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{{Taxobox_begin | color = violet | name = ''Human immunodeficiency virus''}}
{{Taxobox_image | image = [[Image:Aids virus.jpg|200px|]] | caption = Stylized rendering of a cross-section<br/> of the human immunodeficiency virus}}
{{Taxobox_begin_placement_virus}}
{{Taxobox_group_vi_entry}}
{{Taxobox_familia_entry | taxon = ''[[Retroviridae]]''}}
{{Taxobox_genus_entry | taxon = ''[[Lentivirus]]''}}
{{Taxobox_species_entry | taxon = '''''Human immunodeficiency virus 1'''''}}
{{Taxobox_species_entry | taxon = '''''Human immunodeficiency virus 2'''''}}
{{Taxobox_end_placement}}
{{Taxobox_end}}

'''HIV''' ('''human immunodeficiency virus''') is a [[retrovirus]] that infects cells of the human [[immune system]] (mainly CD4+ [[T cell]]s and [[macrophage]]s; vital components of the hosts immune system), and destroys or impairs their function. Infection with HIV results in the progressive depletion of the immune system, leading to "immune deficiency" and has been established as the underlying cause of [[AIDS]].

==Introduction==

The name "'''''HIV'''''" has been used since [[1986]] ([http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3010128&query_hl=23 Coffin et al., 1986]) as the name for the [[retrovirus]] that was first proposed as the cause of [[AIDS]] by [[Luc Montagnier]] of [[France]] (who initially named it '''LAV''', ''Lymphadenopathy-Associated Virus'') ([http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6189183&query_hl=6 Barre-Sinoussi ''et al''., 1983]) and by [[Robert Gallo]] of the [[United States]] (who initially named it '''HTLV-III''', ''Human T Lymphotropic Virus type III'') ([http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6200935&query_hl=9 Popovic ''et al''., 1984]).

[[Image:HIV-SIV-phylogenetic-tree.png|thumb|350px|left|Phylogenetic Tree of the SIV and HIV viruses.<br>(click on image for detailed description.)]]

HIV is a member of the genus [[lentivirus]] [http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/61060000.htm], part of the family of [[retroviridae]] [http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/61000000.htm] that are characterized by long latency periods and a [[lipid]] envelope of host-cell origin surrounding a protein/RNA core. Two species of HIV infect humans: HIV-1 and HIV-2. HIV-1 is more virulent and more easily transmitted. HIV-1 is the source of the majority of HIV infections throughout the world, while HIV-2 is less easily transmitted and is largely confined to West Africa. ([http://dx.doi.org/10.1099/vir.0.18253-0 Reeves and Doms, 2002]) Both HIV-1 and HIV-2 originated in West-Central Africa and jumped species ([[zoonosis]]) from primates to humans. HIV-1 has evolved from a [[Simian Immunodeficiency Virus]] (SIVcpz) found in the [[chimpanzee]] subspecies, Pan troglodyte troglodyte. ([http://dx.doi.org/10.1038/17130 Gao ''et al''., 1999]) HIV-2 crossed species from a different strain of SIV, this one found in [[sooty mangabey|sooty mangabeys]] (an [[Old World monkey]]) of [[Guinea-Bissau]] ([http://dx.doi.org/10.1099/vir.0.18253-0 Reeves and Doms, 2002]).

Three groups of HIV-1 have been identified according to the differences in env: M, N and O ([http://dx.doi.org/10.1016/S1473-3099(02)00343-2 Thomson et al., 2002]). Group M is the most prevalent and is subdivided into eight subtypes based upon the whole genome and are geographically distinct (Carr ''et al''., 1998). The most prevalent are subtypes B (found predominantly in North America and Europe), A, D (found predominantly in Africa) and C (found predominantly in Africa and Asia) that 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 (CRF).
[[Image:subtype.png|right|thumbnail|400px|Map showing HIV-1 subtype prevalence. The bigger the pie chart, the more infections are present]]




The first CRFs to be isolated were the AG recombinant from west and central Africa, the AGI recombinant from Cyprus and Greece, the AB recombinant from Russia and the AE virus from Southeast Asia. However, the parent subtype E of CRF01_AE has not yet been identified.

47% of infections worldwide are of subtype C, 27% are subtype A/CRF02_AG, 12.3% are subtype B, 4% are subtype D, 4% are CRF AE, and the remaining 5.7% is composed of other subtypes and CRFs. Almost 95% of all HIV research currently taking place is focused on subtype B, while few laboratories focus on subtype C ([http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=11832690&query_hl=20 Osmanov ''et al''., 2002]).

==Transmission==

HIV is transmitted through penetrative (anal or vaginal) and oral sex, [[blood transfusion]], the sharing of contaminated needles in health care settings and through drug injection, and between mother and infant during pregnancy, childbirth and breastfeeding according to a leading international health care source UN AIDS in [http://www.unaids.org/en/Resources/faq/faq_transmission.asp#7 UNAIDS transmission]. The use of physical barriers such as the [[latex]] [[condom]] is widely advocated to reduce the risk of sexual transmission of HIV. Recently, it has been proposed that male [[circumcision]] may reduce the risk of HIV transmission [http://www.newsday.com/news/nationworld/wire/sns-ap-brazil-aids-circumcision,0,7464783.story?coll=ny-hs-spotlight&track=mostemailedlink], but UNAIDS believes that it is premature to recommend male circumcision as part of HIV prevention programs. [http://www.who.int/mediacentre/news/releases/2005/pr32/en/]

[[UNAIDS]] estimated that at the end of [[2004]] there were between 36 and 44 million people around the world living with HIV, of whom 25 million were in sub-Saharan Africa. Global estimates for new HIV infection in [[2004]] were 4.3&ndash;6.4 million. ([http://www.unaids.org/wad2004/EPIupdate2004_html_en/epi04_00_en.htm AIDS epidemic update December 2004]).

The epidemic is not homogeneous within regions with some countries more afflicted than others. Even at the country level there are wide variations in infection levels between different areas. Country data indicate that the number of people living with HIV continues to rise in all parts of the world despite the fact that effective prevention strategies exist.

[[AIDS_pandemic#Sub-Saharan_Africa|Sub-Saharan Africa]] remains the hardest-hit region with extremely high HIV prevalence among [[pregnant]] women aged 15&ndash;24 reported in a number of countries. The widespread prevalence of [[sexually transmitted disease]]s (STD), the practice of [[scarification]], [[transfusion]], and the state of [[hygiene]] and [[nutrition]] in Africa may facilitate the transmission of HIV-1 in this region (Bentwich ''et al.'', 1995)). In [[2000]] the [[WHO]] estimated that 25% of the units of blood transfused in Africa were not tested for HIV and 5% to 10% of cases of HIV infection in Africa were transmitted via blood. [http://www.afro.who.int/press/2001/regionalcommittee/rc51004.html]

In [[AIDS_pandemic#Asia|Asia]], the HIV epidemic remains largely concentrated in [[injecting drug user]]s, [[men who have sex with men]], [[sex workers]], clients of sex workers and their immediate sexual partners. Effective prevention programming coverage in these populations is inadequate.

Diverse epidemics are under way in [[AIDS_pandemic#Eastern_Europe_and_Central_Asia|Eastern Europe and Central Asia]]. Injecting drug use is the main driving force behind epidemics across this region. In many high-income countries, sex between men plays an important role in the epidemic whilst drug injecting plays a varying role. In 2002, it accounted for more than 10 % of all reported HIV infections in [[AIDS_pandemic#North_America.2C_Western_and_Central_Europe|Western Europe]] and was responsible for 25% of HIV infections in [[AIDS_pandemic#North_America.2C_Western_and_Central_Europe|North America]]. In [[AIDS_pandemic#Latin_America_and_the_Caribbean| Latin America and the Caribbean]], 11 countries have an estimated national HIV prevalence of 1% or more.

==Structure==
HIV is different in structure from previously described retroviruses. It is around 120 nm in diameter (120 billionths of a meter&mdash;a red blood cell is around 60 times larger at 7 millionths of a meter)&mdash;and roughly spherical.
[[Image:HIV Viron.png|thumb|500px|right|Diagram of the HIV virus.]]

HIV-1 is composed of two copies of single-stranded [[RNA]] enclosed by a conical nucleocapsid comprised of the viral protein [[p24]], typical of [[lentivirus]]es. This is in turn surrounded by a [[plasma membrane]] of host-cell origin. The single-stranded RNA is tightly bound to the nucleocapsid proteins, NCp7 and [[enzymes]] that are indispensable for the development of the virion such as [[reverse transcriptase]], [[protease]]s and [[integrase]]. A matrix composed of an association of the viral protein p17 surrounds the capsid ensuring the integrity of the virion particle. The envelope is formed when the capsid buds from the host protein, taking some of the host-cell membrane with it. The envelope includes the glycoproteins gp120 and gp41, which are derived from the gp160 precursor. gp41 is a transmembrane protein that is covalently linked to gp120.

There are two forms of the virus:

''Immature form:'' When the virus leaves the cell it is not infectious and the inner part of the virus particle contains a spherical core (stains dark on electron micrographs). There are also spikes on the outer membrane that are the Env proteins (gp120 and gp41). Sometimes a virus can be seen during the process of budding, when it looks like a dark arc sitting under the cell membrane&mdash;this observation meant that HIV was originally classed as a type C retrovirus. The Env proteins link together in groups of three (trimers).

''Mature form:'' Once the virus protease has cleaved the Gag proteins, the core rearranges into a truncated cone (imagine a traffic cone sliced at an angle across the top) Some reports also show a small filament linking the core to the membrane. The envelope spikes are often much rarer on mature particles since they are easily dislodged. It is the mature conical core that makes HIV so easily identifiable.

HIV has several major genes coding for structural proteins that are found in all retroviruses, and several nonstructural or "accessory" genes that are unique to HIV.

===General retrovirus genes===
*''gag''. ''gag''-derived proteins make up the cone-shaped viral capsid (p24, i.e. a 24-[[Kilodalton]] protein, CA) the nucleocapsid proteins (p6 and p7, NC) and a matrix protein (p17, MA).
*''pol''. The ''pol'' gene codes for the virus enzymatically active proteins. Most important is the so-called [[reverse transcriptase]] (RT) which performs the unique reverse transcription of the viral [[RNA]] into double-stranded [[DNA]]. The latter is integrated into the genome of the host, which means into a chromosome of an infected cell of an HIV-positive person by the ''pol''-encode integrase (IN). Also, pol encodes a specific viral protease (PR). This enzyme cleaves ''gag''- and ''gag-pol''-derived proteins into functional pieces.
*''env''. ''env'' stands for "envelope". The proteins derived from ''env'' are a surface (gp120) and a transmembrane protein (gp41). They are located at the outer part of the virus particle and enable the virus to attach to and to fuse with the target cells to initiate the infectious cycle. The gene product has a knoblike structure.

===Specific HIV genes===
*''tat''. A portion of the HIV RNA structure is a hairpin structure which initially prevents full transcription taking place. A small amount of RNA transcripts will be made, however, which allows for the ''tat'' protein to be produced. Tat binds to CdK9/CycT and phosphorylates it, helping to alter its shape and eliminating the effect of the hairpin RNA structure. This itself increases the rate of transcription, providing a [[positive feedback]] cycle. This allows HIV to have an explosive response once a threshold amount of tat is produced, a useful tool in defeating the body's response. Despite the lack of a signal sequence, Tat is released by infected cells and is found in detectable levels (0.01&ndash;0.1 nM) in the culture supernatants of cells infected with HIV-1 and in the sera of HIV-1 infected patient’s. It is also efficiently taken up by a variety of cells. Extracellular Tat has many functions which are thought to play a major role in enabling HIV to escape immune surveillance and act as a viral [[toxin]] in contributing to AIDS [[pathology]]. One such role of Tat is in the [[apoptosis]] of uninfected naive bystander [[T cell]]s, contributing to the progressive loss of these cells and the progression towards [[AIDS]].
*''rev''. ''rev'' allows fragments of HIV mRNA that contain a ''rev'' Response Unit (RRE) to be exported from the nucleus to the cytoplasm. In the absence of ''rev'', RNA splicing machinery in the nucleus quickly splices the RNA so that only the smaller, regulatory proteins can be produced; in the presence of ''rev'', RNA is exported from the nucleus before it can be spliced so that the structural proteins and RNA genome can be produced. Again, this mechanism allows a positive feedback loop and allows HIV to overwhelm the host's defenses, and it also provides time-dependant regulation of replication (a common theme in virus infections).
*''nef''. ''nef'' is involved in how pathogenic the virus is. It downregulates the CD4 molecule on T cells (so they can't respond to infections as well). One group of people in Sydney, Australia were infected with a nef-deleted virus and took much longer than expected to progress to AIDS. Unfortunately they did, and a nef-deleted virus vaccine has failed also (in animals; it never made it to human trials).
*''vif''. ''vif'' helps the virus infect cells after it leaves the one it's in. It appears to be involved in how the RNA genome and Gag protein bind to each other and also inhibits a cellular protein that modifies RNA.
*''vpr''. ''vpr'' is involved in getting the virus into the nucleus of the cell so it can integrate. It also causes the cell to stop growing, which can result in immune dysfunction.
*''vpu''. ''vpu'' is involved in getting the virus out of the cell. It enhances virion release from the cell. In HIV-2 the gene is called ''vpx''.

==Life cycle of HIV==
[[Image:Hiv gross.png|right|thumbnail|250px|HIV replication]]

===Viral tropism===
HIV can infect a variety of cells such as [[Helper_T_cell|CD4+ helper T-cells]] and [[macrophage]]s that express the CD4 molecule on its surface. HIV-1 entry to macrophages and T helper cells is mediated not only through interaction of the virion envelope glycoproteins (gp120) with the CD4 molecule on the target cells but also with its chemokine coreceptors. Macrophage (M-tropic) strains of HIV-1, or non-syncitia-inducing strains (NSI) use the beta-[[chemokine]] receptor [[CCR5]] for entry and are thus able to replicate in macrophages and CD4+ T-cells. The normal [[ligand]]s for this receptor, [[RANTES]], macrophage inflammatory protein (MIP)-1-beta and MIP-1-alpha, are able to suppress HIV-1 infection ''in vitro''. This CCR5 coreceptor is used by almost all primary HIV-1 isolates regardless of viral genetic subtype. T-tropic isolates, or [[syncitia]]-inducing (SI) strains replicate in primary CD4+ T-cells as well as in macrophages and use the alpha-chemokine receptor, [[CXCR4]], for entry. The alpha-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. Viruses that use only the CCR5 receptor are terme R5, those that only use 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 (Coakley ''et al''., 2005).

HIV can also infect [[dendritic cell]]s (Knight ''et al''., 1990).

===Viral entry to the cell===

The interaction between the gp120, coreceptor and CD4 provokes conformational changes in gp120 that exposes a previously buried portion of the transmembrane glycoprotein, gp41, and allows access of the V3 loop of gp120 to the coreceptor. gp41 causes the fusion of the viral envelope and the host-cell envelope, allowing the capsid to enter the target cell. The exact mechanism by which gp41 causes the fusion is still largely unknown (Chan and Kim, 1998; Wyatt and Sodroski, 1998).

Once HIV has bound to the CD4+ T-cell a viral protein known as gp41 penetrates the cell membrane and the HIV [[RNA]] and various [[enzymes]] including but not limited to reverse transcriptase, integrase and protease are injected into the cell.

===Viral replication and transcription===
Once the viral capsid has entered the cell, an [[enzyme]] called ''[[reverse transcriptase]]'' liberates the single-stranded (+)[[RNA]] from the attached viral proteins and copies it into a negatively sensed viral complementary [[DNA]] of 9 kb pairs (cDNA). This process of reverse transcription is extremely error prone and it is during this step that mutations (such as drug resistance) are likely to arise. The reverse transcriptase then makes a complementary DNA strand to form a double-stranded viral DNA intermediate (vDNA). This new vDNA is then transported into the [[nucleus]]. The integration of the proviral DNA into the host [[genome]] is carried out by another viral enzyme called ''[[integrase]]''. This is called the latent stage of an HIV infection (Zheng ''et al''., 2005).

To actively produce virus, certain [[transcription factors]] need to be present in the cell. The most important is called [[NF-kB]] (NF Kappa B) and is present once the T cells becomes activated. This means that those cells most likely to be killed by HIV are in fact those currently fighting infection.

The production of the virus is regulated, like that of many viruses. Initially the integrated [[provirus]] is copied to [[mRNA]] which is then [[Splicing_(genetics)|spliced]] into smaller chunks. These small chunks produce the regulatory proteins [[Tat]] (which encourages new virus production) and [[Rev]]. As Rev accumulates it gradually starts to inhibit [[mRNA]] [[splicing]] (Pollard and Malim, 1998). At this stage the structural proteins Gag and Env are produced from the full-length mRNA. Additionally the full-length RNA is actually the virus genome, so it binds to the Gag protein and is packaged into new virus particles.

Interestingly, HIV-1 and HIV-2 appear to package their RNA differently&mdash;HIV-1 will bind to any appropriate RNA whereas HIV-2 will preferentially bind to the mRNA which was used to create the Gag protein itself. This may mean that HIV-1 is better able to mutate (HIV-1 causes AIDS faster than HIV-2 and is the majority species of the virus).

===Viral assembly and release===

The final step of the viral cycle is the assembly of new HIV-1 virions, 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 either occurs in the forming bud or in the immature virion after it buds from the host cell. During maturation, HIV proteases (proteinases) cleave the polyproteins into individual functional HIV proteins and enzymes. The various structural components then assemble to produce a mature HIV virion (Gelderblom et al., 1997). This step can be inhibited by drugs. The virus is then able to infect a further cell.

==Signs and symptoms of HIV-1 infection==
[[Image:hiv-timecourse.png|right|thumbnail|500px|Graph showing HIV virus and CD4<sup>+</sup> levels over the course of an untreated infection]]
The development of [[antibodies]] to HIV usually takes place between 6 weeks and 3 months after an infection has occurred. Most people infected with HIV do not know that they have become infected, because no symptoms develop immediately after the initial infection. However, within the first weeks after infection most patients will develop a syndrome known as "acute HIV syndrome". The symptoms ([[fever]], [[rash]], [[arthralgia|joint pains]] and [[lymphadenopathy|enlarged lymph nodes]]) are similar to those of [[influenza]], [[infectious mononucleosis]] and a number of other infectious diseases (Kahn & Walker 1998). Some people develop no symptoms at all. The symptoms are usually transient and disappear after one or two weeks. Because of the nonspecific nature of the syndrome, it is often not recognized as a sign 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. Since not all patients develop it, and since the same symptoms can be caused by many other common diseases, it cannot be used as an indicator of HIV infection. However, recognizing the syndrome is important because the patient is much more infectious during this period of infection. Also, some studies have indicated that this stage of infection offers unique treatment possibilities and that treatment during this stage may lead to a better prognosis. This has not been proven and is being researched by numerous studies.

After the symptoms have disappeared the infected person will usually not show any signs of infections for several years, but they can still transmit the infection to others. The person may later experience some nonspecific symptoms such as chronic low-grade fever and enlarged lymph nodes which may easily go unnoticed. This is followed by the emergence of more serious symptoms consistent with an impaired immune system. For more information about symptoms and the various stages of disease, see the next section. It should be emphasized that one can not diagnose HIV based on symptoms alone. The only reliable way to know if a person has become infected is by taking an HIV test.

Acute HIV infection progresses over time to asymptomatic HIV infection and then to early symptomatic HIV infection and later, to [[AIDS]], which is identified on the basis of certain infections. In 1990, the World Health Organization (WHO) grouped these infections and conditions together by introduced a staging system for patients infected with HIV-1. Most of these conditions are opportunistic infections that can be easily treated in healthy people.

* ''Stage I:'' HIV disease is asymptomatic and not categorized as AIDS
* ''Stage II:'' include minor mucocutaneous manifestations and recurrent upper respiratory tract infections
* ''Stage III:'' includes unexplained chronic diarrhea for longer than a month, severe bacterial infections and pulmonary tuberculosis or
* ''Stage IV'' includes [[toxoplasmosis]] of the brain, [[candidiasis]] of the esophagus, trachea, bronchi or lungs and [[Kaposi's sarcoma]]; these diseases are used as indicators of AIDS.

{{see details|WHO Disease Staging System for HIV Infection and Disease}}

Most individuals infected with HIV will progress to [[AIDS]], but the time course that this will take depends upon a variety of factors.

{{see details|HIV Disease Progression Rates}}

In 1993, the Centers for Disease Control and Prevention [[CDC]] expanded their definition of [[AIDS]] to include healthy HIV positive people with a CD4 positive T cell count of less than 200 per mm{{sup|3}} of blood. The majority of new [[AIDS_defining_clinical_condition|AIDS cases in the United States]] are reported on the basis of a low [[T cell]] count in the presence of HIV infection.

==Treatment==
HIV infection is a [[chronic]] infectious disease that can be treated, but not yet cured. There are effective means of preventing [[complication (medicine)|complications]] and delaying, but not preventing, progression to [[AIDS]]. At the present time, not all persons infected with HIV have progressed to [[AIDS]], but it is generally believed that the majority will. People with HIV infection need to receive education about the disease and treatment so that they can be active partners in decision making with their health care provider.

A combination of several antiretroviral agents, termed Highly Active Anti-Retroviral Therapy [[antiretroviral drug|HAART]], has been highly effective in reducing the number of HIV particles in the blood stream (as measured by a [[HIV test|blood test called the viral load]]). This can improve [[T-cell]] counts. This is not a cure for HIV, and people on [[antiretroviral drug|HAART]] with suppressed levels of HIV can still transmit the virus to others through sex or sharing of needles. There is good evidence that if the levels of HIV remain suppressed and the CD4 count remains greater than 200, then life and quality of life can be significantly prolonged and improved.

Treatment guidelines are changing constantly. The [http://www.who.int/hiv/pub/prev_care/en/arvrevision2003en.pdf|current guidelines for antiretroviral therapy] from the [[World Health Organization]] reflect the [[2003]] changes to the guidelines and recommend that in resource-limited settings, HIV-infected adults and adolescents should start ARV therapy when HIV infection has been confirmed and one of the following conditions is present:
* Clinically advanced HIV disease:
* WHO Stage IV HIV disease, irrespective of the CD4 cell count;
* WHO Stage III disease with consideration of using CD4 cell counts <350/µl to assist decision making.
* WHO Stage I or II HIV disease with CD4 cell counts <200/µl

The U.S. Department of Health and Human Services have recently stated on [[April 7]], [[2005]] that:
* All patients with history of an AIDS-defining illness or severe symptoms of HIV infection regardless of CD4+ T cell count receive ART.
* Antiretroviral therapy is also recommended for asymptomatic patients with <200 CD4+ T cells/µl
* Asymptomatic patients with CD4+ T cell counts of 201–350 cells/µl should be offered treatment.
* For asymptomatic patients with CD4+ T cell of >350 cells/mm3 and plasma HIV RNA >100,000 copies/ml most experienced clinicians defer therapy but some clinicians may consider initiating treatment.
* Therapy should be deferred for patients with CD4+ T cell counts of >350 cells/µl and plasma HIV RNA <100,000 copies/mL.

There are several concerns about antiretroviral regimens. The drugs can have serious side effects. Regimens can be complicated, requiring patients to take several pills at various times during the day. If patients miss doses, drug resistance can develop. [http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=12617573&query_hl=1]

In 2004, a possible therapeutic vaccine was developed. In order for the vaccine to work, the patient must first be diagnosed with the virus. Once the patient is treated, T-cell counts have been found to stop dropping. [http://my.webmd.com/content/article/97/104268.htm?z=1727_00000_5024_hv_03]

As yet, no vaccine has been developed to prevent HIV infection or disease in in people who are not yet infected with HIV, but the potential worldwide public health benefits of such a preventive vaccine are vast. Researchers in many countries are seeking to produce such a vaccine, including through the [[International aids vaccine initiative]].

In 2005, the Centers for Disease Control and Prevention in the United States recommended a 28-day HIV drug regimen for those who have been exposed to HIV (HIV Postexposure Prophylaxis [PEP][http://www.cdc.gov/hiv/treatment.htm#prophylaxis]). The drugs have demonstrated effectiveness in preventing the virus nearly 100% of the time in those who received treatment within the initial 24 hours of exposure. The effectiveness falls to 52% of the time in those who are treated within 72 hours; those not treated within the first 72 hours are not recommended candidates for the regimen.

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* Thomson, M. M., Perez-Alvarez, L. and Najera, R. (2002) Molecular epidemiology of HIV-1 genetic forms and its significance for vaccine development and therapy. ''Lancet Infect Dis.'' '''2''', 461-71 PMID 12150845
* Wyatt, R. and Sodroski, J. (1998) The HIV-1 envelope glycoproteins: fusogens, antigens, and immunogens. ''Science'' '''280''', 1884-1888 PMID 9632381
* Zheng, Y. H., Lovsin, N. and Peterlin, B. M. (2005) Newly identified host factors modulate HIV replication. ''Immunol Lett.'' '''97''', 225-234 PMID 15752562

==See also==
* [[Criminal Transmission of HIV]]
* [[HIV positive people]]
* [[HIV test]]
* [[List of HIV-positive people]]
* [[Post-exposure prophylaxis]]

==External links==
* [http://www.ericdigests.org/pre-9212/hiv.htm AIDS/HIV Education]
* [http://www.cmeonhiv.com Continuing medical education about HIV for healthcare providers]
*[http://www.un.org/ga/aids/coverage/FinalDeclarationHIVAIDS.html Declaration of Commitment on HIV/AIDS] UN 2001
*[http://fightaidsathome.scripps.edu/ FightAIDS@Home]
* [http://www.hivatis.org HIV/AIDS Treatment Information Service]
* [http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?val=NC_001802 Genome (HIV-1)]
* [http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?val=NC_001722 Genome (HIV-2)]
* [http://www.ericdigests.org/1997-3/hiv.html HIV/AIDS Education in Teacher Preparation Programs]
* [http://hivinsite.org/InSite HIV InSite]
* [http://health.howstuffworks.com/aids.htm How Aids Works] (with animation)
*[http://www.doctorswithoutborders.org/news/hiv-aids/index.cfm Medecins Sans Frontieres/Doctors Without Borders HIV/AIDS Pages]
* [http://www.niaid.nih.gov/daids/ NIH/NIAD/DAIDS]
* [http://www.mcld.co.uk/hiv/ &quot;The Molecules of HIV&quot; information resource]
* [http://www.phrusa.org/campaigns/aids/release080103.html Unsafe Health Care and the HIV/AIDS Pandemic] 2003

{{AIDS}}

[[Category:HIV/AIDS|*]]
[[Category:Sexually-transmitted diseases]]

[[Category:Retroviruses]]
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Revision as of 17:48, 27 August 2005

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