Name	Pristina
Official name	PristinaPrishtina / PrishtinëПриштина / Priština
Settlement type	Municipality and city
Other name
Image seal	Prishtina-Kosovo.jpg
Pushpin map	Kosovo
Pushpin label position	above
Pushpin map caption	Location in Kosovo
Coordinates region	RS-KM
Subdivision type	Country
Subdivision name	Kosovo/Serbia
Subdivision type1	District
Subdivision name1	District of Pristina
Subdivision name2
Established date
Area total km2	854
Area land km2
Area metro sq mi
Population as of	2006
Population total	198.214
Population density km2	661
Population density urban sq mi
Timezone	CET
Utc offset	+1
Timezone dst	CEST
Utc offset dst	+2
Elevation footnotes
Elevation m	652
Elevation ft
Postal code type
Postal code	10000
Area code	+381 38
Website	Municipality of Pristina
Footnotes	}}

Pristina, also spelled Prishtina (Serbian: Приштина or Priština, or ''Prishtina''; ) is the capital and largest city of Kosovo. It is the administrative centre of the homonymous municipality and district.

It is estimated that the current population of the city stands between 500,000 and 600,000. Preliminary results of 2011 census puts population of Pristina at 200.000 The city has a majority Albanian population, alongside other smaller communities including Bosniaks, Roma and others. It is the administrative, educational, and cultural centre of Kosovo. The city is home to the University of Pristina and is served by the Pristina International Airport.

Name

The name of the city is derived from a Slavic form *''Prišьčь'', a possessive adjective from the personal name *''Prišьkъ'', (preserved in the Kajkavian surname ''Prišek'', in the Old Polish personal name ''Przyszek'', and in the Polish surname ''Przyszek'') and the derivational suffix ''-ina'' 'belonging to X and his kin'. The name is most likely a patronymic of the personal name *''Prišь'', preserved as a surname in Polish ''Przysz'' and Sorbian ''Priš'', a hypochoristic of the Slavic personal name ''Pribyslavъ''. A false etymology connects the name Priština with Serbo-Croatian ''prišt'' (пришт), meaning 'ulcer' or 'tumour', referring to its 'boiling'. However, this explanation cannot be correct, as Slavic place names ending in ''-ina'' corresponding to an adjective and/or name of an inhabitant lacking this suffix are built from personal names or denote a person and never derive, under these conditions, from common nouns (SNOJ 2007: ''loc. cit.''). The inhabitants of this city call themselves ''Prishtinali'' in local Gheg Albanian or ''Prištevci'' (Приштевци) in the local Serbian dialect.

Geography

Pristina is located at the geographical coordinates 42° 40' 0" North and 21° 10' 0" East and covers . It lies in the north-eastern part of Kosovo close to the Goljak mountains. From Pristina there is a good view of the Šar Mountains which lie several kilometres away in the south of Kosovo. Pristina is located beside two large towns, Obilić and Kosovo Polje. In fact Pristina has grown so much these past years that it has connected with Kosovo Polje. Lake Badovac is just a few kilometres to the south of the city.

There is no river passing through the city of Pristina now but there was one that passed through the centre. The river flows through underground tunnels and is let out into the surface when it passes the city. The reason for covering the river was because the river passed by the local market and everyone dumped their waste there. This caused an awful smell and the river had to be covered.

The river now only flows through Pristina's suburbs in the north and in the south.

Climate

Pristina has a humid continental climate with very warm summers and cold and often snowy winters.

History

Early history

In Roman times, a large town called ''Ulpiana'' existed 15 kilometers (9 miles) to the south of modern-day Pristina. This city was destroyed but was restored by the Emperor Justinian I. Today the town of Lipljan stands on the site of the Roman city, and remains of the old city can still be seen.

After the fall of Rome, Pristina grew from the ruins of the former Roman city. The city was located at a junction of roads leading in all directions throughout the Balkans. For this reason Pristina rose to become an important trading centre on the main trade routes across south-eastern Europe.

Pristina came to be of great importance to the medieval Serbian state, and served as the capital of King Milutin (1282–1321) and other Serbian rulers from the Nemanjić and Branković dynasties until the Battle of Kosovo in 1389, when an invading Ottoman army decisively defeated the Balkans coalition army. In the following decades the area gradually came under Ottoman control, there was an Ottoman law-court in Pristina in 1423. The whole of Serbia was subsequently conquered by the Ottoman Empire in 1459.

Pjeter Bogdani, who is the most original writer of early literature in Albanian, lived and worked in Kosovo. After his return to the Balkans in March 1686 and spent the next years promoting resistance to the armies of the Ottoman Empire, in particular in Kosovo. In 1686 Pristina was briefly liberated by Pjeter Bogdani with aid of Austrians. He published his book ''Cuneus Profetarum'' (Alb: ''Ceta e Profeteve'' roughly ''Vanguard of the Prophets'') in 1685. At the same time, simultaneously with the Ottoman conquest, the Great Serb exodus has started; tens of thousands of Kosovo Serb families have withdrawn from Kosovo towards Habsburg Empire, led by their patriarch Arsenije III Carnojevic, along with the Habsburg army. Demographic balanced slowly started to shift in favour of Albanians.

During the Ottoman Empire, Pristina became increasingly Ottoman in character following the conversion to Islam of many of its inhabitants, both Albanians and Slavs.

From the 1870s onwards Albanians in the region formed the League of Prizren to resist Ottoman rule, and a provisional government was formed in 1881. In 1912 Pristina along with the rest of Kosovo was briefly included in the newly independent state of Albania. But the following year the Great Powers forced Albania to cede the region to the Kingdom of Serbia. In 1918 Kosovo became a part of the newly formed Yugoslavia, though without any of the autonomy that the region later enjoyed.

Before World War II, Pristina was an ethnically mixed town with large communities of Albanians and Serbs. However, a mass series of both ethnic cleansing and genocide perpetrated by ethnic Albanians backed by the Nazis swung this largely in the Albanian's favour.

Before the 1999 war over 25,000 Serbs lived in Pristina, as a result of a post war ethnic cleansing, there is anything from several dozen to several thousand.

Balkan Wars

After the Serbian army took the city of Pristina in October 1912, the retaliation against the civilian population was fierce. Reports say that immediately upon entering the city, the Serbian army began "hunting" the Albanians, making bloodshed and "literally decimated" Pristina population.

Number of Albanians of Pristina killed in the early days of the Serbian rule is estimated at 5,000.

World War II

The Second World War saw the decline of Pristina's Serbian community as well as a large-scale settling of Albanians in the town. Between 1941 and 1945 Pristina was incorporated into the Italian-occupied Greater Albania.

Pristina after World War II

In 1946, Pristina became the capital of the Socialist Autonomous Region of Kosovo. Between 1953 and 1999, the population increased from around 24,000 to over 300,000. All of the national communities of the city increased over this period, but the greatest increase was among the Albanian population, a large number of whom had moved from mountain areas to settle in the city. The Albanian population increased from around 9,000 in 1953 to nearly 76,000 in 1981. The Serbian and Montenegrin population increased too but by a far more modest number, from just under 8,000 in 1953 to around 21,000 by 1981. By the start of the 1980s, Albanians constituted over 70% of the city's population.

Although Kosovo was under the rule of local Albanian members of the Communist Party, economic decline and political instability in the late 1960s and at the start of the 1980s led to outbreaks of nationalist unrest. In November 1968, student demonstrations and riots in Belgrade spread to Pristina, but were put down by the Yugoslav security forces. Some of the demands of the students were nonetheless met by the Tito government, including the establishment in 1970 of the University of Pristina as an independent institution. This ended a long period when the institution had been run as an outpost of Belgrade University and gave a major boost to Albanian-language education and culture in Kosovo. The Albanians were also allowed to use the Albanian flag.

In March 1981, students at Pristina University rioted over poor food in their university canteen. This seemingly trivial dispute rapidly spread throughout Kosovo and took on the character of a national revolt, with massive popular demonstrations in Pristina and other Kosovo towns. The Communist Yugoslav presidency quelled the disturbances by sending in riot police and the army and proclaiming a state of emergency, with several people being killed in clashes and thousands subsequently being imprisoned or disciplined.

Pristina in the Kosovo War and afterwards

Following the reduction of Kosovo's autonomy by Serbian President Slobodan Milošević in 1989, a harshly repressive regime was imposed throughout Kosovo by the Serbian government with Albanians largely being purged from state industries and institutions. The University of Pristina was seen as a hotbed of Albanian nationalism and was duly purged: 800 lecturers were sacked and 22,500 of the 23,000 students expelled. In response, the Kosovo Albanians set up a "shadow government" under the authority of the Democratic League of Kosovo (LDK), led by the writer Ibrahim Rugova. Although the city was formally controlled by Serbs appointed by the Milošević government, the LDK established parallel structures, funded by private contributions, to provide free services such as health care and education that were largely denied to the Albanian population.

The LDK's role meant, that when the Kosovo Liberation Army began to attack Serbian and Yugoslav forces from 1996 onwards, Pristina remained largely calm until the outbreak of the Kosovo War in March 1999. The city was placed under a state of emergency at the end of March and large areas were sealed off. After NATO began air strikes against Yugoslavia on March 24, 1999, widespread violence broke out in Pristina. Serbian and Yugoslav forces shelled several districts and, in conjunction with paramilitaries, conducted large-scale expulsions of ethnic Albanians accompanied by widespread looting and destruction of Albanian properties. Many of those expelled were directed onto trains apparently brought to Pristina's main station for the express purpose of deporting them to the border of the Republic of Macedonia, where they were forced into exile. The United States Department of State estimated in May 1999 that between 100,000-120,000 people had been driven out of Pristina by government forces and paramilitaries.

|War Crimes Indictment against Milosevic and others}}

Several strategic targets in Pristina were attacked by NATO during the war, but physical damage appears to have largely been restricted to a few specific neighbourhoods shelled by Yugoslav security forces. At the end of the war, most of the city's 40,000 Serbs fled. The few who remained were subjected to harassment and violence in revenge by Albanian gangs, which reduced Pristina's Serb population still further. Other national groups accused by Albanians of collaboration with the Serbian war effort; notably the Roma– were also driven out. According to the United Nations High Commissioner for Refugees, by August 1999 fewer than 2,000 Serbs were left in the city. The number reportedly fell even further after the March 2004 unrest in Kosovo.

Economy

The number of registered businesses in Pristina is currently at 8,725, with a total of 75,089 employees. The exact number of businesses is unknown due to the fact that not all are registered. Since independence the Mayor of Pristina, Isa Mustafa has built many new roads in Pristina. Also he has plans to construct a ring road around the city. The national government is taking part in modernising the roadways as well, building motorways to Uroševac and other cities. An Albanian millionaire in Croatia is building the largest building in the Balkans with a projected height of up to and capacity to hold 20,000 people. The cost for this is 400 million Euro. The Lakriste area is designated by Municipality as high-rise area with many complex building. The buildings such as ENK, World Trade Centre, Hysi and AXIS towers are being constructed in an area which previously served as an industrial zone.

Limak Holding and French firm Aéroport de Lyon won the concession tender for Pristina International Airport. Two companies pledged investment of 140 million euros by 2012.

Places around Pristina

{| style="width:100%;" class="wikitable" |- ! style="width:8%;"| Name ! style="width:24%;"| Description ! style="width:8%;"| Picture |- | style="text-align:center;"|New Born ||align="left"|The Newborn Obelisk inaugurated for Kosovo's Independence on the 17/02/2008.|| style="text-align:center;"| |- | style="text-align:center;"|Rilindja Tower||align="left"|The building of the former "Rilindja" newspaper, also the tallest in Pristina.|| style="text-align:center;"| |- | style="text-align:center;"|UNMIK Headquarters||align="left"|United Nations Interim Administration Mission in Kosovo Headquarters|| style="text-align:center;"| |- | style="text-align:center;"|Mother Teresa Boulevard||align="left"|The Mother Teresa Boulevard.|| style="text-align:center;"| |- | style="text-align:center;"|The Ministry of Culture||align="left"|The Ministry of Culture|| style="text-align:center;"| |- | style="text-align:center;"|OSCE Building||align="left"|OSCE Building|| style="text-align:center;"| |- | style="text-align:center;"|The museum of Kosovo||align="left"|The Kosovo Museum has an extensive collection of archaeological and ethnological artifacts, including the Neolithic ''Goddess on the Throne'' terracotta, unearthed near Pristina in 1960|| style="text-align:center;"| |- | style="text-align:center;"|City Stadium||align="left"|Home to football club, KF Prishtina|| style="text-align:center;"| |}

Culture

The Museum of Kosovo is located in an Austro-Hungarian inspired building originally built for the regional administration of the Ottoman Vilayet of Kosovo. From 1945 until 1975 it served as headquarters for the Yugoslav National Army. In 1963 it was sold to the Kosovo Museum. From 1999 until 2002, the European Agency for Reconstruction had its main office in the museum building.

The Kosovo Museum has an extensive collection of archaeological and ethnological artifacts, including the Neolithic ''Goddess on the Throne'' terracotta, unearthed near Pristina in 1960 and depicted in the city's emblem. Although a large number of artifacts from antiquity is still in Belgrade, even though the museum was looted in 1999.

The Clock Tower (''Sahat Kulla'') dates back to the 19th century. Following a fire, the tower has been reconstructed using bricks. The original bell was brought to Kosovo from Moldavia. It bore an inscription reading "this bell was made in 1764 for ''Jon Moldova Rumen''." In 2001, the original bell was stolen. The same year, French KFOR troops replaced the old clock mechanism with an electric one. Given Kosovo's electricity problems the tower is struggling to keep time.

Environment

left|thumb|View from city centerthumb|right|Pristina City Park City Park was a badly managed, and was the only real green place in Pristina. Three markets (one of them very large) used to be a hotspot for dumping waste and other materials on the roads.

After the war of 1999, Pristina has changed dramatically. City Park has been fully changed. It now has stone pathways, tall trees, flowers have been planted and a public area has been built for children. The much larger Gërmia Park, located to the east of the city is the best place for a family to go and relax. Restaurants, small paths for people to have a run and a large outdoor swimming pool, basketball and volleyball court have been built for the pleasure of the citizens. Lately a new green place called Tauk Bashqe has been made half way between Gërmia and City Park.

After the construction of the new Mother Teresa Square, many trees and flowers have been planted. This had a big impact on the city because of the trees releasing oxygen in the air. Many old buildings in front of the government building have been cleared to provide open space.

Education

Universities

AAB University

American University in Kosovo

Iliria Royal University

University of Pristina

Sport

Basketball has been, since 2000, one of the most popular sports in Pristina. In this sport Pristina is represented in the Basketball National League by two teams. Streetball Kosova is a traditionally organized sport and cultural event in Germia Lake in Pristina, since Year 2000, too. Football is also very popular. Pristina's representatives KF Prishtina play their home games in the city's stadium.

Handball is also very popular. Pristina's representatives are recognised internationally and play international matches.

Demographics

Ottoman Empire

The Ottomans started conducting census surveys in Rumelia in 1486. Approximate populations reported were:

1486: 392 families

1487: 412 Christian households and 94 Muslim households

1569: 692 families

1669: 2,060 families

1685: 3,000 families

1689: 4,000 families

From 1850, surveys were conducted in the Vilayet of Kosovo. Populations reported were:

1850: 12,000 citizens, in 3,000 families

1902: 18,000 citizens, in 3,760 families

Serbia and Kingdom of Yugoslavia

The 1921 official population census conducted by the Kingdom of Serbs, Croats and Slovenes listed 14,338 citizens.

The 1931 official population census organised by the Kingdom of Yugoslavia listed 18,358 inhabitants by mother languages:

:* Turkish - 7,573 (''41%'') :* Serbian - 5,738 (''31%'') :* Albanian - 2,351 (''13%'') :* ''other languages'' (Romani, Circassian etc.) - 2,651 (''14%'')

Socialist Yugoslavia

The 1948 official population census of the Autonomous Province of Kosovo and Metohija organised by the government of the People's Republic of Serbia under the Federal People's Republic of Yugoslavia government recorded 19,631 citizens in 4,667 families.

The 1953 official population census of the Autonomous Province of Kosovo and Metohija organised by the government of Serbia under the Yugoslav government recorded 24,229 citizens: :* 9,034 Albanians (''37%'') :* 7,951 Serbs and Montenegrins (''33%'') :* 4,726 Turks (''20%'') :* 2,518 Roma and ''others'' (''10%'')

The 1961 official population census of the Autonomous Province of Kosovo and Metohija organised by the government of the Socialist Republic of Serbia under the Socialist Federal Republic of Yugoslavia government recorded 38,593 citizens in 9,095 families: :* 19,060 Albanians (''49%'') :* 14,695 Serbs and Montenegrins (''38%'') :* 404 Croats (''1%'') :* 195 Roma

The 1971 official population census of the Socialist Autonomous Province of Kosovo organised by the government of the Socialist Republic of Serbia under the Socialist Federal Republic of Yugoslavia government 69,514 citizens in 14,813 families: :* 40,873 Albanians (''59%'') :* 19,767 Serbs and Montenegrins (''28%'') :* 4,119 Roma (''6%'')

The 1981 official population census of the Socialist Autonomous Province of Kosovo organised by the government of the Socialist Republic of Serbia under the Socialist Federal Republic of Yugoslavia government 108,083 citizens in 21,017 families: :* 75,803 Albanians (''70%'') :* 21,067 Serbs and Montenegrins (''19%'') :* 5,101 Roma (''5%'') :* 2,504 Muslims (''2%'')

According to the last census in 1991 (boycotted by the Albanian majority), the population of the Pristina municipality was 199,654, including 77.63% Albanians, 15.43% Serbs and Montenegrins, 1.72% Muslims by nationality, and others. This census cannot be considered accurate as it is based on previous records and estimates.

In 2004 it was estimated that the population exceeded half a million, and that Albanians form around ''98%'' of it. The Serbian population in the city has fallen significantly since 1999, many of the city's Serbs having fled or been expelled following the end of the war. In early 1999 Pristina had about 230,000 inhabitants. There were more than 40,000 Serbs and about 6,500 Romas with the remainder being Albanians.

{|border="2" cellspacing="0" cellpadding="4" rules="all" style="width:75%%; clear:all; margin:5px 0 1em 1em; border-style:solid; border-width:1px; border-collapse:collapse; font-size:95%; empty-cells:show;" |- |colspan="10" align=centre style="background:#778899; color:white;"|Ethnic Composition, Including IDPs¹ |- style="background:#ffebcd;" !Year !Albanians ! % !Serbs ! % !Roma ! % !Others² ! % !Total |- style="background:#f5f5f5;" |1991 census³ | 161,314 | 78.7 | 27,293 | 13.3 | 6,625 | 3.2 | 9,861 | 4.8 | 205,093 |- style="background:#fffaf0;" |1998⁴ | N/A | N/A | N/A | N/A | N/A | N/A | N/A | N/A | 225,388 |- style="background:#f5f5f5;" |February 2000 estimate⁵ | 550,000 | 97.4 | 12,000 | 2.2 | 1,000 | 0.1 | 1,800 | 0.3 | 564,800 |- | colspan="10" style="text-align:left; background:#ffebcd;"|Source: , June 2006, page 2 (Table 1.1). 1. IDP: Internally displaced person. 2. Others include Montenegrins, Muslim Slavs, Turks, etc. 3. 1991 figures from Federal Republic of Yugoslavia (FRY) Institute for Statistics. It is noted that the 1991 census was highly politicised and is thus unreliable. 4. 1999 figures from UNHCR, "Kosovo Village List", 9 March 1999 (1998 population estimate excluding forced displacement). 5. 2001 figures from KFOR – MNB (c) and for minority figures OSCE/UNHCR ‘Situation of Ethnic Minorities in Kosovo’, February 2001. |}

International relations

Twin towns — Sister cities

	town twinning>twinned with:	* Ankara, Turkey.	* Bursa, Turkey.	* Durrës, Albania.	* Tirana, Albania.	* Karachi, Pakistan.

See also

District of Pristina

Kosovo War

University of Pristina

Bregu i Diellit

Pristina City Stadium

Pristina International Airport

References

External links

Pristina In Your Pocket city guide

University of Pristina

Pristina Airport

Interactive map of Pristina

.

Category:Capitals in Europe Pristina Category:Gegëri Category:Municipalities of Kosovo

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name	James Blunt
background	solo_singer
birth name	James Hillier Blount
born	February 22, 1974Tidworth, Wiltshire, England, UK
instrument	Vocals, guitar, piano, keyboards, violin
genre	Pop rock, soft rock, folk rock, Brit-pop
occupation	Singer-songwriter, musician
years active	2004 – present
label	Warner Bros. Records, Atlantic, Custard
notable instruments	Seagull acoustic guitars
website	}}

James Hillier Blount (born 22 February 1974), better known by his stage name James Blunt, is an English singer-songwriter and musician, and former army officer, whose debut album, ''Back to Bedlam'' and single releases, including "You're Beautiful" and "Goodbye My Lover", brought him to fame in 2005. His repertoire can be best described as a mix of acoustic-tinged pop, rock and folk. After recording on the independent American label Custard Records, Blunt won two BRIT Awards, two Ivor Novello Awards, and by 2006 was nominated for five Grammy Awards. The following year, he released his second album ''All the Lost Souls'' (2007). Blunt's third studio album, ''Some Kind of Trouble'', was released in November 2010. Worldwide, Blunt has sold over 15 million albums, and his debut album, ''Back to Bedlam'', is the best-selling album of the 2000s in the UK.

Blunt was an officer in the Life Guards, a Cavalry regiment of the British Army, and served under NATO in Kosovo during the conflict there in 1999. While posted to Kosovo, Blunt was introduced to the work of Médecins Sans Frontières (MSF or "Doctors Without Borders"). Since then, Blunt has supported MSF by holding meet-and-greet auctions at many of his concerts. As of 4 October 2009 Blunt's primary residence is on the Spanish island of Ibiza.

Early life

James Blunt was born at an army hospital in Tidworth, Wiltshire, England; the first child born to Jane A.F. ( Amos) and Charles Blount. James spent his early childhood living in England, Cyprus, and Germany, where his father, a Colonel in the British Army Air Corps, and military helicopter pilot, was posted at various times.

James Blunt has two younger siblings. The Blount family has a long history of military service, dating from the 10th century.His father instilled in him a love of flying, and he earned his pilot's licence at age 16.He has a keen interest in motorcycles after learning to ride when he was 16.

Education

Blunt was educated at two independent schools: at the age of seven, he was enrolled at Elstree School in Woolhampton in Berkshire, before continuing to Harrow School in Harrow on the Hill in north-west London (Elmfield House) on an army bursary. From Harrow School he gained an army-sponsored place at the University of Bristol, where he first studied Aerospace Manufacturing Engineering and then subsequently moved on to the study of Sociology. He graduated with a BSc(Hons) in Sociology in 1996.

Military service

Because the British Army sponsored his university education, Blunt was obliged to serve a minimum of four years in the armed forces. James stated on an interview in his ''Back to Bedlam'' sessions that he chose to join the military as "his Father was pushing for it, so that Blunt could obtain a secure work placement and income". Blunt trained at the Royal Military Academy Sandhurst. He was commissioned as a second lieutenant in the Life Guards, a unit of the Household Cavalry, where he rose to the rank of captain. One of his first assignments was to British Army Training Unit Suffield in Alberta, Canada, where his battalion was posted for six months in 1998 to act as the opposing army in combat training exercises.

In 1999, he served as an armoured reconnaissance officer in the NATO deployment in Kosovo. Initially assigned to reconnaissance of the Macedonia-Yugoslavia border, Blunt and his unit worked ahead of the front lines directing forces and targeting Serb positions for the NATO bombing campaign. His unit was given the assignment of securing the Pristina International Airport in advance of the 30,000-strong peacekeeping force; the Russian army had moved in and taken control of the airport before his unit's arrival. According to Blunt's own account of the incident he refused to follow orders from NATO command to attack the Russians. There were less intense moments during Blunt's Kosovo assignment, however. Blunt had brought along his guitar, strapped to the outside of his tank. At some places, the peacekeepers would share a meal with hospitable locals, and Blunt would perform. It was while on duty there that he wrote the song "No Bravery".

A keen skier, Blunt captained the Household Cavalry Alpine Ski Team in Verbier, Switzerland, eventually becoming champion skier of the entire Royal Armoured Corps. He had extended his military service in November 2000, and after an intensive six-month army riding course was posted to the Household Cavalry Mounted Regiment in London, England. During this posting, Blunt was interviewed about his responsibilities on the television programme "Girls on Top", a series highlighting unusual career choices. He stood guard at the coffin of the Queen Mother during the days of her lying in State and was part of the funeral procession on 9 April 2002. Blunt left the army on 1 October 2002 having served six years.

Music career

Early career

Blunt took piano and violin lessons as a child, but his first significant exposure to popular music was at Harrow School. There, he was introduced to the guitar by a fellow student, and started playing guitar and writing songs at age 14. At University of Bristol, his undergraduate thesis was ''The Commodification of Image – Production of a Pop Idol''; one of his main references for the thesis was Simon Frith, a sociologist and rock critic, and current chair of the Mercury Music Prize.

Blunt left the British Army in 2002 so that he could pursue his musical career. It was at that period of time that he started using the stage name "Blunt", in part to make it easier for others to spell; "Blount" is pronounced the same way, and remains his legal surname. Shortly after leaving the Army, he was signed to EMI music publishers, and to Twenty-First Artists management. A record contract remained elusive however, with recording label executives pointing to Blunt's "posh" speaking voice as a barrier in class-divided Britain. Linda Perry, who was just launching her own Custard Records label in early 2003, heard Blunt's promotional tape when visiting London, and soon after heard him perform live at the South by Southwest Music Festival. She made an offer to him the same night and within a few days, Blunt signed a recording contract with Perry, and one month later he was in Los Angeles working with producer Tom Rothrock.

''Back to Bedlam''

Blunt recorded ''Back to Bedlam'' in 2003 with producer Tom Rothrock at Rothrock's home studio, using session musicians and performing on many different instruments himself. While in Los Angeles, he lodged with actress Carrie Fisher, whom he had met through the family of a former girlfriend. Fisher was very supportive of Blunt's aspirations, suggesting the name of the album and providing use of a bathroom in her home for Blunt to record the song "Goodbye My Lover". ''Back to Bedlam'' was finally released in the UK in October 2004. Blunt's debut single in the UK was "High" (co-written with Ricky Ross of Deacon Blue). This song initially peaked below the Top 100 of the UK Singles Chart, however after the subsequent success of "You're Beautiful" it finally made the Top 75 before eventually being re-released. However, the song was chosen to appear in a Vodafone commercial in Italy, and was a Top 10 hit in that country.

The debut album from the unknown Blunt initially attracted little critical attention, and there were no published reviews from major UK music journals. His live performances, mainly in support of better known musicians, received somewhat mixed but generally favourable reviews. Blunt's lack of performing experience and inconsistent approach with audiences was commented upon, while his music was likened to that of Damien Rice and David Gray. In March 2004, with Blunt performing in the support role for Katie Melua in Manchester, Alex McCann of ''Designer Magazine'' wrote, "Blunt's ascendance is a dead cert and this time next year it isn't that far removed from reality to suggest that a number 1 album, Brit Award and countless accolade's [sic] will be his for the taking." After release of the album, Concert support slots for Elton John and Lloyd Cole and the Commotions in late 2004 and early 2005 followed, as did a band residency at London club 93 Feet East. In March 2005, his second single, "Wisemen," was released.

Blunt's third single "You're Beautiful" was his break-out hit. The song debuted at number 12 in the UK, and rose all the way to the number one position six weeks after its debut. The song also received massive airplay in the UK, which helped propel ''Back to Bedlam'' to number one on the UK Albums Chart. The extensive airplay ultimately led to Blunt and his co-writers being awarded the Ivor Novello Award for Most Performed Work. After the success of "You're Beautiful" in the UK, the song crossed over to mainland Europe, becoming one of the biggest hits of summer 2005 across the continent. In the U.S., "You're Beautiful" made its debut in the summer of 2005 on WPLJ, a prominent radio station in New York City, despite not having been released to radio yet. Once the song was released to radio stations in the fall of 2005, the song climbed into the Top 10 in three radio formats: Adult Contemporary Music, Hot Adult Top 40 Tracks, and Adult album alternative. Blunt became the first British artist to top the American singles chart in nearly a decade when his song "You're Beautiful" reached number one on the Billboard Hot 100 in 2006; the last British artist to do so had been Elton John in 1997 with the song "Candle in the Wind 1997". "Goodbye My Lover" was released as the fourth UK single from the album in December 2005, and was later the second US single. The songs "High" and "Wisemen" were subsequently re-released in 2006. Blunt started off 2006 celebrating five BRIT Award nominations, going on to win Best British male solo artist and Best pop act categories, having already started an 11-month tour that would take him around the world.

There was extensive promotion in the United States starting in the autumn of 2005, with Blunt making appearances on ''The Oprah Winfrey Show'' and as a musical guest on ''Saturday Night Live''. Eight of the songs on the album were featured in television shows (''The O.C.'', ''Grey's Anatomy'' and many more), films (''Undiscovered''), and advertising campaigns (Hilton Hotels, Sprint telecommunications) throughout 2005 and 2006. Blunt performed "You're Beautiful" at the 49th Grammy Awards in February 2007, dedicating the song to the late Ahmet Ertegün of Atlantic Records, but he did not win in any of the five categories for which he had received nominations (includes one for Best New Artist Grammy, but lost to Carrie Underwood).

The album eventually sold 11 million copies and topped the album charts in 16 territories worldwide. It sold 2.6 million in the U.S. and was certified 2x platinum. In Britain the album was certified 10x platinum, sold over three million copies, and entered the ''Guinness Book of World Records'' for the fastest selling album in one year. In 2005, Blunt performed in 90 live shows, mainly across the UK and Europe, ending the year supporting Jason Mraz in a North American tour. The "Back to Bedlam World Tour" started off in January 2006, covering cities in Europe, the UK, Australia, New Zealand, and Japan, as well as three separate headline tours in North America, ending in November of that year. Not including promotional appearances, Blunt performed over 140 live shows in 2006. He enjoys the touring experience, saying in July 2006 that he and his band were having the time of their lives going to new places every day. The videos for all of Blunt's singles released from ''Back To Bedlam'' feature symbolism and dark imagery. In the first video for "High", he is buried in a desert. In the first video for "Wisemen", he is kidnapped and taken hostage. In the video for "You're Beautiful", he alludes to suicide by jumping off a cliff into the sea. In the "Goodbye My Lover" video, he is the outsider in a love triangle, imagining the couple, a man and woman (played by Matt Dallas of ''Kyle XY'' and Mischa Barton of ''The O.C.'') together. The re-release video for "High" features Blunt running in a forest. The re-release video for "Wisemen" has Blunt burning identification papers, and then walking through a forest while he is on fire.

Blunt appeared on an episode of ''Sesame Street'' which aired on 14 November 2007, singing about triangles to the tune of "You're Beautiful".

A parody of "You're Beautiful" titled "You're Pitiful" was recorded by Weird Al Yankovic. Blunt gave personal permission for this parody to be included on a Weird Al album, but Atlantic Records, Blunt's label, stepped in to forbid the commercial release of the song. Weird Al has since made the song available as a free MP3 download on his website. In a request by Yankovic to include the song on an upcoming compilation CD, Blunt's manager replied via email, "Thanks for your email, but both James and I will never approve this parody to be released on any label."

On 28 December 2009, BBC Radio 1 announced that ''Back to Bedlam'' was the biggest selling album of the noughties decade in the United Kingdom.

''All the Lost Souls''

Blunt's second studio album, ''All the Lost Souls'', was released on 17 September 2007 in the United Kingdom and one day later in North America. It sold 65,000 units in its first week, and was certified gold in the UK after only four days. By the end of January 2008, the album had sold 600,000 copies in the UK, and 4.5 million copies internationally. Blunt completed the album's songs at his home in Ibiza in the winter of 2006–2007. He performed five of the ten album tracks during his 2005–2006 tours; lyrics, melodies, and harmonies were refined for the studio recording, on which his touring band played and Tom Rothrock worked as producer.

While Blunt’s first album received very little critical attention, critics from every major music publication, and newspapers around the world, weighed in on ''All the Lost Souls''. The album maintains a 53/100 rating at ''Metacritic'', which the website describes as "mixed or average reviews." Eric Danton, of the ''Milwaukee Journal Sentinel'' and ''The Hartford Courant'' wrote that the album is "a collection so bland, it makes hardtack seem sumptuous", while ''Rolling Stone'' said that the album contains "forgettable ballads that make Coldplay seem like the Arctic Monkeys." Yet, in her review of the album, Kerri Mason of ''Billboard'' said Blunt "shows the abandon and confidence of a long-term artist, not just a one-hit wonder". And of the album, Mason wrote, "there is not a misstep throughout". Equally effusive, Liz Hoggard of ''The Observer'' wrote that "it’s impossible to resist Blunt’s troubadour yearning.”

The first single from ''All the Lost Souls'', "1973", was inspired by Blunt's nights out at Pacha, an Ibiza club, which opened in that year. The song became another hit for Blunt reaching number one the Billboard European Hot 100 Singles chart. D.J. Pete Tong remixed "1973" and played the track during his set at Pacha over the summer of 2007. The second single, "Same Mistake", was released in early December 2007 but did not fare well in the UK charts, peaking at number 57. It was Number 1 in Brazil and a hit in many South American countries. The third single from the album was "Carry You Home", released in March 2008, peaking at number 20 in the U.K charts and bringing the album back into the Top 10, six months after its release. The fourth and final single from the original "All The Lost Souls" album was "I Really Want You".

Blunt collaborated twice during this album cycle. In the end of 2007, he worked with French rapper Sinik. They released "Je Réalise", which took elements of Blunt's song "I'll Take Everything", which hit the top 3 in France. On 14 November 2008, "Primavera in anticipo", Laura Pausini new album, was released. The title track is a duet with Blunt. The album reached the Number 1 in Italy.

Throughout 2007 and 2008, Blunt went on his second world tour, including a performance in London's O2 Arena.

On 24 November 2008, ''All The Lost Souls'' was re-released as a deluxe edition, with new album artwork, new single "Love, Love, Love" and the documentary ''James Blunt: Return to Kosovo''.

''Some Kind of Trouble''

James Blunt's third studio album titled ''Some Kind of Trouble'', was released on November 8, 2010. The album debuted at #4 in the UK with over 100,000 copies sold in the first week. The album's first single "Stay the Night" was released on October 27, 2010. The single charted in the UK top 40 at number 37, and sat at Number 2 on the European Airplay Chart for 5 consecutive weeks. The second single from the album, "So Far Gone" was for released on the UK on January 3, 2011. Overall critical reception has been mixed and as of February 2011, worldwide sales stand at over one million copies, making it a commercial success. The third single from the album, "If Time Is All I Have" was released in the UK on April 4, 2011.

Personal life

Blunt says that he has become closer to his family since his musical success. His father manages his finances and his mother arranged for the purchase of his principal residence in Ibiza, where Blunt has holidayed since he was a teenager. Blunt also owns a châlet in the Swiss town of Verbier, which he purchased in February 2007, and he was named "godfather" of one of the town's new ski lifts.

Blunt was instrumental in introducing his sister to her eventual husband after offering her for "sale" on eBay. She was having difficulty obtaining transport to a funeral in Ireland, and Blunt listed her as a "damsel in distress". A person responded saying his friend had a helicopter his sister could charter, but it turned out he was in Sweden and she did not attend the funeral. But the respondent suggested she still meet up with the helicopter owner, Guy Harrison, and they began a relationship and eventually married.

The musician's social life has been the subject of significant commentary, particularly in the tabloid press. Blunt himself has found the degree of interest in his personal life to be bizarre, stating that "fame and celebrity is something that other people have constructed that I'm not really party to".

Charitable and environmental causes

Blunt has raised funds for the medical charity Médecins Sans Frontières through benefit concerts and by auctioning opportunities to meet him at his own shows. He first encountered MSF medical care workers during his tour of duty in Kosovo, and was impressed with the work they did under conditions of minimal support and limited security.

He also supports environmental causes. He screened the trailer for ''An Inconvenient Truth'' at his concerts, and for each advance sales concert ticket purchased through his designated website a tree is planted. On 7 July 2007, Blunt performed at the Live Earth concert at Wembley Stadium, London, and is the owner of one of two prototype electric cars made by Hybrid Technologies under a Space Act partnership with NASA.

As a former soldier, Blunt is a patron of Help for Heroes, a charity aiming to raise money to provide better facilities for wounded British servicemen, and has also held benefit concerts for this charity.

Blunt has also contributed with his vocals for the charity single, "Everybody Hurts" in aid of the 2010 Haiti Earthquake Appeal.

Discography

''Back to Bedlam'' (13-06-2005)

''All the Lost Souls'' (17-09-2007)

''Some Kind of Trouble'' (08-11-2010)

''James Blunt Live at Manchester Apollo'' (Jan. 2008)

''High (18-10-2004)

''Wisemen (07-03-2005)

''You're Beautiful (30-05-2005)

''Goodbye My Lover (19-12-2005)

''1973 (23-07-2007)

''Same Mistake (03-12-2007)

''Carry You Home (07-07-2008)

''I Really Want You (04-08-2008)

''Love Love Love (10-11-2008)

''Live From London EP (28-06-05)

''iTunes Live: London Festival EP (18-04-2008)

''Chasing Time: The Bedlam Sessions (Live at the BBC) (13-02-2006)

Awards

Grammy Awards

|- | rowspan=5|2007 || James Blunt || Best New Artist || |- | rowspan=3 |"You're Beautiful" || Record of the Year|| |- | Song of the Year || |- | Best Male Pop Vocal Performance || |- | ''Back to Bedlam ''|| Best Pop Vocal Album ||

;2005

MTV Europe Music Awards – Best New Act

Q Awards – Best New Act

Digital Music Awards – Best Pop Act

;2006

NRJ Music Awards (France) – Best International Newcomer

BRIT Awards – Best pop act and Best Male Vocalist

ECHO Awards (Germany) – Best International Newcomer

NME Awards – Worst Album

MTV Australia Video Music Awards – Song of the Year for ''You're Beautiful''

Ivor Novello Awards – Most Performed Work and International Hit of the Year

MTV Video Music Awards – Best Male Video and Best Cinematography

World Music Awards – Best New Artist in the World and Biggest Selling British Artist in the World

Teen Choice Awards (United States) – Choice Music Male Artist

;2008

ECHO Awards (Germany) – Best International Male Artist

;2010

Virgin Media Music Awards – The Hottest Male

;2011

Regenbogen Awards (Germany) – Best International Male Artist

References

Further reading

TV interview with ''The Hour'' on CBC

James Blunt interview and video on and ''POP''

External links

JamesBlunt.com Official James Blunt website

Category:1974 births Category:Alumni of the University of Bristol Category:British Life Guards officers Category:Custard Records artists Category:English folk singers Category:English guitarists Category:English keyboardists Category:English-language singers Category:English male singers Category:English multi-instrumentalists Category:English pianists Category:English singer-songwriters Category:BRIT Award winners Category:Ivor Novello Award winners Category:Living people Category:Military brats Category:Old Harrovians Category:People from Tidworth Category:Sandhurst graduates Category:Warner Music Group artists Category:Atlantic Records artists Category:British expatriates in Spain

ar:جيمس بلانت bn:জেমস ব্লান্ট bs:James Blunt bg:Джеймс Блънт ca:James Blunt cs:James Blunt da:James Blunt de:James Blunt et:James Blunt el:Τζέιμς Μπλαντ es:James Blunt eo:James Blunt eu:James Blunt fa:جیمز بلانت fr:James Blunt ko:제임스 블런트 hy:Ջեյմս Բլանտ hi:जेम्स ब्लंट hr:James Blunt id:James Blunt is:James Blunt it:James Blunt he:ג'יימס בלאנט kn:ಜೇಮ್ಸ್ ಬ್ಲಂಟ್ ka:ჯეიმზ ბლანტი lv:Džeimss Blants lt:James Blunt hu:James Blunt mk:Џејмс Блант nah:James Blunt nl:James Blunt ja:ジェームス・ブラント no:James Blunt nn:James Blunt pl:James Blunt pt:James Blunt ro:James Blunt ru:Блант, Джеймс sq:James Blunt simple:James Blunt sr:Džejms Blant fi:James Blunt sv:James Blunt ta:ஜேம்ஸ் பிளண்ட் th:เจมส์ บลันท์ tr:James Blunt uk:Джеймс Блант vi:James Blunt zh:詹姆仕·布朗特

Name	Rita Ora
Background	solo_singer
Birth name	Rita Sahatçiu Ora
Born	November 26, 1990 Prishtina, Republic of Kosovo
Origin	London, Greater London,United Kingdom
Instrument	Vocals
Genre	R&B;
Occupation	Musician, Singer-songwriter
Years active	2008–present
Label	Roc Nation
Associated acts	Jay-ZDrakeCraig David
Website
Notable instruments	}}

Rita Sahatçiu Ora (born November 26, 1990) is an Kosovar-born British R&B; recording artist. She is currently signed to Roc Nation.

Early life and career

Rita Ora was born in Prishtina, Republic of Kosovo, to Kosovar Albanian parents. She moved to the United Kingdom in the same year of her birth, and grew up in London. She attended and graduated Sylvia Young Theatre School and then St Charles Catholic Sixth Form College. She began singing from a very young age. She acted in the movie Spivs. She also auditioned for Your Country Needs You on BBC One for the Eurovision Song Contest and got through but later on removed herself from the competition due to the fact she did not feel ready. In 2009, Rita caught the attention of Jay-Z and he quietly signed her to Roc Nation, in which she was featured in one of the commercials for Roc Nation + Skullcandy Aviator Headphones

Music career

Guest appearances

In 2008, Rita appeared on Craig David's track entitled "''Awkward''" as well as "''Where's Your Love''" featuring Tinchy Stryder and in the music video. In 2009, Rita made a cameo on Jay-Z 's video, "''Young Forever''".

References

External links

Category:1990 births Category:Living people Category:British female singers Category:Kosovo singers Category:British people of Kosovar descent Category:British people of Albanian descent Category:Kosovar Albanians Category:Kosovar people Category:Kosovar people of Albanian descent Category:People of Albanian descent Category:People from London Category:People from Pristina

30px ''This Republic of Kosovo biographical article is a stub. You can help Wikipedia by expanding it''.

{{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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