HIV: Perbedaan antara revisi
Konten dihapus Konten ditambahkan
Tidak ada ringkasan suntingan |
k ←Membatalkan revisi 1626637 oleh 125.162.119.107 (Bicara) |
||
Baris 1:
{{terjemah|Inggris}}
{{Taxobox_begin | color = violet | name = ''Human immunodeficiency virus''}}
{{Taxobox_image | image = [[Berkas:Human_Immunodeficency_Virus_-_stylized_rendering.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''') adalah sebuah [[retrovirus]] yang menginfeksi sel [[sistem kekebalan tubuh]] manusia - terutama CD4+ [[T cell]] dan [[macrophage]], komponen vital dari sistem sistem kekebalan tubuh "tuan rumah" - dan menghancurkan atau merusak fungsi mereka. Infeksi dari HIV menyebabkan pengurangan cepat dari sistem kekebalan tubuh, yang menyebabkan kekurangan imun. HIV merupakan penyebab dasar [[AIDS]].
Baris 32 ⟶ 45:
Pada tahun 2000, [[WHO]] memperkirakan bahwa 25% unit darah yang ditransfusikan di Afrika tidak dites untuk HIV, dan bahwa 10% infeksi HIV di benua itu terjadi lewat darah. [http://www.afro.who.int/press/2001/regionalcommittee/rc51004.html].
Di [[Asia]], [[wabah]] HIV terutama disebabkan oleh para pengguna obat bius lewat jarum suntik, hubungan seks baik antarpria maupun dengan [[pekerja seks komersial]], dan pelanggannya, serta pasangan seks mereka. Pencegahannya masih kurang memadai.
<!--
Epidemics of HIV are occurring in [[AIDS_pandemic#Eastern_Europe_and_Central_Asia|Eastern Europe and Central Asia]]. Injecting drug use is the main driving force behind epidemics across these regions. In many high-income countries, sex between men plays an important role in the epidemic; drug injecting plays a varying role, accounting in 2002 for more than 10% of reported HIV infections in [[AIDS_pandemic#North_America.2C_Western_and_Central_Europe|Western Europe]] and 25% inn [[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.
-->
== Struktur ==
HIV berbeda dalam struktur dengan retrovirus yang dijelaskan sebelumnya. Besarnya sekitar 120 nm dalam diameter (seper 120 milyar meter-kira-kira 60 kali lebih kecil dari sel darah merah) dan kasarnya "spherical"
[[Berkas: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 comprising the viral protein [[p24]], typical of [[lentivirus]]es. This is in turn surrounded by a [[plasma membrane]] of host-cell origin. The single-strand 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 (Gelderborn, 1997).
There are two forms of the virus:
The ''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 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—this observation meant that HIV was originally classed as a type C retrovirus. The Env proteins link together in groups of three (trimers).
The ''mature form'': Once the virus protease has cleaved the gag proteins, the core rearranges into a truncated cone (like 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, because they are easily dislodged. It is the mature conical core that makes HIV easily identifiable.
HIV has several major genes coding for structural proteins that are found in all retroviruses, and several nonstructural ('accessory') genes that are unique to HIV.
===General retrovirus genes===
*'''gag''': gag-derived proteins make up the cone-shaped viral capsid (p24, i.e., CA, a 24-[[kilodalton]] protein), the nucleocapsid proteins (p6 and p7, i.e., NC) and a matrix protein (p17, i.e., MA).
*'''pol''', a gene that codes for the virus [[enzyme]]s. The most important of which is the [[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''-encoded integrase (IN). Also, ''pol'' encodes a specific viral protease (PR). This enzyme cleaves gag- and gag-pol-derived proteins into functional proteins.
*'''env''', which stands for 'envelope'. The proteins derived from env are the surface (gp120) and a transmembrane (gp41) proteins. They are located at the outer part of the virus particle and enable the virus to attach to and fuse with the target cells to initiate the infectious cycle. The gene product has a knob-like structure.
===Specific HIV genes===
*''tat'' codes for the Tat protein. The HIV RNA initially has a hairpin-structured portion which prevents full transcription occurring. However, a small number of RNA transcripts will be made, which allow the Tat protein to be produced. Tat binds to P-TEF-b (CdK9/Cyclin T) and phosphorylates it, helping to alter its shape and eliminating the effect of the hairpin RNA structure (Kim and Sharp, 2001). This itself increases the rate of transcription, providing a [[positive feedback]] cycle. This in turn allows HIV to have an explosive response once a threshold amount of tat is produced, a useful tool for defeating the body's response. Despite the lack of a signal sequence, Tat is released by infected cells and is found in detectable levels (0.1 nM–40 nM) in the culture supernatants of cells infected with HIV-1, and in the sera of HIV-1 infected patient’s (Xiao et al., 2000). It is also efficiently taken up by a variety of cells. Extracellular Tat has many functions that are thought to play a major role in enabling HIV to escape immune surveillance and to act as a viral [[toxin]] in 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]] (Campbell et al., 2004).
*''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 to allow HIV to overwhelm the host's defenses, and provides time-dependant regulation of replication (a common process in viral infections) (Strebel, 2003).
*''nef''. This is involved in the pathogenicity of the virus. It downregulates the CD4 molecule on T cells, reducing the effectiveness of their response to infections. One group of patients in Sydney were infected with a nef-deleted virus and took much longer than expected to progress to AIDS (Learmont et al., 1999). A nef-deleted virus vaccine has not been trialed in humans and has failed in nonhuman animals.
*''vif''. The exact role of Vif is as yet unclear (Strebel, 2003). However, it is thought that vif helps the virus to infect other cells after it leaves a host cell; Vif appears to be involved in determining how the RNA genome and Gag protein bind to each other, and inhibits a cellular protein that modifies RNA.
*''vpr''. Vpr plays an important role in regulating nuclear import of the HIV-1 pre-integration complex, and is required for virus replication in non-dividing cells. Vpr also induces cell cycle arrest in proliferating cells, which can result in immune dysfunction (Bukrinsky and Adzhubei, 1999).
*''vpu''. This is involved in viral budding, enhancing virion release from the cell. In HIV-2, this 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 termed 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 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—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.
{{see details|CDC Classification System for 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/µl 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.
-->
== Referensi ==
* Barré-Sinoussi, F., Chermann, J. C., Rey, F., Nugeyre, M. T., Chamaret, S., Gruest, J., Dauguet, C., Axler-Blin, C., Vezinet-Brun, F., Rouzioux, C., Rozenbaum, W. and Montagnier, L. (1983) Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS) ''Science'' '''220''', 868-871 PMID 6189183
* Bentwich, Z., Kalinkovich., A. and Weisman, Z. (1995) Immune activation is a dominant factor in the pathogenesis of African AIDS. ''Immunol. Today'' '''16''', 187-191 PMID 7734046
* Bukrinsky M, Adzhubei A. (1999) Viral protein R of HIV-1. ''Rev Med Virol'' '''9''', 39-49 PMID 10371671
* Campbell GR, Pasquier E, Watkins J, Bourgarel-Rey V, Peyrot V, Esquieu D, Barbier P, de Mareuil J, Braguer D, Kaleebu P, Yirrell DL, Loret EP. (2004) The glutamine-rich region of the HIV-1 Tat protein is involved in T-cell apoptosis. ''J. Biol. Chem.'' '''279''', 48197-48204 PMID 15331610
* Carr, J. K., Foley, B. T., Leitner, T., Salminen, M., Korber, B. and McCutchan, F. (1998) Reference Sequences Representing the Principal Genetic Diversity of HIV-1 in the Pandemic. In: Los Alamos National Laboratory (Ed) HIV Sequence Compendium, pp. 10-19
* Chan, D. C. and Kim, P. S. (1998) HIV entry and its inhibition. ''Cell'' '''93''', 681-684 PMID 9630213
* Coakley, E., Petropoulos, C. J. and Whitcomb, J. M. (2005) Assessing chemokine co-receptor usage in HIV. ''Curr Opin Infect Dis.'' '''18''', 9-15. PMID 15647694
* Coffin, J., Haase, A., Levy, J. A., Montagnier, L., Oroszlan, S., Teich, N., Temin, H., Toyoshima, K., Varmus, H., Vogt, P. and Weiss, R. A. (1986) What to call the AIDS virus? ''Nature'' '''321''', 10. PMID 3010128.
* Dybul, M., Fauci, A. S., Bartlett, J. G., Kaplan, J. E., Pau, A. K., and the Panel on Clinical Practices for Treatment of HIV. (2002) Guidelines for using antiretroviral agents among HIV-infected adults and adolescents. ''Ann Intern Med'' '''137''', 381-433 PMID 12617573.
* Gao, F., Bailes, E., Robertson, D. L., Chen, Y., Rodenburg, C. M., Michael, S. F., Cummins, L. B., Arthur, L. O., Peeters, M., Shaw, G. M., Sharp, P. M. and Hahn, B. H. (1999) [http://dx.doi.org/10.1038/17130 Origin of HIV-1 in the chimpanzee Pantroglodytes troglodytes]. ''Nature'' '''397''', 436-441 PMID 9989410
* Gelderblom, H. R. (1997) Fine structure of HIV and SIV. In: Los Alamos National Laboratory (Ed) HIV Sequence Compendium, 31-44.
* Kahn, J. O. and Walker, B. D. (1998) Acute Human Immunodeficiency Virus type 1 infection. ''N Engl J Med'' '''331''', 33-39 PMID 9647878.
* Kim JB, Sharp PA. (2001) Positive transcription elongation factor B phosphorylates hSPT5 and RNA polymerase II carboxyl-terminal domain independently of cyclin-dependent kinase-activating kinase. ''J. Biol. Chem.'' '''276''', 12317-12323 PMID 11145967
* Knight, S. C., Macatonia, S. E. and Patterson, S. (1990) HIV I infection of dendritic cells. ''Int Rev Immunol.'' '''6''',163-75 PMID 2152500
* Learmont JC, Geczy AF, Mills J, Ashton LJ, Raynes-Greenow CH, Garsia RJ, Dyer WB, McIntyre L, Oelrichs RB, Rhodes DI, Deacon NJ, Sullivan JS. (1999) Immunologic and virologic status after 14 to 18 years of infection with an attenuated strain of HIV-1. A report from the Sydney Blood Bank Cohort. ''N Engl J Med'' '''340''', 1715-1722 PMID 10352163
* Osmanov, S., Pattou, C., Walker, N., Schwardlander, B., Esparza, J. and the WHO-UNAIDS Network for HIV Isolation and Characterization. (2002) Estimated global distribution and regional spread of HIV-1 genetic subtypes in the year 2000. ''J. Acquir. Immune. Defic. Syndr.'' '''29''', 184-190 PMID 11832690
* Pollard, V. W. and Malim, M. H. (1998) The HIV-1 Rev protein. ''Annu Rev Microbiol.'' '''52''', 491-532 PMID 9891806
* Popovic, M., Sarngadharan, M. G., Read, E. and Gallo, R. C. (1984) Detection, isolation, and continuous production of cytopathic retroviruses (HTLV-III) from patients with AIDS and pre-AIDS. ''Science'' '''224''', 497-500 PMID 6200935
* Reeves, J. D. and Doms, R. W. (2002) [http://dx.doi.org/10.1099/vir.0.18253-0 Human immunodeficiency virus type 2]. ''J. Gen. Virol.'' '''83''', 1253-1265 PMID 12029140
* Strebel, K (2003) Virus-host interactions: role of HIV proteins Vif, Tat, and Rev. ''AIDS'' '''17 Suppl 4''', S25-S34 PMID 15080177
* Thomson, M. M., Perez-Alvarez, L. and Najera, R. (2002) [http://dx.doi.org/10.1016/S1473-3099(02)00343-2 Molecular epidemiology of HIV-1 genetic forms and its significance for vaccine development and therapy]. ''Lancet Infect Dis.'' '''2''', 461-71 PMID 12150845
* Xiao, H., Neuveut, C., Tiffany, H. L., Benkirane, M., Rich, E. A., Murphy, P. M. and Jeang, K. T. (2000) Selective CXCR4 antagonism by Tat: implications for in vivo expansion of coreceptor use by HIV-1. ''Proc. Natl. Acad. Sci. U. S. A.'' '''97''', 11466-11471 PMID 11027346
* 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
== Lihat pula ==
* [[Penularan kriminal HIV]]
* [[Orang HIV positif]]
* [[Tes HIV]]
* [[Daftar orang HIV-positif]]
* [[Post-exposure prophylaxis]]
== Pranala luar ==
* [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/ "The Molecules of HIV" information resource]
* [http://www.phrusa.org/campaigns/aids/release080103.html Unsafe Health Care and the HIV/AIDS Pandemic] 2003
[[Kategori:AIDS]]
[[Kategori:Retrovirus]]
[[Kategori:Penyakit yang ditularkan melalui hubungan seksual]]
[[af:MIV]]
[[als:HIV]]
[[am:ኤችአይቪ]]
[[ar:فيروس نقص المناعة]]
[[bg:ХИВ]]
[[bn:এইচআইভি]]
[[bs:HIV]]
[[ca:Virus de la Immunodeficiència Humana]]
[[cs:HIV]]
[[cy:HIV]]
[[da:HIV]]
[[de:Humanes Immundefizienz-Virus]]
[[el:HIV]]
[[en:HIV]]
[[eo:HIV]]
[[es:VIH]]
[[et:HIV]]
[[eu:GIB]]
[[fa:اچآیوی]]
[[fi:HIV]]
[[fr:Virus de l'immunodéficience humaine]]
[[he:HIV]]
[[hi:एचआईवी]]
[[hr:HIV]]
[[hu:HIV]]
[[hy:ՄԻԱՎ]]
[[ilo:HIV]]
[[it:HIV]]
[[iu:ᐊᓴᐱ/asapi]]
[[ja:ヒト免疫不全ウイルス]]
[[ko:HIV]]
[[ln:Virus de l'Immunodéfience Humaine]]
[[mk:ХИВ]]
[[ml:എച്ച്.ഐ.വി.]]
[[mr:एच.आय.व्ही.]]
[[nl:Hiv]]
[[no:Humant immunsviktvirus]]
[[oc:Virus de l'immunodeficiéncia umana]]
[[pl:Wirus zespołu nabytego braku odporności]]
[[ps:اېچ آی وي(HIV)]]
[[pt:Vírus da imunodeficiência humana]]
[[ro:HIV]]
[[ru:ВИЧ]]
[[sh:HIV]]
[[simple:HIV]]
[[sk:HIV]]
[[sl:HIV]]
[[sq:HIV]]
[[sr:ХИВ]]
[[su:HIV]]
[[sv:HIV]]
[[th:เอชไอวี]]
[[tr:HIV]]
[[uk:ВІЛ (вірус)]]
[[yo:HIV]]
[[zh:人類免疫缺陷病毒]]
[[zh-min-nan:HIV]]
| |||