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Name | Acquired immunodeficiency syndrome (AIDS) |
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Caption | The red ribbon is a symbol for solidarity with HIV-positive people and those living with AIDS. |
Width | 120 |
Diseasesdb | 5938 |
Icd10 | |
Icd9 | |
Medlineplus | 000594 |
Emedicinesubj | emerg |
Emedicinetopic | 253 |
Meshid | D000163 |
{| style="float: right; clear:right; margin: 0 0 0.5em 1em; padding: 0.5em; background: #fffff4; border: 1px solid #ddb; width: 250px; font-size:90%;" |- |List of abbreviations used in this article AIDS: Acquired immune deficiency syndrome HIV: Human immunodeficiency virus CD4+: CD4+ T helper cells CCR5: Chemokine (C-C motif) receptor 5 CDC: Centers for Disease Control and Prevention WHO: World Health Organization PCP: Pneumocystis pneumonia TB: Tuberculosis MTCT: Mother-to-child transmission HAART: Highly active antiretroviral therapy STI/STD: Sexually transmitted infection/disease |} Acquired immune deficiency syndrome or acquired immunodeficiency syndrome (AIDS) is a disease of the human immune system caused by the human immunodeficiency virus (HIV). This condition progressively reduces the effectiveness of the immune system and leaves individuals susceptible to opportunistic infections and tumors. HIV is transmitted through direct contact of a mucous membrane or the bloodstream with a bodily fluid containing HIV, such as blood, semen, vaginal fluid, preseminal fluid, and breast milk. This transmission can involve anal, vaginal or oral sex, blood transfusion, contaminated hypodermic needles, exchange between mother and baby during pregnancy, childbirth, breastfeeding or other exposure to one of the above bodily fluids.
AIDS is now a pandemic.
Genetic research indicates that HIV originated in west-central Africa during the late nineteenth or early twentieth century. AIDS was first recognized by the U.S. Centers for Disease Control and Prevention in 1981 and its cause, HIV, identified in the early 1980s.
Although treatments for AIDS and HIV can slow the course of the disease, there is no known cure or vaccine. Antiretroviral treatment reduces both the mortality and the morbidity of HIV infection, but these drugs are expensive and routine access to antiretroviral medication is not available in all countries. Due to the difficulty in treating HIV infection, preventing infection is a key aim in controlling the AIDS pandemic, with health organizations promoting safe sex and needle-exchange programmes in attempts to slow the spread of the virus.
Opportunistic infections are common in people with AIDS. These infections affect nearly every organ system.
People with AIDS also have an increased risk of developing various cancers such as Kaposi's sarcoma, cervical cancer and cancers of the immune system known as lymphomas. Additionally, people with AIDS often have systemic symptoms of infection like fevers, sweats (particularly at night), swollen glands, chills, weakness, and weight loss. The specific opportunistic infections that AIDS patients develop depend in part on the prevalence of these infections in the geographic area in which the patient lives.
Before the advent of effective diagnosis, treatment and routine prophylaxis in Western countries, it was a common immediate cause of death. In developing countries, it is still one of the first indications of AIDS in untested individuals, although it does not generally occur unless the CD4 count is less than 200 cells per µL of blood.
Tuberculosis (TB) is unique among infections associated with HIV because it is transmissible to immunocompetent people via the respiratory route, and is not easily treatable once identified, Multidrug resistance is a serious problem. Tuberculosis with HIV co-infection (TB/HIV) is a major world health problem according to the World Health Organization: in 2007, 456,000 deaths among incident TB cases were HIV-positive, a third of all TB deaths and nearly a quarter of the estimated 2 million HIV deaths in that year.
Even though its incidence has declined because of the use of directly observed therapy and other improved practices in Western countries, this is not the case in developing countries where HIV is most prevalent. In early-stage HIV infection (CD4 count >300 cells per µL), TB typically presents as a pulmonary disease. In advanced HIV infection, TB often presents atypically with extrapulmonary (systemic) disease a common feature. Symptoms are usually constitutional and are not localized to one particular site, often affecting bone marrow, bone, urinary and gastrointestinal tracts, liver, regional lymph nodes, and the central nervous system.
Unexplained chronic diarrhea in HIV infection is due to many possible causes, including common bacterial (Salmonella, Shigella, Listeria or Campylobacter) and parasitic infections; and uncommon opportunistic infections such as cryptosporidiosis, microsporidiosis, Mycobacterium avium complex (MAC) and viruses, astrovirus, adenovirus, rotavirus and cytomegalovirus, (the latter as a course of colitis).
In some cases, diarrhea may be a side effect of several drugs used to treat HIV, or it may simply accompany HIV infection, particularly during primary HIV infection. It may also be a side effect of antibiotics used to treat bacterial causes of diarrhea (common for Clostridium difficile). In the later stages of HIV infection, diarrhea is thought to be a reflection of changes in the way the intestinal tract absorbs nutrients, and may be an important component of HIV-related wasting.
Toxoplasmosis is a disease caused by the single-celled parasite called Toxoplasma gondii; it usually infects the brain, causing toxoplasma encephalitis, but it can also infect and cause disease in the eyes and lungs. Cryptococcal meningitis is an infection of the meninx (the membrane covering the brain and spinal cord) by the fungus Cryptococcus neoformans. It can cause fevers, headache, fatigue, nausea, and vomiting. Patients may also develop seizures and confusion; left untreated, it can be lethal.
Progressive multifocal leukoencephalopathy (PML) is a demyelinating disease, in which the gradual destruction of the myelin sheath covering the axons of nerve cells impairs the transmission of nerve impulses. It is caused by a virus called JC virus which occurs in 70% of the population in latent form, causing disease only when the immune system has been severely weakened, as is the case for AIDS patients. It progresses rapidly, usually causing death within months of diagnosis.
AIDS dementia complex (ADC) is a metabolic encephalopathy induced by HIV infection and fueled by immune activation of HIV infected brain macrophages and microglia. These cells are productively infected by HIV and secrete neurotoxins of both host and viral origin. Specific neurological impairments are manifested by cognitive, behavioral, and motor abnormalities that occur after years of HIV infection and are associated with low CD4+ T cell levels and high plasma viral loads.
Prevalence is 10–20% in Western countries but only 1–2% of HIV infections in India. This difference is possibly due to the HIV subtype in India. AIDS related mania is sometimes seen in patients with advanced HIV illness; it presents with more irritability and cognitive impairment and less euphoria than a manic episode associated with true bipolar disorder. Unlike the latter condition, it may have a more chronic course. This syndrome is less often seen with the advent of multi-drug therapy.
Patients with HIV infection have substantially increased incidence of several cancers. This is primarily due to co-infection with an oncogenic DNA virus, especially Epstein-Barr virus (EBV), Kaposi's sarcoma-associated herpesvirus (KSHV) (also known as human herpesvirus-8 [HHV-8]), and human papillomavirus (HPV).
Kaposi's sarcoma (KS) is the most common tumor in HIV-infected patients. The appearance of this tumor in young homosexual men in 1981 was one of the first signals of the AIDS epidemic. Caused by a gammaherpes virus called Kaposi's sarcoma-associated herpes virus (KSHV), it often appears as purplish nodules on the skin, but can affect other organs, especially the mouth, gastrointestinal tract, and lungs. High-grade B cell lymphomas such as Burkitt's lymphoma, Burkitt's-like lymphoma, diffuse large B-cell lymphoma (DLBCL), and primary central nervous system lymphoma present more often in HIV-infected patients. These particular cancers often foreshadow a poor prognosis. Epstein-Barr virus (EBV) or KSHV cause many of these lymphomas. In HIV-infected patients, lymphoma often arises in extranodal sites such as the gastrointestinal tract. When they occur in an HIV-infected patient, KS and aggressive B cell lymphomas confer a diagnosis of AIDS.
Invasive cervical cancer in HIV-infected women is also considered AIDS-defining, it is caused by human papillomavirus (HPV).
In addition to the AIDS-defining tumors listed above, HIV-infected patients are at increased risk of certain other tumors, notably Hodgkin's disease, anal and rectal carcinomas, hepatocellular carcinomas, head and neck cancers, and lung cancer. Some of these are causes by viruses, such as Hodgkin's disease (EBV), anal/rectal cancers (HPV), head and neck cancers (HPV), and hepatocellular carcinoma (hepatitis B or C). Other contributing factors include exposure to carcinogens (cigarette smoke for lung cancer), or living for years with subtle immune defects.
Interestingly, the incidence of many common tumors, such as breast cancer or colon cancer, does not increase in HIV-infected patients. In areas where HAART is extensively used to treat AIDS, the incidence of many AIDS-related malignancies has decreased, but at the same time malignant cancers overall have become the most common cause of death of HIV-infected patients. In recent years, an increasing proportion of these deaths have been from non-AIDS-defining cancers.
Penicilliosis due to Penicillium marneffei is now the third most common opportunistic infection (after extrapulmonary tuberculosis and cryptococcosis) in HIV-positive individuals within the endemic area of Southeast Asia.
An infection that often goes unrecognized in AIDS patients is Parvovirus B19. Its main consequence is anemia, which is difficult to distinguish from the effects of antiretroviral drugs used to treat AIDS itself.
Once HIV has killed so many CD4+ T cells that there are fewer than 200 of these cells per microliter (µL) of blood, cellular immunity is lost. Acute HIV infection usually progresses over time to clinical latent HIV infection and then to early symptomatic HIV infection and later to AIDS, which is identified either on the basis of the amount of CD4+ T cells remaining in the blood, and/or the presence of certain infections, as noted above.
In the absence of antiretroviral therapy, the median time of progression from HIV infection to AIDS is nine to ten years, and the median survival time after developing AIDS is only 9.2 months. However, the rate of clinical disease progression varies widely between individuals, from two weeks up to 20 years.
Many factors affect the rate of progression. These include factors that influence the body's ability to defend against HIV such as the infected person's general immune function. Older people have weaker immune systems, and therefore have a greater risk of rapid disease progression than younger people.
Poor access to health care and the existence of coexisting infections such as tuberculosis also may predispose people to faster disease progression. The infected person's genetic inheritance plays an important role and some people are resistant to certain strains of HIV. An example of this is people with the homozygous CCR5-Δ32 variation are resistant to infection with certain strains of HIV. HIV is genetically variable and exists as different strains, which cause different rates of clinical disease progression.
There are a number HIV and AIDS misconceptions. Three of the most common are that AIDS can spread through casual contact, that sexual intercourse with a virgin will cure AIDS, and that HIV can infect only homosexual men and drug users. Other misconceptions are that any act of anal intercourse between gay men can lead to AIDS infection, and that open discussion of homosexuality and HIV in schools will lead to increased rates of homosexuality and AIDS.
Sexual transmission occurs with the contact between sexual secretions of one person with the rectal, genital or oral mucous membranes of another. Unprotected sexual acts are riskier for the receptive partner than for the insertive partner, and the risk for transmitting HIV through unprotected anal intercourse is greater than the risk from vaginal intercourse or oral sex.
However, oral sex is not entirely safe, as HIV can be transmitted through both insertive and receptive oral sex. Sexual assault greatly increases the risk of HIV transmission as condoms are rarely employed and physical trauma to the vagina or rectum occurs frequently, facilitating the transmission of HIV. Drug use has been studied as a possible predictor of HIV transmission. Perry N. Halkitis found that methamphetamine usage does significantly relate to unprotected sexual behavior. As a result of these findings, methamphetamine users are at a higher risk for contracting HIV.
Other sexually transmitted infections (STI) increase the risk of HIV transmission and infection, because they cause the disruption of the normal epithelial barrier by genital ulceration and/or microulceration; and by accumulation of pools of HIV-susceptible or HIV-infected cells (lymphocytes and macrophages) in semen and vaginal secretions. Epidemiological studies from sub-Saharan Africa, Europe and North America suggest that genital ulcers, such as those caused by syphilis and/or chancroid, increase the risk of becoming infected with HIV by about fourfold. There is also a significant although lesser increase in risk from STIs such as gonorrhea, chlamydia and trichomoniasis, which all cause local accumulations of lymphocytes and macrophages.
Transmission of HIV depends on the infectiousness of the index case and the susceptibility of the uninfected partner. Infectivity seems to vary during the course of illness and is not constant between individuals. An undetectable plasma viral load does not necessarily indicate a low viral load in the seminal liquid or genital secretions.
However, each 10-fold increase in the level of HIV in the blood is associated with an 81% increased rate of HIV transmission. Women are more susceptible to HIV-1 infection due to hormonal changes, vaginal microbial ecology and physiology, and a higher prevalence of sexually transmitted diseases.
People who have been infected with one strain of HIV can still be infected later on in their lives by other, more virulent strains.
Infection is unlikely in a single encounter. High rates of infection have been linked to a pattern of overlapping long-term sexual relationships. This allows the virus to quickly spread to multiple partners who in turn infect their partners. A pattern of serial monogamy or occasional casual encounters is associated with lower rates of infection.
HIV spreads readily through heterosexual sex in Africa, but less so elsewhere. One possibility being researched is that schistosomiasis, which affects up to 50% of women in parts of Africa, damages the lining of the vagina.
Needle sharing is the cause of one third of all new HIV-infections in North America, China, and Eastern Europe. The risk of being infected with HIV from a single prick with a needle that has been used on an HIV-infected person is thought to be about 1 in 150 (see table above). Post-exposure prophylaxis with anti-HIV drugs can further reduce this risk.
This route can also affect people who give and receive tattoos and piercings. Universal precautions are frequently not followed in both sub-Saharan Africa and much of Asia because of both a shortage of supplies and inadequate training.
The WHO estimates that approximately 2.5% of all HIV infections in sub-Saharan Africa are transmitted through unsafe healthcare injections. Because of this, the United Nations General Assembly has urged the nations of the world to implement precautions to prevent HIV transmission by health workers.
The risk of transmitting HIV to blood transfusion recipients is extremely low in developed countries where improved donor selection and HIV screening is performed. However, according to the WHO, the overwhelming majority of the world's population does not have access to safe blood and between 5% and 10% of the world's HIV infections come from transfusion of infected blood and blood products.
However, when the mother takes antiretroviral therapy and gives birth by caesarean section, the rate of transmission is just 1%.
During the acute phase, HIV-induced cell lysis and killing of infected cells by cytotoxic T cells accounts for CD4+ T cell depletion, although apoptosis may also be a factor. During the chronic phase, the consequences of generalized immune activation coupled with the gradual loss of the ability of the immune system to generate new T cells appear to account for the slow decline in CD4+ T cell numbers.
Although the symptoms of immune deficiency characteristic of AIDS do not appear for years after a person is infected, the bulk of CD4+ T cell loss occurs during the first weeks of infection, especially in the intestinal mucosa, which harbors the majority of the lymphocytes found in the body. The reason for the preferential loss of mucosal CD4+ T cells is that a majority of mucosal CD4+ T cells express the CCR5 coreceptor, whereas a small fraction of CD4+ T cells in the bloodstream do so.
HIV seeks out and destroys CCR5 expressing CD4+ cells during acute infection. A vigorous immune response eventually controls the infection and initiates the clinically latent phase. However, CD4+ T cells in mucosal tissues remain depleted throughout the infection, although enough remain to initially ward off life-threatening infections.
Continuous HIV replication results in a state of generalized immune activation persisting throughout the chronic phase. Immune activation, which is reflected by the increased activation state of immune cells and release of proinflammatory cytokines, results from the activity of several HIV gene products and the immune response to ongoing HIV replication. Another cause is the breakdown of the immune surveillance system of the mucosal barrier caused by the depletion of mucosal CD4+ T cells during the acute phase of disease.
This results in the systemic exposure of the immune system to microbial components of the gut’s normal flora, which in a healthy person is kept in check by the mucosal immune system. The activation and proliferation of T cells that results from immune activation provides fresh targets for HIV infection. However, direct killing by HIV alone cannot account for the observed depletion of CD4+ T cells since only 0.01–0.10% of CD4+ T cells in the blood are infected.
A major cause of CD4+ T cell loss appears to result from their heightened susceptibility to apoptosis when the immune system remains activated. Although new T cells are continuously produced by the thymus to replace the ones lost, the regenerative capacity of the thymus is slowly destroyed by direct infection of its thymocytes by HIV. Eventually, the minimal number of CD4+ T cells necessary to maintain a sufficient immune response is lost, leading to AIDS
There are two main definitions for AIDS, both produced by the Centers for Disease Control and Prevention (CDC). The older definition is to referring to AIDS using the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus. In 1993, the CDC expanded their definition of AIDS to include all HIV positive people with a CD4+ T cell count below 200 per µL of blood or 14% of all lymphocytes. The majority of new AIDS cases in developed countries use either this definition or the pre-1993 CDC definition. The AIDS diagnosis still stands even if, after treatment, the CD4+ T cell count rises to above 200 per µL of blood or other AIDS-defining illnesses are cured.
Many people are unaware that they are infected with HIV. Less than 1% of the sexually active urban population in Africa has been tested, and this proportion is even lower in rural populations. Furthermore, only 0.5% of pregnant women attending urban health facilities are counseled, tested or receive their test results. Again, this proportion is even lower in rural health facilities. Routinely used HIV tests for infection in neonates and infants (i.e., patients younger than 2 years), born to HIV-positive mothers, have no value because of the presence of maternal antibody to HIV in the child's blood. HIV infection can only be diagnosed by PCR, testing for HIV pro-viral DNA in the children's lymphocytes.
During a sexual act, only male or female condoms can reduce the risk of infection with HIV and other STDs. The best evidence to date indicates that typical condom use reduces the risk of heterosexual HIV transmission by approximately 80% over the long-term, though the benefit is likely to be higher if condoms are used correctly on every occasion.
The male latex condom, if used correctly without oil-based lubricants, is the single most effective available technology to reduce the sexual transmission of HIV and other sexually transmitted infections. Manufacturers recommend that oil-based lubricants such as petroleum jelly, butter, and lard not be used with latex condoms, because they dissolve the latex, making the condoms porous. If lubrication is desired, manufacturers recommend using water-based lubricants. Oil-based lubricants can be used with polyurethane condoms.
Female condoms are commonly made from polyurethane, but are also made from nitrile and latex. They are larger than male condoms and have a stiffened ring-shaped opening with an inner ring designed to be inserted into the vagina keeping the condom in place; inserting the female condom requires squeezing this ring. Female condoms have been shown to be an important HIV prevention strategy by preliminary studies which suggest that overall protected sexual acts increase relative to unprotected sexual acts where female condoms are available. At present, availability of female condoms is very low and the price remains prohibitive for many women.
Studies on couples where one partner is infected show that with consistent condom use, HIV infection rates for the uninfected partner are below 1% per year. Prevention strategies are well-known in developed countries, but epidemiological and behavioral studies in Europe and North America suggest that a substantial minority of young people continue to engage in high-risk practices despite HIV/AIDS knowledge, underestimating their own risk of becoming infected with HIV.
Randomized controlled trials have shown that male circumcision lowers the risk of HIV infection among heterosexual men by up to 60%. It is expected that this procedure will be actively promoted in many of the countries affected by HIV, although doing so will involve confronting a number of practical, cultural and attitudinal issues. However, programs to encourage condom use, including providing them free to those in poverty, are estimated to be 95 times more cost effective than circumcision at reducing the rate of HIV in sub-Saharan Africa.
Some experts fear that a lower perception of vulnerability among circumcised men may result in more sexual risk-taking behavior, thus negating its preventive effects. However, one randomized controlled trial indicated that adult male circumcision was not associated with increased HIV risk behavior.
Studies of HIV infection rates among women who have undergone female genital cutting (FGC) have reported mixed results; for details see Female genital cutting#HIV.
A three-year study in South Africa, completed in 2010, found that an anti-microbial vaginal gel could reduce infection rates among women by 50% after one year of use, and by 39% after two and a half years. The results of the study, which was conducted by the Centre for the Aids Programme of Research in South Africa (Caprisa), were published in Science magazine in July 2010, and were then presented at an international aids conference in Vienna.
Standard goals of HAART include improvement in the patient’s quality of life, reduction in complications, and reduction of HIV viremia below the limit of detection, but it does not cure the patient of HIV nor does it prevent the return, once treatment is stopped, of high blood levels of HIV, often HAART resistant. Moreover, it would take more than the lifetime of an individual to be cleared of HIV infection using HAART.
Despite this, many HIV-infected individuals have experienced remarkable improvements in their general health and quality of life, which has led to the plummeting of HIV-associated morbidity and mortality. In the absence of HAART, progression from HIV infection to AIDS occurs at a median of between nine to ten years and the median survival time after developing AIDS is only 9.2 months.
For some patients, which can be more than fifty percent of patients, HAART achieves far less than optimal results, due to medication intolerance/side effects, prior ineffective antiretroviral therapy and infection with a drug-resistant strain of HIV. Non-adherence and non-persistence with therapy are the major reasons why some people do not benefit from HAART. The reasons for non-adherence and non-persistence are varied. Major psychosocial issues include poor access to medical care, inadequate social supports, psychiatric disease and drug abuse. HAART regimens can also be complex and thus hard to follow, with large numbers of pills taken frequently.
Side effects can also deter people from persisting with HAART, these include lipodystrophy, dyslipidaemia, diarrhoea, 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. However, the costs of anti-retroviral drugs have fallen recently in low-income countries. Moreover, a study in South Africa showed that patients' quality of life indices benefit from anti-retroviral treatment (Bhargava and Booysen, 2010) especially if healthcare services are adequate. In the absence of a cure for AIDS, anti-retroviral treatment is likely to be a cost-effective strategy for enhancing well-being of AIDS patients and their dependents.
Vitamin or mineral supplementation has shown benefit in some studies. Daily doses of selenium can suppress HIV viral burden with an associated improvement of the CD4 count. Selenium can be used as an adjunct therapy to standard antiviral treatments, but cannot itself cure the infection. More evidence is needed before it can be established that selenium supplementation reduces mortality rates. There is some evidence that vitamin A supplementation in children reduces mortality and improves growth. Dietary intake of micronutrients at RDA levels by HIV-infected adults is recommended by the World Health Organization (WHO). The WHO further states that several studies indicate that supplementation of vitamin A, zinc, and iron can produce adverse effects in HIV positive adults. 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 about 20 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. 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
Even with anti-retroviral treatment, over the long term HIV-infected patients may experience neurocognitive disorders, osteoporosis, neuropathy, cancers, nephropathy, and cardiovascular disease. It is not always clear whether these conditions result from the infection, related complications, or are side effects of treatment.
The largest cause of AIDS morbidity today, globally, is tuberculosis co-infection, see AIDS#Pulmonary_infections. In Africa, HIV is the single most important factor contributing to the increase in the incidence of TB since 1990.
The AIDS pandemic can also be seen as several epidemics of separate subtypes; the major factors in its spread are sexual transmission and vertical transmission from mother to child at birth and through breast milk. Globally, an estimated 33.2 million people lived with HIV in 2007, including 2.5 million children. An estimated 2.5 million (range 1.8–4.1 million) people were newly infected in 2007, including 420,000 children. South & South East Asia are second worst affected; in 2007 this region contained an estimated 18% of all people living with AIDS, and an estimated 300,000 deaths from AIDS.
In the United States, young African-American women are also at unusually high risk for HIV infection. African Americans make up 10% of the population but about half of the HIV/AIDS cases nationwide. This is due in part to a lack of information about AIDS and a perception that they are not vulnerable, as well as to limited access to health-care resources and a higher likelihood of sexual contact with at-risk male sexual partners.
There are also geographic disparities in AIDS prevalence in the United States, where it is most common in rural areas and in the southern states, particularly in the Appalachian and Mississippi Delta regions and along the border with Mexico. Approximately 1.1 million persons are living with HIV/AIDS in the United States, and more than 56,000 new infections occur every single year.
AIDS was first reported June 5, 1981, when the U.S. Centers for Disease Control (CDC) recorded a cluster of Pneumocystis carinii pneumonia (now still classified as PCP but known to be caused by Pneumocystis jirovecii) in five homosexual men in Los Angeles. In the beginning, the CDC did not have an official name for the disease, often referring to it by way of the diseases that were associated with it, for example, lymphadenopathy, the disease after which the discoverers of HIV originally named the virus.
In the general press, the term GRID, which stood for Gay-related immune deficiency, had been coined. The CDC, in search of a name, and looking at the infected communities coined “the 4H disease,” as it seemed to single out Haitians, homosexuals, hemophiliacs, and heroin users. However, after determining that AIDS was not isolated to the homosexual community, By September 1982 the CDC started using the name AIDS, and properly defined the illness.
The earliest known positive identification of the HIV-1 virus comes from the Congo in 1959 and 1960 though genetic studies indicate that it passed into the human population from chimpanzees around fifty years earlier.
The HIV virus descends from the related simian immunodeficiency virus (SIV), which infects apes and monkeys in Africa. There is evidence that humans who participate in bushmeat activities, either as hunters or as bushmeat vendors, commonly acquire SIV. However, only a few of these infections were able to cause epidemics in humans, and all did so in the late 19th—early 20th century. To explain why HIV became epidemic only by that time, there are several theories, each invoking specific driving factors that may have promoted SIV adaptation to humans, or initial spread: social changes following colonialism, rapid transmission of SIV through unsafe or unsterile injections (that is, injections in which the needle is reused without being sterilised), colonial abuses and unsafe smallpox vaccinations or injections, or prostitution and the concomitant high frequency of genital ulcer diseases (such as syphilis) in nascent colonial cities. See the main article Origin of AIDS.
A more controversial theory known as the OPV AIDS hypothesis suggests that the AIDS epidemic was inadvertently started in the late 1950s in the Belgian Congo by Hilary Koprowski's research into a poliomyelitis vaccine. According to scientific consensus, this scenario is not supported by the available evidence.
AIDS stigma has been further divided into the following three categories:
Instrumental AIDS stigma—a reflection of the fear and apprehension that are likely to be associated with any deadly and transmissible illness. Symbolic AIDS stigma—the use of HIV/AIDS to express attitudes toward the social groups or lifestyles perceived to be associated with the disease.
Often, AIDS stigma is expressed in conjunction with one or more other stigmas, particularly those associated with homosexuality, bisexuality, promiscuity, prostitution, and intravenous drug use.
In many developed countries, there is an association between AIDS and homosexuality or bisexuality, and this association is correlated with higher levels of sexual prejudice such as anti-homosexual attitudes. There is also a perceived association between AIDS and all male-male sexual behavior, including sex between uninfected men. Without proper nutrition, health care and medicine that is available in developed countries, large numbers of people suffer and die from AIDS-related complications. They will not only be unable to work, but will also require significant medical care. The forecast is that this will probably cause a collapse of economies and societies in countries with a significant AIDS population. In some heavily infected areas, the epidemic has left behind many orphans cared for by elderly grandparents.
The increased mortality has results in a smaller skilled population and labor force. This smaller labor force consists of increasingly younger people, with reduced knowledge and work experience leading to reduced productivity. An increase in workers’ time off to look after sick family members or for sick leave lowers productivity. Increased mortality reduces the mechanisms that generate human capital and investment in people, through loss of income and the death of parents.
By affecting mainly young adults, AIDS reduces the taxable population, in turn reducing the resources available for public expenditures such as education and health services not related to AIDS resulting in increasing pressure for the state's finances and slower growth of the economy. This results in a slower growth of the tax base, an effect that is reinforced if there are growing expenditures on treating the sick, training (to replace sick workers), sick pay and caring for AIDS orphans. This is especially true if the sharp increase in adult mortality shifts the responsibility and blame from the family to the government in caring for these orphans.
A small number of activists question the connection between HIV and AIDS, the existence of HIV, or the validity of current treatment methods (even going so far as to claim that the drug therapy itself was the cause of AIDS deaths). Though these claims have been examined and thoroughly rejected by the scientific community, they continue to be promulgated through the Internet and have had a significant political impact. In South Africa, former President Thabo Mbeki's embrace of AIDS denialism resulted in an ineffective governmental response to the AIDS epidemic that has been blamed for hundreds of thousands of AIDS-related deaths.
Operation INFEKTION was a worldwide Soviet active measures operation to spread information that the United States had created HIV/AIDS. Surveys show that a significant number of people believed - and continue to believe - in such claims.
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. A number of studies have shown that measures to prevent opportunistic infections can be beneficial when treating patients with HIV infection or AIDS. Vaccination against hepatitis A and B is advised for patients who are not infected with these viruses and are at risk of becoming infected. Patients with substantial immunosuppression are also advised to receive prophylactic therapy for Pneumocystis jiroveci pneumonia (PCP), and many patients may benefit from prophylactic therapy for toxoplasmosis and Cryptococcus meningitis as well.
Researchers have discovered an abzyme that can destroy the protein gp120 CD4 binding site. This protein is common to all HIV variants as it is the attachment point for B lymphocytes and subsequent compromising of the immune system.
Researchers from the Hebrew University of Jerusalem have also discovered that a combination of peptides that stimulate integration together with the protease inhibitor Ro 31-8959 caused apoptotic cell death of HIV-infected cells with total extermination of the virus but did not harm healthy cells. It could take several years before a commercial treatment based on this discovery becomes available.
Reactivation of the retrocyclin pseudogene has been proposed as a possible prevention method, as was demonstrated in a proof-of-concept study in tissue culture cells.
In Berlin, Germany, a 42-year-old leukemia patient, Timothy Ray Brown (also referred to as the "Berlin Patient"), infected with HIV for more than a decade was given an experimental transplant of bone marrow with cells that contained an unusual natural variant of the CCR5 cell-surface receptor. This CCR5-Δ32 variant has been shown to make some cells from people who are born with it resistant to infection with some strains of HIV. Almost two years after the transplant, and even after the patient reportedly stopped taking antiretroviral medications, HIV has not been detected in the patient's blood. As of December 2010, three years after the transplant, Brown was still free of any detectable HIV in his blood and was described, in a paper in the journal Blood, as "cured."
Category:Acronyms Category:AIDS origin hypotheses Category:HIV/AIDS Category:Immune system disorders Category:Immunodeficiency Category:Infectious diseases Category:Health disasters Category:Microbiology Category:Pandemics Category:Sexually transmitted diseases and infections Category:Syndromes Category:Viral diseases Category:Virology
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Name | George Mason |
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Birth name | George Mason |
Birth date | December 11, 1725 |
Birth place | Fairfax County, Colony of Virginia |
Death date | October 07, 1792 |
Death place | Gunston Hall, Fairfax County, Virginia |
Death cause | natural causes |
Resting place coordinates | |
Residence | Gunston Hall, Fairfax County, Virginia |
Nationality | British, American |
Ethnicity | English American |
Citizenship | Kingdom of Great BritainUnited States |
Occupation | patriot, statesman, and delegate from Virginia to the U.S. Constitutional Convention |
Religion | Anglican, Episcopalian |
Spouse | Ann EilbeckSarah Brent |
Children | George Mason VAnn Eilbeck Mason JohnsonWilliam MasonWilliam MasonThomson MasonSarah Eilbeck Mason McCartyMary Thomson Mason CookeJohn MasonElizabeth Mason ThorntonThomas MasonJames MasonRichard Mason |
Parents | George Mason IIIAnn Stevens Thomson |
Like anti-federalist Patrick Henry, Mason was a leader of those who pressed for the addition of explicit States rights and individual rights to the U.S. Constitution as a balance to the increased federal powers, and did not sign the document in part because it lacked such a statement. His efforts eventually succeeded in convincing the Federalists to add the first ten amendments of the Constitution. These amendments, collectively known as the Bill of Rights, were based on the earlier Virginia Declaration of Rights, which Mason had drafted in 1776.
On the nagging issue of slavery, Mason walked a fine line. Although a slaveholder himself, he found slavery repugnant for a variety of reasons. He wanted to ban further importation of slaves from Africa and prevent slavery from spreading to more states. However, he did not want the new federal government to be able to ban slavery where it already existed, because he anticipated that such an act would be difficult and controversial.
George Mason's sixth child, christened Sarah Eilbeck Mason but fondly known as Sally, was born on December 11, 1760 and married in 1778. She had ten children with her husband Daniel McCarty, Jr. before dying on September 11, 1823. The seventh of the Mason children was another girl, Mary Thomson Mason. She was born on January 24, 1764, and married John Travers Cooke on November 18, 1784, with whom she had ten children before dying in 1806. John Mason was Mason's eighth child, being born on April 4, 1766. He married Anna Marie Murray on February 14, 1796, had ten children, and died on March 19, 1849. The ninth child was a daughter named Elizabeth Mason. She was born on April 19, 1768 and died sometime between 1792 and June of 1797. She married William Thornton in 1789 and they had two children. The tenth child, Thomas Mason, was born on May 1, 1770 and died on September 18, 1800. He married Sarah Barnes Hooe on April 22, 1793 and the two had four children together.
George Mason's last two children were James and Richard Mason; twins who were born in December, 1772 but died six weeks later. Their mother died three months later on March 9, 1773 due to complications. George Mason remarried on April 11, 1780 but did not have any children with his new wife, Sarah Brent. George Mason also suffered from the condition known as gout for a large part of his life, and in accordance with current medical treatment, relied upon bloodletting.
Mason had virtually no formal schooling and essentially educated himself from his uncle's library.
Mason was appointed in 1786 to represent Virginia as a delegate to a Federal Convention, to meet in Philadelphia for the purpose of revising the Articles of Confederation. He served at the Federal Convention in Philadelphia from May to September 1787 and contributed significantly to the formation of the Constitution. "He refused to sign the Constitution, however, and returned to his native state as an outspoken opponent in the ratification contest." One objection to the proposed Constitution was that it lacked a "declaration of rights". As a delegate to Virginia's ratification convention, he opposed ratification without amendment. Among the amendments he desired was a bill of rights. This opposition, both before and during the convention, may have cost Mason his long friendship with his neighbor George Washington, and is probably a leading reason why George Mason became less well-known than other U.S. founding fathers in later years. On December 15, 1791, the U.S. Bill of Rights, based primarily on George Mason's Virginia Declaration of Rights, was ratified in response to the agitation of Mason and others.
At the convention, Mason was one of the five most frequent speakers. Mason believed in the disestablishment of the church. Mason was a strong anti-federalist who wanted a weak central government, divided into three parts, with little power, leaving the several States with a preponderance of political power. congratulating him on victory at Boston, April 1776]]
Two of Mason's stated reasons for opposing the U.S. Constitution were seemingly contradictory: on the one hand, he said that the draft Constitution did not specifically protect the right of states to let slavery continue where it already existed, and on the other hand he also said that the draft Constitution did not allow Congress to immediately stop the importation of slaves. Mason's immediate concern was to prevent more slaves from being imported, and to prevent slavery from spreading into more states. He was not eager to ban slavery where it already existed: "It is far from being a desirable property. But it will involve us in great difficulties and infelicity to be now deprived of them."
Because of his efforts to stop the spread of slavery, and his recognition of the undesirability of slavery, some historians have said that Mason should be categorized as an abolitionist. Other historians have disagreed.
Category:1725 births Category:1792 deaths Category:18th-century American Episcopalians Category:American planters Category:British North American Anglicans Category:American people of English descent Category:Mason family Category:People from Fairfax County, Virginia Category:People from Stafford County, Virginia Category:People of Virginia in the American Revolution Category:Virginia politicians Category:Virginia lawyers Category:Virginia colonial people
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Name | Sir Mix-a-Lot |
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Background | solo_singer |
Birth name | Anthony Ray |
Born | August 12, 1963 |
Origin | Seattle, Washington, U.S. |
Genre | Hip hop |
Occupation | Rapper, record producer, songwriter |
Years active | 1985–present |
Label | Nastymix/Ichiban Records, American Recordings/Warner Bros. Records, Artist Direct/BMG Records |
Url | www.sirmixalot.com |
Sir Mix-A-Lot debuted on the Def American label, which also bought the rights of his first two albums, with Mack Daddy in 1992. Its single "Baby Got Back" was a number-one hit that went double platinum MTV aired the video for "Baby Got Back" only during evening hours because of its sexual nature. In 1993, Sir Mix-a-Lot collaborated with Seattle-based grunge group Mudhoney for the song "Freak Momma" on the Judgment Night soundtrack. Despite having taken several years off from recording, Sir Mix-a-Lot is still known to mix frequently.
In 2006, Sir Mix-a-Lot appeared as himself in the second season episode of Tom Goes to the Mayor, , in which he raps the jingle for Tom's latest commercial enterprise, a store that sells big cups. He is currently trying to make a comeback with a new label that should make its release at the end of 2011.
Sir Mix-a-Lot provides narration and commentary in Wheedle's Groove, a 2009 documentary about the Seattle '60s/'70s funk and soul scene.
Category:1963 births Category:Living people Category:African American rappers Category:People from Seattle, Washington Category:Grammy Award winners Category:rappers from Washington (U.S. state)
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Name | Alison Gertz |
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Birth name | Alison L. Gertz |
Birth date | February 27, 1966 |
Birth place | Manhattan, New York |
Death date | August 08, 1992 |
Death place | Manhattan, New York |
Alison Gertz (February 27, 1966 – August 8, 1992) was a prominent AIDS activist in the late 1980s and early 1990s, who died from AIDS related complications in 1992.
During Gertz' time as an activist, she was voted Woman of the Year by Esquire magazine, received the Secretary's Award for Excellence in Public Service from the United States Department of Health and Human Services, and a based on her life starring Molly Ringwald was released.
Gertz died of complications arising from AIDS on August 8, 1992. She was 26 years old.
Alison Gertz was referred to in the song "Life Support" from the rock opera RENT. At the beginning of the song, various members of the group say their names. Jonathan Larson used the names of his HIV-positive friends as the characters in this song. At the beginning of the song, the character who refers to herself as "Ali" was named after Gertz.
Category:1966 births Category:1992 deaths Category:AIDS activists Category:AIDS-related deaths in New York Category:Horace Mann School alumni Category:People from Manhattan Category:American health activists
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