-American. The more recent African immigrants may sometimes view themselves, and be viewed, as culturally distinct from native-born people who are descendants of African slaves.

The U.S. census race definitions says a black is a person having origins in any of the black racial groups of Africa. It includes people who indicate their race as "Black, African Am., or Negro," or who provide written entries such as African-American, Afro-American, Kenyan, Nigerian, or Haitian. However, the Census Bureau notes that these classifications are socio-political constructs and should not be interpreted as scientific or anthropological.

A considerable portion of the U.S. population identified as ''black'' also has some Native American or European ancestry. For instance, genetic studies of African-American people show an ancestry that is on average 17–18% European.

One-drop rule

Since the late nineteenth century, the South used a colloquial term, the ''one-drop rule'', to classify as black a person of any known African ancestry. This practice of hypodescent was not put into law until the early twentieth century. Legally the definition varied from state to state, and was more flexible in the eighteenth and nineteenth centuries before the American Civil War. For instance, Thomas Jefferson held persons who were legally white (less than 25% Black) according to Virginia law at the time, but, because they were born to slave mothers, they were born into slavery, according to the principle of ''partus sequitur ventrem,'' which Virginia adopted into law in 1662.

Outside of the US, some other countries have adopted the one-drop rule, but the definition of who is black and the extent to which the one-drop "rule" applies varies greatly from country to country.

The one-drop rule may have originated as a means of increasing the number of black slaves and been maintained as an attempt to keep the white race pure. One of the results of the one-drop rule was uniting the African-American community. Some of the most prominent civil-rights activists were multiracial, and advocated equality for all.

Blackness

The concept of blackness in the United States has been described as the degree to which one associates themselves with mainstream African-American culture and values. To a certain extent, this concept is not so much about race but more about culture and behavior. Blackness can be contrasted with "acting white," where black Americans are said to behave with assumed characteristics of stereotypical white Americans, with regard to fashion, dialect, taste in music, and possibly, from the perspective of a significant number of black youth, academic achievement.

The notion of blackness can also be extended to non-black people. Toni Morrison once described Bill Clinton as the first black president, because of his warm relations with African Americans, his poor upbringing and also because he is a jazz musician. Christopher Hitchens was offended by the notion of Clinton as the first black president noting "we can still define blackness by the following symptoms: alcoholic mothers, under-the-bridge habits...the tendency to sexual predation and shameless perjury about the same". Some black activists were also offended, claiming Clinton used his knowledge of black culture to exploit black people like no other president before for political gain, while not serving black interests. They note his lack of action during the Rwanda genocide and his welfare reform which some claim led to the worst child poverty since the 1960s along with the fact that the number of black people in jail increased during his administration.

The question of blackness also arose in Democrat Barack Obama's 2008 presidential campaign. Commentators have questioned whether Obama, who was elected the first black President of the United States, is black enough, as his mother was white American, and his father was a black Kenyan immigrant. Obama refers to himself interchangeably as black and African-American. "Is Barack Obama the first black President of the United States?"

Brazil

The topic of race in Brazil is a complex and diverse one. A Brazilian child was never automatically identified with the racial type of one or both parents, nor were there only two categories to choose from. Between a pure black and a very light mulatto over a dozen racial categories would be recognized in conformity with the combinations of hair color, hair texture, eye color, and skin color. These types grade into each other like the colors of the spectrum, and no one category stands significantly isolated from the rest. That is, race referred to appearance, not heredity. There is some disagreement among scholars over the effects of social status on racial classifications in Brazil. It is generally believed that upward mobility and education results in reclassification of individuals into lighter skinned categories. The popular claim is that in Brazil poor whites are considered black and wealthy blacks are considered white. Some scholars disagree arguing that whitening of one's social status may be open to people of mixed race, but a typically black person will consistently be identified as black regardless of wealth or social status. Multiracial persons can even reappreciate their African heritage and start to declare themselves as black persons with increasings of social status and education.

Statistics

!Ethnic group 3,787,289 26,171,778 75,704,927

Brazilian Population, by Race, from 1872 to 1991 (Census Data)
|	White	Black	Brown	Yellow (Asian)	Undeclared	Total
1872	|	1,954,452	4,188,737	-	-	9,930,478
1940	|	6,035,869	8,744,365	242,320	41,983	41,236,315
1991	|	7,335,136	62,316,064	630,656	534,878	146,521,661

+Demographics of Brazil
Year!! White !! Pardo!! Black
1835	24.4%	18.2%	51.4%
2000	53.7%	38.5%
2010	48.4%	42.4%

From the year 1500 to 1850 an estimated 3.5 million Africans were forcibly shipped to Brazil. It is estimated that more than half of the Brazilian population is at least in part descendants of these Africans. Brazil has the largest population of Afro-descendants outside of Africa. In contrast to the US there were no segregation or anti-miscegenation laws in Brazil and as a result intermarriage has affected a large majority of the Brazilian population. Even much of the white/Asian population has either African or Amerindian blood. According to the last census of the twentieth century 54% identified themselves as white, 6.2% identified themselves as black and 39.5% identified themselves as Pardo (brown) — a broad multiracial category.

A philosophy of whitening emerged in Brazil in the nineteenth century. Until recently the government did not keep data on race. However, statisticians estimate that in 1835 half the population was black, one fifth was Pardo (brown) and one fourth white. By 2000 the black population had fallen to only 6.2% and the Pardo had increased to 40% and white to 55%. Essentially most of the black population was absorbed into the multiracial category by intermixing. A recent study found that at least 29% of the middle class white Brazilian population had some recent African ancestry.

Race relations in Brazil

Because of the ideology of miscegenation, Brazil has avoided the polarization of society into black and white. The bitter and sometimes violent racial tensions that divide the US are notably absent in Brazil. According to the census, 6.7% of Brazilians said they were black, compared with 6.2% in 2000, and 43.1% said they were mixed race, up from 38.5%. According to Brazil's minister for racial equality, Elio Ferreira de Araujo, attributed the change to growing pride among his country's black and indigenous communities.

However, the philosophy of the racial democracy in Brazil has drawn criticism from some quarters. Brazil has one of the largest gaps in income distribution in the world. The richest 10% of the population earn 28 times the average income of the bottom 40%. The richest 10 percent is almost exclusively white. One-third of the population lives under the poverty line, with blacks and other non-whites accounting for 70 percent of the poor. In the US, black people earn 75% of what white people earn. In Brazil, non-whites earn less than 50% of what whites earn. Some have posited that Brazil does in fact practice the one-drop rule when social economic factors are considered. This is because the gap in income between blacks and other non-whites is relatively small compared to the large gap between whites and non-whites. Other factors such as illiteracy and education level show the same patterns. Unlike in the US where African Americans were united in the civil-rights struggle, in Brazil the philosophy of whitening has helped divide blacks from other non-whites and prevented a more active civil rights movement.

Though Brazilians of African heritage make up a large percentage the population there are very few black politicians. The city of Salvador, Bahia, for instance, is 80% Afro-Brazilian but has never had a black mayor. Critics indicate that US cities that have a black majority, such as Detroit and New Orleans, have never had white mayors since first electing black mayors in the 1970s. Non-white people also have limited media visibility. The Latin American media, in particular the Brazilian media, has been accused of hiding its Black, Indigenous, Multiracial and East Asian population. For example the telenovelas or soaps are said to be a hotbed of largely light-eyed white and light-skinned mulattoes and mestizos (often deemed as white persons in Brazil if achieving the middle class or higher social status) actors. Most rare empowered persons of color represented in Latin American media possess typically Caucasian features due to a mix of racist standards of beauty, colourism and lookism. Nevertheless, in the last years, the number of empowered afrodescendants (either economically or by other ways) increased in Brazilian media coverage. Despite Brazil also possessing criminal black man stereotypes, it is considered a huge prejudice and mostly not used in a disordered way by the media, in spite of sometimes common "humouristic" sexist jokes and LGBT stereotyping and as such lack of politically correctness in native race issues is not a major problem (there are way more stereotypes of Asian people, Europeans or U.S. Americans, for example).

These patterns of discrimination against non-whites have led some to advocate for the use of the Portuguese term 'negro' to encompass non-whites so as to renew a black consciousness and identity, in effect an African descent rule. It generates criticism since Pardo, or Brown people, is intended to include caboclos (mestizos), assimilated Amerindians and tri-racials, not only afrodescendants — thus Brazilian of some or no recent African descent, as most White Brazilians, become 60–70% of the population, breaking the argument of possible Brazilian one-drop rule since real noticeable mulattoes, cafuzos (zambos) and black persons are a minority and the Brazilian poor represents larger percents in Brazil. As one would expect from an underdeveloped country, there are pockets of poverty in White-majority and Japanese Brazilian-majority areas, rarer in urban developments but common in rural areas. They are even more common among Mestizo-majority areas, and Amerindian communities.

In Asia and Australasia

China

As of August, 2008, ''The Migration Information Source'' article noted that "A Nigerian Embassy spokesman estimated that Nigerians possibly make up the largest group of Black Africans in China, with about 2,000 to 3,000 Nigerians in Guangdong in 2006. Most businessmen only stay temporarily."

India and Southeast Asia

The Great Andamanese are one of five Negrito ethnic groups (Adivasi or tribal) native to the Andaman and Nicobar Islands; they are among the first inhabitants of what is now India, arriving over 70,000 years ago. They are facing extinction. The other four ethnic groups are the Jangil, Jarawa, Onge and Sentinelese. By their external physical appearance (phenotype) such people resemble Black Africans with dark skin and sometimes tightly coiled hair. There have been suggestions of a Black African origin. However, in the case of the Andamanese people, a study conducted by the NCBI indicated that the Andamanese people possessed closer affinities with the Southeast Asian population than with the Black African population.

In South India there are also several communities of Black African descent, such as the Sheedis/Siddis, specifically the Siddis of Karnataka, who descend from Black African slaves. In Pakistan, these descendants are known as the Makrani.

Other black people of Southeast Asia, collectively known as Negritos, include the Semang peoples of Malaysia, the Mani of Thailand the Aeta of Luzon and the Ati of Panay in the Philippines.

Melanesia

There are several groups of dark-skinned people who live in various parts of Asia, Australia and Oceania who sometimes are referred to as black people. They include the Indigenous Australians, the Melanesians (now divided into Austronesian-speaking populations and Papuans, and including the great genetic diversity of New Guinea), the Semang people of the Malay peninsula, and indigenous first nation Fijians. They are as genetically, anthropologically and culturally related to Africans only as much as all other non-Africans are related to Africans, and because of this it has been deemed controversial to label them black people in the sense of some relation to the native African peoples and the African diaspora that is not similarly present in other Asian, Oceanic or European populations.

In Europe

United Kingdom

According to the Office for National Statistics, as of the 2001 census, there are over a million black people in the United Kingdom; 1% of the total population describe themselves as "Black Caribbean", 0.8% as "Black African", and 0.2% as "Black other". Britain encouraged the immigration of workers from the Caribbean after World War II; the first symbolic movement was those who came on the ship the ''Empire Windrush''. The preferred official umbrella term is "black and minority ethnic" (BME), but sometimes the term "black" is used on its own, to express unified opposition to racism, as in the Southall Black Sisters, which started with a mainly British Asian constituency, and the National Black Police Association, which has a membership of "African, African-Caribbean and Asian origin".

France

While census collection of ethnic background is illegal in France, it is estimated that there are about 2.5 – 5 million black people residing there.

Balkans

Due to the Ottoman slave trade that had flourished in the Balkans, the coastal town of Ulcinj in Montenegro had its own black community. As a consequence of the slave trade and privateer activity, a considerable number of Ulcinj inhabitants until 1878 were black. The Ottoman Army also sent an estimated 30,000 Black African troops and cavalrymen to its expedition in Hungary during the Austro-Turkish War of 1716–18.

Eastern Europe

As African states became independent in the 1960s, the Soviet Union offered many of their citizens the chance to study in Russia. Over a period of 40 years, about 400,000 African students from various countries moved to Russia to pursue higher studies, including many Black Africans. This extended beyond the Soviet Union to many countries of the Eastern bloc.

A cultural classification of people as "black" exists in Russia. Certain groups of people who are ethnically different, and generally darker, than ethnic Russians are pejoratively referred to as "blacks" (''chernye''), and face specific sorts of social exclusion (see Racism in Russia). Roma, Georgians, and Tatars fall into this category. Those referred to as "black" are from the former Soviet republics, predominantly peoples of the Caucasus, for example, Chechens. Although "Caucasian" is used in American English to mean "white people", in Russian – and most other varieties of English – it only refers to the Caucasus, not European people in general.

See also

African-American

African diaspora

African Jews

Afro-Europeans

Afro-Asian

Afro Asians (African Asians)

Afro-Latino

Afro-Trinbagonian

Black British

Black Canadians

Black Hispanic and Latino Americans

Black Indians

Black Jews

Black nationalism

Black Power

Black pride

Black separatism

Black supremacy

Creole peoples

List of topics related to the Black Diaspora

Mulatto

Negritos

Négritude

Stereotypes of black people

Sub-Saharan Africa

''The Minds of Marginalized Black Men'' (book)

Footnotes

Category:Latin American caste system Category:Race

ca:Raça negra de:Schwarze et:Neegrid es:Negro (persona) eo:Nigrulo fr:Noir (humain) ko:흑인 la:Nigrita pt:Negros simple:Black people sv:Svart (hudfärg) uk:Негр ug:قارا تەنلىكلەر wuu:黑人 yi:שווארצע zh-yue:黑人 bat-smg:Negrā zh:黑人

"The Man" is a slang phrase that may refer to the government or to some other authority in a position of power. In addition to this derogatory connotation, it may also serve as a term of respect and praise.

The phrase "the Man is keeping me down" is commonly used to describe oppression. The phrase "stick it to the Man" encourages resistance to authority, and essentially means "fight back" or "resist", either openly or via sabotage.

History

The term "the Man" in the American sense dates back to the late 19th Century. In the Southern U.S. states, the phrase came to be applied to any man or any group in a position of authority, or to authority in the abstract. From about the 1950s the phrase was also an underworld code word for police, the warden of a prison or other law enforcement or penal authorities.

It was also used as a term for a drug dealer in the 1950s and 1960s and can be seen in such media as Curtis Mayfield's "No Thing On Me", William Burroughs's novel ''Naked Lunch'', and in the Velvet Underground song "I'm Waiting for the Man", in which Lou Reed sings about going to Uptown Manhattan, specifically Lexington Avenue and 125th Street, to buy heroin.

The use of this term was expanded to counterculture groups and their battles against authority, such as the Yippies, which, according to a May 19, 1969 article in ''U.S. News and World Report'', had the "avowed aim ... to destroy 'The Man', their term for the present system of government". The term eventually found its way into humorous usage, such as in a December 1979 motorcycle ad from the magazine ''Easyriders'' which featured the tagline, "California residents: Add 6% sales tax for The Man."

In present day, the phrase has been popularized in commercials and cinema.

Use as praise

The term has also been used as an approbation or form of praise. This may refer to the recipient's status as the leader or authority within a particular context, or it might be assumed to be a shortened form of a phrase like "He is the man (who is in charge)." One example of this usage dates to 1879 when Otto von Bismarck commented, referring to Benjamin Disraeli's pre-eminent position at the Congress of Berlin, "The old Jew, he is the man."

In more modern usage, it can be a superlative compliment ("you da man!") indicating that the subject is currently standing out amongst his peers even though they have no special designation or rank, such as a basketball player who is performing better than the other players on the court. It can also be used as a genuine compliment with an implied, slightly exaggerated or sarcastic tone, usually indicating that the person has indeed impressed the speaker but by doing something relatively trivial.

See also

Absentee landlord

Big Brother (''Nineteen Eighty-Four'')

New World Order (conspiracy theory)

Ruling class

The Establishment

Power elite

Corrections officer

YTMND

Notes

References

Lighter, J.E. (Ed.). (1997). ''Random House Dictionary of American Slang''. New York: Random House.

Category:Slang expressions Category:Stock characters Category:English idioms Category:Pejorative terms for people Category:Military-industrial complex