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{{infobox spesies
{{terjemah|Inggris}}
| color = {{Tc2|virus}}
| item = Q374232
| subdivision_ranks = Spesies
| subdivision =
* '''''Human immunodeficiency virus 1'''''
* '''''Human immunodeficiency virus 2'''''
}}<!--
{{DiseaseDisorder infobox
| Name = International Statistical Classification of Diseases and Related Health Problems Codes
| ICD10 = B20-B24
| ICD9 = {{ICD9|042}}-{{ICD9|044}}
}}-->
 
'''Virus imunodefisiensi manusia'''<ref name="ref1">[http://kateglo.bahtera.org/index.php?mod=glossary&op=1&phrase=human+immunodeficiency+virus&dc=&lang=&src=&srch=Cari Kateglo- virus imunodifisiensi manusia]{{Pranala mati|date=Mei 2021 |bot=InternetArchiveBot |fix-attempted=yes }}</ref> atau '''virus lemah kebal manusia''' ([[bahasa Inggris]]: '''''human immunodeficiency virus'''''; sering disingkat '''HIV''') adalah virus mematikan dari dua spesies [[lentivirus]] penyebab [[AIDS]].<ref name="his1">Jenny Page, Maylani Louw, Delene Pakkiri, Monica Jacobs. 2006. Working with HIV/AIDS. Cape Town: Juta Legal and Academic Publishers</ref> Virus ini menyerang manusia dan menyerang [[sistem kekebalan]] tubuh, sehingga tubuh menjadi lemah dalam melawan infeksi. Jika virus ini terus menyerang tubuh, sistem pertahanan tubuh kita akan semakin lemah. Tanpa pengobatan, seorang dengan HIV bisa bertahan hidup selama 9-11 tahun setelah terinfeksi, tergantung tipenya. Dengan kata lain, kehadiran virus ini dalam tubuh akan menyebabkan penurunan [[sistem imun]].<ref name="his1" /> Penyaluran virus HIV bisa melalui penyaluran [[Semen (reproduksi)]], [[Darah]], cairan vagina, dan ASI. HIV bekerja dengan membunuh sel-sel penting yang dibutuhkan oleh manusia, salah satunya adalah [[Sel T pembantu]], [[Makrofaga]], [[Sel dendritik]].
{{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/AIDS kini masih menjadi permasalahan besar global dengan sebanyak 39,0 juta terjangkit infeksi HIV pada tahun 2022 dengan angka kasus infeksi baru sebesar 1,3 juta.<ref>{{Cite journal|last=Joint United Nations Programme on HIV/AIDS (UNAIDS)|date=2024|title=Fact Sheet 2024 - Latest Global and Regional HIV Statistics on The Status of The AIDS Epidemic|url=https://www.unaids.org/en|journal=}}</ref><ref>{{Cite journal|last=Joint United Nations Programme on HIV/AIDS|date=2023|title=The Path That Ends AIDS|url=http://www.unaids.org/|journal=Unaids Glob Aids Updat}}</ref> Afrika Timur dan Selatan menyumbang penambahan kasus infeksi HIV terbesar sebesar, yaitu lima ratus ribu jiwa diikuti Asia Pasifik sebesar tiga ratus ribu jiwa. Di Indonesia sendiri, terdapat sebanyak 515.455 ODHA (orang dengan HIV/AIDS) berdasarkan Laporan Eksekutif Perkembangan HIV/AIDS dan PIMS Triwulan 1 Tahun 2023<ref>{{Cite journal|last=Sistem Informasi HIV-AIDS dan IMS (SIHA)|date=2023|title=Laporan Eksekutif Perkembangan HIV/AIDS Dan Penyakit Infeksi Menular Seksual (PIMS) Triwulan I Tahun 2023|url=https://siha.kemkes.go.id/|journal=|pages=1-15}}</ref>. Angka ini lebih rendah dari perkiraan Kemenkes pada tahun 2016, yaitu sebesar 631.524 jiwa ODHA. Insidensi HIV di Indonesia pun juga lebih rendah dari target asli, yaitu sebesar 0,09.<ref name=":0">{{Cite book|last=Rondowunu|first=MR|last2=Trisnantoro|first2=L|last3=Pramono|first3=Y|last4=Pambudi|first4=I|date=2022|title=Tahunan HIV/AIDS 2022|url-status=live}}</ref>
'''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]].
 
Namun, salah satu masalah terbesar infeksi HIV di Indonesia adalah cara agar para ODHA mengalami penekanan virus. ''Joint United Nations Programme on HIV and AIDS'' (UNAIDS) menetapkan target 95-95-95 pada tahun 2030 yang berarti sebanyak 95% ODHA mengetahui statusnya, 95% ODHA mendapatkan terapi ARV, dan 95% ODHA yang mendapatkan terapi ARV mengalami penekanan virus. Nyatanya, sampai dengan Desember 2022, baru sebesar 81% ODHA di Indonesia yang mengetahui statusnya. Sekitar setengah dari ODHA yang mengetahui statusnya mendapatkan terapi ARV dan kurang dari setengah ODHA yang mendapat terapi mengalami penekanan virus. Lebih buruknya lagi, lebih dari setengah (54%) ODHA yang mendapat terapi ARV tidak melanjutkan pengobatan. Dari 51% itu, 54% ODHA mangkir, 40% meninggal dunia, dan 6% berhenti sendiri.<ref name=":0" />
== Perkenalan ==
Istilah HIV telah digunakan sejak 1986 (Coffin et al., 1986) sebagai nama untuk retrovirus yang diusulkan pertama kali sebagai penyebab AIDS oleh [[Luc Montagnier]] dari Perancis, yang awalnya menamakannya LAV (lymphadenopathy-associated virus) (Barre-Sinoussi et al., 1983) dan oleh [[Robert Gallo]] dari Amerika Serikat, yang awalnya menamakannya HTLV-III (human T lymphotropic virus type III) (Popovic et al., 1984).
 
[[Berkas:HIV-SIV-phylogenetic-tree.png|thumb|350px|left|The phylogenetic tree of the SIV and HIV viruses.<br />(click on image for a detailed description.)]]
 
HIV adalah anggota dari genus [[lentivirus]] [http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/61060000.htm], bagian dari keluarga [[retroviridae]] [http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/61000000.htm] yang ditandai dengan periode latensi yang panjang dan sebuah sampul [[lipid]] dari sel-host awal yang mengelilingi sebuah pusat protein/RNA. Dua spesies HIV menginfeksi manusia: HIV-1 dan HIV-2. HIV-1 adalah yang lebih "virulent" dan lebih mudah menular, dan merupakan sumber dari kebanyakan infeksi HIV di seluruh dunia; HIV-2 kebanyakan masih terkurung di Afrika barat (Reeves and Doms, 2002). Kedua spesies berawal di Afrika barat dan tengah, melompat dari [[primata]] ke manusia dalam sebuah proses yang dikenal sebagai [[zoonosis]].
 
*
HIV-1 telah berevolusi dari sebuah [[simian immunodeficiency virus]] (SIVcpz) yang ditemukan dalam subspesies [[chimpanzee]], Pan troglodyte troglodyte (Gao et al., 1999).HIV-2 melompat spesies dari sebuah strain SIV yang berbeda, ditemukan dalam [[sooty mangabey]]s, [[monyet dunia lama]] [[Guinea-Bissau]] (Reeves and Doms, 2002).
 
== Sejarah ==
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Pada tahun 1983, Jean Claude Chermann dan [[Françoise Barré-Sinoussi]] dari [[Prancis]] berhasil mengisolasi HIV untuk pertama kalinya dari seorang penderita sindrom [[limfadenopati]].<ref name="his2">Jay A. Levy. 2007. HIV and the pathogenesis of AIDS. ASM Press.</ref> Pada awalnya, virus itu disebut ALV (''lymphadenopathy-associated virus'')<ref name="barre">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</ref> Bersama dengan [[Luc Montagnier]], mereka membuktikan bahwa virus tersebut merupakan penyebab [[AIDS]].<ref name="barre" /> Pada awal tahun 1984, [[Robert Gallo]] dari [[Amerika Serikat]] juga meneliti tentang virus penyebab AIDS yang disebut HTLV-III.<ref name="his2" /><ref name="popo">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</ref> Setelah diteliti lebih lanjut, terbukti bahwa ALV dan HTLV-III merupakan virus yang sama dan pada tahun 1986, istilah yang digunakan untuk menyebut virus tersebut adalah HIV, atau lebih spesifik lagi disebut HIV-1.<ref name="coffin">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.</ref>
Three groups of HIV-1 have been identified on the basis of differences in env: M, N and O (Thomson et al., 2002). Group M is the most prevalent and is subdivided into eight subtypes, based on the whole genome, that are each geographically distinct (Carr et al., 1998). The most prevalent are subtypes B (found predominantly in North America and Europe), A and D (found predominantly in Africa), and C (found predominantly 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).
[[Image:subtype.png|right|thumbnail|400px|Map showing HIV-1 subtype prevalence. The bigger the pie chart, the more infections are present.]]
 
Tidak lama setelah HIV-1 ditemukan, suatu subtipe baru ditemukan di [[Portugal]] dari pasien yang berasal dari [[Afrika Barat]] dan kemudian disebut HIV-2.<ref name="his2" /> Melalui kloning dan analisis sekuens (susunan genetik), HIV-2 memiliki perbedaan sebesar 55% dari HIV-1 dan secara antigenik berbeda.<ref name="his2" /> Perbedaan terbesar lainnya antara kedua strain (galur) virus tersebut terletak pada glikoprotein selubung.<ref name="his2" /> Penelitian lanjutan memperkirakan bahwa HIV-2 berasal dari SIV (retrovirus yang menginfeksi [[primata]]) karena adanya kemiripan sekuens dan reaksi silang antara antibodi terhadap kedua jenis virus tersebut.<ref name="his2" />
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.
 
== Klasifikasi ==
47% of infections worldwide are of subtype C, 27% are of subtype A/CRF02_AG, 12.3% are of subtype B, 4% are of subtype D, 4% are of CRF AE, and the remaining 5.7% are composed of other subtypes and CRFs. Almost 95% of all HIV research currently taking place is focused on subtype B, while a few laboratories focus on subtype C (Osmanov et al., 2002).
[[Berkas:HIV-SIV-phylogenetic-tree.png|jmpl|350px|kiri|Pohon kekerabatan (filogenetik) yang menunjukkan kedekatan SIV dan HIV.{{br}}]]
-->
Kedua spesies HIV yang menginfeksi manusia (HIV-1 dan -2) pada mulanya berasal dari Afrika barat dan tengah, berpindah dari [[primata]] ke manusia dalam sebuah proses yang dikenal sebagai [[zoonosis]].<ref name="re" /> HIV-1 merupakan hasil evolusi dari'' [[simian immunodeficiency virus]]'' (SIVcpz) yang ditemukan dalam subspesies [[simpanse]], ''Pan troglodyte troglodyte''. Sedangkan, HIV-2 merupakan spesies virus hasil evolusi strain SIV yang berbeda (SIVsmm), ditemukan pada ''[[Sooty Mangabey|Sooty mangabey]]'', [[monyet dunia lama]] [[Guinea-Bissau]].<ref name="re"/> Sebagian besar infeksi HIV di dunia disebabkan oleh HIV-1 karena spesies virus ini lebih virulen dan lebih mudah menular dibandingkan HIV-2.<ref name="re"/> Sedangkan, HIV-2 kebanyakan masih terkurung di Afrika barat.<ref name="re">Reeves, J. D. and Doms, R. W. (2002) [http://dx.doi.org/10.1099/vir.0.18253-0 Human immunodeficiency virus type 2] {{Webarchive|url=https://web.archive.org/web/20230812122622/https://www.pharmacists.org/statistics/|date=2023-08-12}}. ''J. Gen. Virol.'' '''83''', 1253-1265 PMID 12029140</ref>
 
Berdasarkan susunan genetiknya, HIV-1 dibagi menjadi tiga kelompok utama, yaitu M, N, dan O.<ref name="test"/> Kelompok HIV-1 M terdiri dari 16 subtipe yang berbeda.<ref name="test"/> Sementara pada kelompok N dan O belum diketahui secara jelas jumlah subtipe virus yang tergabung di dalamnya.<ref name="test"/> Namun, kedua kelompok tersebut memiliki kekerabatan dengan SIV dari simpanse.<ref name="test"/> HIV-2 memiliki 8 jenis subtipe yang diduga berasal dari ''[[Sooty Mangabey|Sooty mangabey]]'' yang berbeda-beda.<ref name="test"/>
== Penularan ==
HIV menular melalui hubungan kelamin dan hubungan seks oral, atau melalui anus, [[transfusi darah]], penggunaan bersama jarum terkontaminasi melalui injeksi obat dan dalam perawatan kesehatan, dan antara ibu dan bayinya selama masa hamil, kelahiran dan masa menyusui.
[http://www.unaids.org/en/Resources/faq/faq_transmission.asp#7 UNAIDS transmission]. Penggunaan pelindung fisik seperti [[kondom]] [[latex]] dianjurkan untuk mengurangi penularan HIV melalui seks. Belakangan ini, diusulkan bahwa [[penyunatan]] dapat mengurangi risiko penyebaran virus HIV
[http://www.newsday.com/news/nationworld/wire/sns-ap-brazil-aids-circumcision,0,7464783.story?coll=ny-hs-spotlight&track=mostemailedlink], tetapi banyak ahli percaya bahwa hal ini masih terlalu awal untuk merekomendasikan penyunatan lelaki dalam rangka mencegah HIV
[http://www.who.int/mediacentre/news/releases/2005/pr32/en/].
 
Apabila beberapa virus HIV dengan subtipe yang berbeda menginfeksi satu individu yang sama, maka akan terjadi bentuk rekombinan sirkulasi ''(circulating recombinant forms''-CRF)<ref>{{en}} {{cite web
Pada akhir tahun [[2004]] diperkirakan antara 36 hingga 44 juta orang yang hidup dengan HIV, 25 juta di antaranya adalah penduduk sub-Sahara Afrika. Perkiraan jumlah orang yang terinfeksi HIV di seluruh dunia pada tahun 2004 adalah antara 4,3 juta hingga 6,4 juta orang. ([http://www.unaids.org/wad2004/EPIupdate2004_html_en/epi04_00_en.htm AIDS epidemic update December 2004]).
| url = http://www.hiv.lanl.gov/content/sequence/HIV/CRFs/CRFs.html
| title = The Circulating Recombinant Forms (CRFs)
| accessdate = 2010-04-02
| work = Los Alamos National Laboratory
| archive-date = 2023-03-20
| archive-url = https://web.archive.org/web/20230320110747/https://www.hiv.lanl.gov/content/sequence/HIV/CRFs/CRFs.html
| dead-url = no
}}</ref> ({{lang-en|circulating recombinant form, CRF}}). Bagian dari genom beberapa subtipe HIV yang berbeda akan bergabung dan membentuk satu genom utuh yang baru.<ref name="hivor" /> Bentuk rekombinan yang pertama kali ditemukan adalah rekombinan AG dari Afrika tengah dan barat, kemudian rekombinan AGI dari [[Yunani]] dan [[Siprus]], kemudian rekombinan AB dari [[Rusia]] dan [[AE]] dari [[Asia]] tenggara.<ref name="hivor">[http://www.metapathogen.com/HIV-1/HIV-origin-classification.html MetaPathogen.com] {{Webarchive|url=https://web.archive.org/web/20110603121835/http://www.metapathogen.com/HIV-1/HIV-origin-classification.html |date=2011-06-03 }} Human Immunodeficiency Virus 1 (HIV-1). Diakses pada 19 Juni 2011.</ref> Dari seluruh infeksi HIV yang terjadi di dunia, sebanyak 47% kasus disebabkan oleh subtipe C, 27% berupa CRF02_AG, 12,3% berupa subtipe B, 5.3% adalah subtipe D dan 3.2% merupakan CRF AE, sedangkan sisanya berasal dari subtipe dan CRF lain.<ref name="hivor" />
 
== Struktur dan materi genetik ==
[[Wabah]] ini tidak merata di wilayah-wilayan tertentu karena ada negara-negara yang lebih menderita daripada yang lainnya. Bahkan pada tingkatan negara pun ada perbedaan tingkatan infeksinya pada daerah-daerah yang berlainan. Jumlah orang yang hidup dengan HIV terus meningkat di semua bagian dunia, meskipun telah dilakukan berbagai langkah pencegahan yang ketat.
HIV memiliki diameter 100-150&nbsp;nm dan berbentuk sferis (''spherical'') hingga oval karena bentuk selubung yang menyelimuti partikel virus (''virion'').<ref name="s1" /> Selubung virus berasal dari membran sel inang yang sebagian besar tersusun dari lipida.<ref name="s1" /> Di dalam selubung terdapat bagian yang disebut protein matriks.<ref name="s1">{{en}} B. D. Schoub. 1999. AIDS and HIV in Perspective: A Guide to Understanding the Virus and its Consequences. Cambridge University Press Page. 57-59.</ref>
 
Bagian internal dari HIV terdiri dari dua komponen utama, yaitu genom dan kapsid.<ref name="sh1" /> Genom adalah materi genetik pada bagian inti virus yang berupa dua kopi utas tunggal RNA.<ref name="sh1" /> Sedangkan, kapsid adalah protein yang membungkus dan melindungi genom.<ref name="sh1" />
Sub-Sahara Afrika tetap merupakan daerah yang paling parah terkena HIV di antara kaum perempuan hamil pada usia 15-24 tahun di sejumlah negara di sana. Ini diduga disebabkan oleh banyaknya [[penyakit kelamin]], praktek menoreh tubuh, [[transfusi darah]], dan buruknya tingkat [[kesehatan]] dan [[gizi]] di sana (Bentwich et al., 1995).
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].
 
Berbeda dengan sebagian besar retrovirus yang hanya memiliki tiga gen (''gag'', ''pol'', dan ''env''), HIV memiliki enam gen tambahan (''vif, vpu, vpr, tat, ref,'' dan ''nef'').<ref name="hasilan otomatis1">Mary Ropka, Ann Williams. 1998. HIV nursing and symptom management. Jones & Bartlett. Page. 4</ref> Gen-gen tersebut disandikan oleh RNA virus yang berukuran 9 kb.<ref name="s1" /> Kesembilan gen tersebut dikelompokkan menjadi tiga kategori berdasarkan fungsinya, yaitu gen penyandi protein struktural (Gag, Pol, Env), protein regulator (Tat, Rev), dan gen aksesoris (Vpu hanya pada HIV-1, Vpx hanya pada HIV-2; Vpr, Vif, Nef).<ref name="sh1" />
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.
 
{| class="wikitable" border="1" cellpadding="3" cellspacing="0" align="center"
<!--
! Nama Gen dan Protein yang disandikan !! Ukuran !! Lokalisasi !! Fungsi
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.
|- align="center"
-->
! Tat (trans-aktivator transkripsi)
| 86 asam amino (AA), 2 ekson, 14 kDalton || nukleus, nukleolus, protein awal || Penting untuk replikasi; Trans-aktivasi ekspresi mRNA virus, mengatur ekspresi sitokin dan reseptor.<ref name="prot">Andreas Holzenburg, Elke Bogner. 2002. Structure-function relationships of human pathogenic viruses. New York: Kluwer Academic/Plenum Publisher. Page. 303</ref>
|- align="center"
! Rev (regulator ekspresi protein virus)
| 116 AA, 2 ekson, 19 kDalton|| [[nukleus]], di antara [[sitoplasma]] dan [[nukleolus]]|| Penting untuk replikasi; mengatur [[transkripsi]] dan [[Ekspresi gen|ekspresi protein]] Gag, Pol, Env, Vif, Vpu, dan Vpr.<ref name="prot"/>
|- align="center"
! Vif (faktor infektivitas virus)
| 192 AA, 23 kDalton || sitoplasma, beberapa [[molekul]] yang terbungkus dalam virion dewasa || Penting untuk infektivitas dan [[Replikasi DNA|replikasi]] pada sel primer; berperan dalam tahap awal replikasi HIV<ref name="prot"/>
|- align="center"
! Vpr (Protein R virus)
| 96-106 AA, 10-15 kDalton || komponen dari inti virus dan kompleks membran || Mediasi replikasi di sel yang tidak membelah<ref name="prot"/>
|- align="center"
! Vpx (Protein X virus)
| 112 AA, 12-16 kDalton|| komponen virion || Berfungsi seperti Vpr<ref name="prot"/>
|- align="center"
! Vpu (Protein U virus)
| 81 AA (terfosforilasi), 9,2 & 16 kDalton|| [[retikulum endoplasma]], protein transmembran || Degradasi CD4; meningkatkan pelepasan HIV; pembentukan membran protein integral; regulasi ekpresi permukaan sel terhadap [[Kompleks histokompatibilitas utama|MHC I]]<ref name="prot"/>
|- align="center"
! Nef (Faktor Negatif)
| 206 AA, 27 kDalton|| virion, sitoplasma, nukleus || Meningkatkan produksi HIV di tahap akhir; mengatur ekspresi MHC I dan CD4<ref name="prot"/>
|- align="center"
|}
 
== StrukturSiklus ==
[[Berkas:Struktur HIV.png|jmpl|400px|ka|Struktur HIV.]]
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"
Seperti virus lain pada umumnya, HIV hanya dapat bereplikasi dengan memanfaatkan sel inang. Siklus HIV diawali dengan penempelan partikel virus (''virion'') dengan reseptor pada permukaan sel inang, di antaranya adalah CD4, CXCR5, dan CXCR5. Sel-sel yang menjadi target HIV adalah [[sel dendritik]], [[sel T]], dan [[makrofaga]].<ref name="sh1" /> Sel-sel tersebut terdapat pada permukaan lapisan kulit dalam ([[mukosa]]) [[penis]], [[vagina]], dan [[oral]] yang biasanya menjadi tempat awal infeksi HIV.<ref name="sh1" /> Selain itu, HIV juga dapat langsung masuk ke aliran darah dan masuk serta bereplikasi di [[Limpa|noda limpa]].<ref name="sh1">{{en}} Felissa R. Lashley, Jerry D. Durham. 2009. The person with HIV/AIDS: nursing perspectives. Springer Publishing Company.</ref>
[[Berkas:HIV Viron.png|thumb|500px|right|Diagram of the HIV virus.]]
 
Setelah menempel, selubung virus akan melebur (fusi) dengan membran sel sehingga isi partikel virus akan terlepas di dalam sel.<ref name="sh2">[http://www.avert.org/hiv-virus.htm Avert.org] {{Webarchive|url=https://web.archive.org/web/20130821231238/http://avert.org/hiv-virus.htm |date=2013-08-21 }} HIV Structure and Life Cycle.</ref> Selanjutnya, enzim [[transkriptase balik]] yang dimiliki HIV akan mengubah genom virus yang berupa RNA menjadi DNA.<ref name="sh2" /> Kemudian, DNA virus akan dibawa ke inti sel manusia sehingga dapat menyisip atau terintegrasi dengan DNA manusia.<ref name="sh2" /> DNA virus yang menyisip di DNA manusia disebut sebagai provirus dan dapat bertahan cukup lama di dalam sel.<ref name="sh2" /> Saat sel teraktivasi, enzim-enzim tertentu yang dimiliki sel inang akan memproses provirus sama dengan [[DNA]] manusia, yaitu diubah menjadi mRNA.<ref name="sh2" /> Kemudian, [[mRNA]] akan dibawa keluar dari inti sel dan menjadi cetakan untuk membuat protein dan enzim HIV.<ref name="sh2" /> Sebagian RNA dari provirus yang merupakan genom RNA virus.<ref name="sh2" /> Bagian genom RNA tersebut akan dirakit dengan protein dan enzim hingga menjadi virus utuh.<ref name="sh2" /> Pada tahap perakitan ini, [[HIV-1 protease|enzim HIV protease]] virus berperan penting untuk memotong [[protein]] panjang menjadi bagian pendek yang menyusun inti virus.<ref name="sh2" /> Apabila HIV utuh telah matang, maka virus tersebut dapat keluar dari sel inang dan menginfeksi sel berikutnya.<ref name="sh3" /> Proses pengeluaran virus tersebut melalui pertunasan (budding), di mana virus akan mendapatkan selubung dari [[Membran sel|membran permukaan sel inang]].<ref name="sh3">{{en}} [http://aids.about.com/cs/aidsfactsheets/a/hivlife.htm About.com] {{Webarchive|url=https://web.archive.org/web/20110810025831/http://aids.about.com/cs/aidsfactsheets/a/hivlife.htm |date=2011-08-10 }} Mark Cichocki, R.N. The HIV Life Cycle: Understanding HIV replication. Diakses 29 Mei 2011.</ref>
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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).
 
== Deteksi HIV ==
There are two forms of the virus:
[[Berkas:Oraquick.jpg|200px|jmpl|ka|Seorang wanita sedang menggunakan alat tes HIV.]]
 
Pada saat paling awalpun deteksi HIV dapat dilakukan dengan pemeriksaan darah, walaupun tidak ada gejala apapun. Pada tahap kedua telah ada gejala klinis, misalnya kulitnya jelek, gatal-gatal dan batuk pilek seperti flu biasa. Pada tahap ketiga akan mengalami penurunan berat badan dan terkena TBC. Dan pada tahap keempat telah mengalami komplikasi, sulit disembuhkan dan biasanya diikuti dengan kematian.<ref>{{Cite news |url=http://pontianak.tribunnews.com/2014/11/26/kenali-empat-stadium-hiv |title=Kenali Empat Stadium HIV |date=26 Nopember 2014 |language=id |work=[[Tribunnews|Tribunnews.com]] |access-date=2014-11-26 |archive-date=2023-06-12 |archive-url=https://web.archive.org/web/20230612152240/https://pontianak.tribunnews.com/2014/11/26/kenali-empat-stadium-hiv |dead-url=no }}</ref>
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).
 
Umumnya, ada tiga tipe deteksi HIV, yaitu tes PCR, tes antibodi HIV, dan tes antigen HIV.<ref name="test1">[http://www.avert.org/testing.htm AVERT.org] {{Webarchive|url=https://web.archive.org/web/20130821221223/http://avert.org/testing.htm |date=2013-08-21 }}. HIV Testing: The different types of HIV test. Diakses 18 Juni 2011.</ref> Tes [[Reaksi berantai polimerase|reaksi berantai polimerase (PCR)]] merupakan teknik deteksi berbasis asam nukleat (DNA dan RNA) yang dapat mendeteksi keberadaan materi genetik HIV di dalam tubuh manusia.<ref name="test2" /> Tes ini sering pula dikenal sebagai tes beban virus atau tes amplifikasi asam nukleat (HIV NAAT).<ref name="test1" /> PCR DNA biasa merupakan metode kualitatif yang hanya bisa mendeteksi ada atau tidaknya DNA virus.<ref name="deteksi1" /> Sedangkan, untuk deteksi RNA virus dapat dilakukan dengan metode ''real-time'' PCR yang merupakan metode kuantitatif.<ref name="deteksi1">[http://www.who.int/hiv/paediatric/EarlydiagnostictestingforHIVVer_Final_May07.pdf World Health Organization] {{Webarchive|url=https://web.archive.org/web/20220305190519/http://www.who.int/hiv/paediatric/EarlydiagnostictestingforHIVVer_Final_May07.pdf |date=2022-03-05 }} Early detection of HIV infection in infants and children.</ref> Deteksi asam nukleat ini dapat mendeteksi keberadaan HIV pada 11-16 hari sejak awal infeksi terjadi.<ref name="test">[http://www.contoh.org Microbiology Australia] {{Webarchive|url=https://web.archive.org/web/20130421014703/http://contoh.org/ |date=2013-04-21 }} The Australian Society for Microbiology. Volume 22. Number 1. Maret 2010. Page 17-20.</ref> Tes ini biasanya digunakan untuk mendeteksi HIV pada bayi yang baru lahir, namun jarang digunakan pada individu dewasa karena biaya tes PCR yang mahal dan tingkat kesulitan mengelola dan menafsirkan hasil tes ini lebih tinggi bila dibandingkan tes lainnya.<ref name="test1" />
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.
 
Untuk mendeteksi HIV pada orang dewasa, lebih sering digunakan tes [[antibodi]] HIV yang murah dan akurat.<ref name="test1" /> Seseorang yang terinfeksi HIV akan menghasilkan antibodi untuk melawan infeksi tersebut.<ref name="test1" /> Tes antibodi HIV akan mendeteksi antibodi yang terbentuk di darah, saliva (liur), dan urin.<ref name="test1" /> Sejak tahun 2002, telah dikembangkan suatu penguji cepat (''rapid test'') untuk mendeteksi antibodi HIV dari tetesan darah ataupun sampel liur (saliva) manusia.<ref name="rapid" /> Sampel dari tubuh pasien tersebut akan dicampur dengan larutan tertentu. Kemudian, kepingan alat uji (''test strip'') dimasukkan dan apabila menunjukkan hasil positif maka akan muncul dua pita berwarna ungu kemerahan.<ref name="rapid" /> Tingkat akurasi dari alat uji ini mencapai 99.6%, namun semua hasil positif harus dikonfirmasi kembali dengan [[ELISA]].<ref name="rapid">Hung Fan, Ross F. Conner, Luis P. Villarreal. 2010. AIDS: Science and Society. Jones & Bartlett Publishers. Page.150-151.</ref> Selain ELISA, tes antibodi HIV lain yang dapat digunakan untuk pemeriksaan lanjut adalah ''[[Western blot]]''.<ref name="test2">{{en}} David Mahan Knipe, Peter M. Howley. Fields virology, Volume 1. 2001. Lippincott William & Wilkins. Page 596-598.</ref>
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.
 
Tes antigen dapat mendeteksi antigen (protein P24) pada HIV yang memicu respon antibodi.<ref name="test1" /> Pada tahap awal infeksi HIV, P24 diproduksi dalam jumlah tinggi dan dapat ditemukan dalam serum darah.<ref name="test1" /> Tes antibodi dan tes antigen digunakan secara berkesinambungan untuk memberikan hasil deteksi yang lebih akurat dan lebih awal.<ref name="test1" /> Tes ini jarang digunakan sendiri karena sensitivitasnya yang rendah dan hanya bisa bekerja sebelum antibodi terhadap HIV terbentuk.<ref name="test1" />
===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.
 
Kesemua cara di atas mendeteksi virusnya, tetapi cara paling murah adalah tes CD4 yang hanya Rp 100,000 lebih di RS Kanker. CD4 tidak mengetes kehadiran virus HIVnya, atau antibodi spesifik yang melawan HIV, CD4 mengukur sistem imunitas pasien. Sebelumnya jika CD4 belum mencapai nilai tertentu, walaupun diketahui keberadaan virus HIV, maka belum dilakukan pengobatan apapun, tetapi sekarang ini jika sudah diketahui keberadaan virus HIV, maka berapapun nilai CD4 harus dilakukan pengobatan.Di Indonesia, dimana masalah dana menjadi kendala, maka tes CD4 sudah cukup memadai untuk deteksi awal kemungkinan keberadaan virus HIV. Dan perlu diingat bahwa HIV belum tentu menjadi AIDS dengan pengobatan yang adekuat. CD4 juga berguna sebagai indikasi awal keberadaan kanker atau segala hal yang berhubungan dengan sistem imunitas pasien. Jika CD4 telah mencapai nilai tertentu, maka perlu dilakukan tes CD8.
===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''.
 
== Penularan dan pencegahan ==
==Life cycle of HIV==
HIV dapat ditularkan melalui injeksi langsung ke aliran darah, serta kontak [[membran mukosa]] atau jaringan yang terlukan dengan cairan tubuh tertentu yang berasal dari penderita HIV.<ref name="p3" /> Cairan tertentu itu meliputi [[darah]], semen, sekresi vagina, dan [[ASI]].<ref name="p3">{{Cite web |url=http://www.cdc.gov/hiv/resources/qa/transmission.htm |title=Center for Disease Control and Prevention:HIV Transmission |access-date=2011-05-31 |archive-date=2012-06-07 |archive-url=https://web.archive.org/web/20120607023525/http://www.cdc.gov/hiv/resources/qa/transmission.htm |dead-url=no }}</ref> Beberapa jalur penularan HIV yang telah diketahui adalah melalui hubungan seksual, dari ibu ke anak (perinatal), penggunaan obat-obatan intravena, transfusi dan [[transplantasi]], serta paparan pekerjaan.<ref name="p2" /> Tetapi untuk tiap satu kali tindakan, maka yang paling berisiko adalah [[transfusi darah]] dari donor darah penderita HIV dimana kemungkinan resipien terkena HIV mencapai 90 persen, sedangkan ibu hamil penderita HIV yang melahirkan dan menyusuinya kemungkinan akan menularkan pada bayinya HIV sebesar 25 persen, tetapi dengan pemberian obat-obatan dan penanganan yang tepat pada saat kelahiran dan sesudahnya, maka angka ini dapat ditekan menjadi 1 sampai 2 persen saja.Sekarang ini semua darah dari donor mengalami penapisan HIV, sehingga kasus penularan melalui transfusi darah boleh dikatakan sudah tidak ada lagi.
[[Image:Hiv gross.png|right|thumbnail|250px|HIV replication]]
 
===Viral tropismHubungan seksual ===
Menurut data [[WHO]], pada tahun 1983-1995, sebanyak 70-80% penularan HIV dilakukan melalui hubungan heteroseksual, sedangkan 5-10% terjadi melalui hubungan homoseksual. Kontak seksual melalui vagina dan anal memiliki risiko yang lebih besar untuk menularkan HIV dibandingkan dengan kontak seks secara oral.<ref name="oral">[http://www.cdc.gov/hiv/resources/factsheets/pdf/oralsex.pdf CDC HIV/AIDS Facts] {{Webarchive|url=https://web.archive.org/web/20130510210937/http://www.cdc.gov/hiv/resources/Factsheets/pdf/oralsex.pdf |date=2013-05-10 }}, Oral Sex and HIV Risk. Juni 2009.</ref> Beberapa faktor lain yang dapat meningkatkan risiko penularan melalui hubungan seksual adalah kehadiran [[penyakit menular seksual]], [[beban virus|kuantitas beban virus]], penggunaan [[douche]]. Seseorang yang menderita penyakit menular seksual lain (contohnya: [[sifilis]], [[herpes genitali]], [[kencing nanah]], dsb.) akan lebih mudah menerima dan menularkan HIV kepada orang lain yang berhubungan seksual dengannya.<ref name="hub1">[http://www.hivinfo.us/preventionforpositives.html HIVInfo.us: An HIV Information Site & HIV Educational Resource Site (HIS & HERS)] {{Webarchive|url=https://web.archive.org/web/20230529124237/http://hivinfo.us/preventionforpositives.html |date=2023-05-29 }}, Prevention for Positives: HIV & STD Transmission Issues. Diakeses pada 12 Juni 2011.</ref><ref name="hub2">[http://www.kingcounty.gov/healthservices/health/communicable/hiv/publications/infograms/hivtransmission.aspx Public Health - Seattle & King County] {{Webarchive|url=https://web.archive.org/web/20110522114638/http://www.kingcounty.gov/healthservices/health/communicable/hiv/publications/infograms/hivtransmission.aspx |date=2011-05-22 }}, Update on Sexual Transmission of HIV - March 2002. Diakses pada 17 Juni 2011.</ref> Beban virus merupakan jumlah virus aktif yang ada di dalam tubuh. Penularah HIV tertinggi terjadi selama masa awal dan akhir infeksi HIV karena beban virus paling tinggi pada waku tersebut.<ref name="hub2" /> Pada rentan waktu tersebut, beberapa orang hanya menimbulkan sedikit gejala atau bahkan tidak sama sekali.<ref name="hub2" /> Penggunaan douche dapat meningkatkan risiko penularan HIV karena menghancurkan [[bakteri]] baik di sekitar vagina dan anus yang memiliki fungsi proteksi.<ref name="hub2" /> Selain itu, penggunaan douche setelah berhubungan seksual dapat menekan bakteri penyebab penyakit masuk ke dalam tubuh dan mengakibatkan infeksi.<ref name="hub2" />
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).
 
Pencegahan HIV melalui hubungan seksual dapat dilakukan dengan tidak berganti-ganti pasangan dan menggunakan [[kondom]].<ref name="p2" /> Cara pencegahan lainnya adalah dengan melakukan hubungan seks tanpa menimbulkan paparan cairan tubuh.<ref name="hub1" /> Untuk menurunkan beban virus di dalam saluran kelamin dan darah, dapat digunakan terapi anti-retroviral.<ref name="hub2" />
HIV can also infect [[dendritic cell]]s (Knight ''et al''., 1990).
 
=== Ibu ke anak (transmisi perinatal) ===
===Viral entry to the cell===
Penularan HIV dari ibu ke anak dapat terjadi melalui infeksi ''in utero'', saat proses persalinan, dan melalui pemberian ASI.<ref name="p2" /> Beberapa faktor maternal dan eksternal lainnya dapat mempengaruhi transmisi HIV ke bayi, di antaranya banyaknya virus dan sel imun pada trisemester pertama, kelahiran prematur, dan lain-lain.<ref name="p2" /> Penurunan sel imun (CD4+) pada ibu dan tingginya RNA virus dapat meningkatkan risiko penularan HIV dari ibu ke anak. Selain itu, sebuah studi pada wanita hamil di Malawi dan AS juga menyebutkan bahwa kekurangan vitamin A dapat meningkatkan risiko infeksi HIV. Risiko penularan perinatal dapat dilakukan dengan persalinan secara caesar, tidak memberikan ASI, dan pemberian ARV pada masa akhir kehamilan dan setelah kelahiran bayi.<ref name="p2">[http://trace.tennessee.edu/cgi/viewcontent.cgi?article=1554&context=utk_chanhonoproj&sei-redir=1#search=%22HIV+structure%22 Trace: Tennessee Research and Creative Exchange] {{Webarchive|url=https://web.archive.org/web/20210412114541/https://trace.tennessee.edu/cgi/viewcontent.cgi?article=1554&context=utk_chanhonoproj&sei-redir=1#search=%22HIV+structure%22 |date=2021-04-12 }} Jonathan Richard Hughes. 2002. HIV: Structure, Life Cycle, and Pathogenecity.</ref> Di sebagian negara berkembang, pencegahan pemberian ASI dari penderita HIV/AIDS kepada bayi menghadapi kesulitan karena harga susu formula sebagai pengganti relatif mahal.<ref name="perinatal" /> Selain itu, para ibu juga harus memiliki akses ke air bersih dan memahami cara mempersiapan susu formula yang tepat.<ref name="perinatal">[http://www.rand.org/content/dam/rand/pubs/drafts/2005/DRU3071.pdf RAND Health] {{Webarchive|url=https://web.archive.org/web/20220720001508/https://www.rand.org/content/dam/rand/pubs/drafts/2005/DRU3071.pdf |date=2022-07-20 }} Michael A. Stoto, Ann S. Goldman. 2003. Preventing Perinatal Transmission of HIV.</ref>
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).
 
=== Lain-lain ===
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.
Cara efektif lain untuk penyebaran virus ini adalah melalui penggunaan [[jarum]] atau [[alat suntik]] yang terkontaminasi, terutama di negara-negara yang kesulitan dalam sterilisasi alat kesehatan.<ref name="p2" /> Bagi pengguna obat intravena (dimasukkan melalui [[pembuluh darah]]), HIV dapat dicegah dengan menggunakan jarum dan alat suntik yang bersih.<ref name="p2" /> Penularan HIV melalui [[transplantasi]] dan [[Transfusi darah|transfusi]] hanya menjadi penyebab sebagian kecil kasus HIV di dunia (3-5%).<ref name="p2" /> Hal ini pun dapat dicegah dengan melakukan pemeriksaan produk darah dan transplan sebelum didonorkan dan menghindari donor yang memiliki risiko tinggi terinfeksi HIV.<ref name="p2" />
 
Penularan dari pasien ke petugas kesehatan yang merawatnya juga sangat jarang terjadi (< 0.0001% dari keseluruhan kasus di dunia).<ref name="p2" /> Hal ini dicegah dengan memeberikan pengajaran atau edukasi kepada petugas kesehatan, pemakaian pakaian pelindung, [[sarung tangan]], dan pembuangan alat dan bahan yang telah terkontaminasi sesuai dengan prosedur.<ref name="p2" /> Pada tahun 2005, sempat diusulkan untuk melakukan [[sunat]] dalam rangka pencegahan HIV. Namun menurut WHO, tindakan pencegahan tersebut masih terlalu awal untuk direkomendasikan.<ref name="p1">{{en}}[http://www.who.int/mediacentre/news/releases/2005/pr32/en/ WHO:UNAIDS statement on South African trial findings regarding male circumcision and HIV] {{Webarchive|url=https://web.archive.org/web/20210126015524/http://www.who.int/mediacentre/news/releases/2005/pr32/en/ |date=2021-01-26 }}</ref>
===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).
 
Ada beberapa jalur penularan yang ditakutkan dapat menyebarkan HIV, yaitu melalui [[ludah]], gigitan [[nyamuk]], dan kontak sehari-hari (berjabat tangan, terekspos batuk dan bersin dari penderita HIV, menggunakan [[toilet]] dan alat makan bersama, [[Peluk|berpelukan]]).<ref name="p3" /> Namun, CDC (Pusat Pengendalian dan Pencegahan Penyakit) menyatakan bahwa aktivitas tersebut tidak mengakibatkan penularan HIV.<ref name="p3" /> Beberapa aktivitas lain yang sangat jarang menyebabkan penularan HIV adalah melalui gigitan manusia dan beberapa tipe ciuman tertentu.<ref name="p3" />
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.
 
Sub-Sahara Afrika tetap merupakan daerah yang paling parah terkena HIV di antara kaum perempuan hamil pada usia 15-24 tahun di sejumlah negara di sana. Ini diduga disebabkan oleh banyaknya [[penyakit kelamin]], praktik menoreh tubuh, [[transfusi darah]], dan buruknya tingkat [[kesehatan]] dan [[gizi]] di sana.<ref name="p4">{{en}}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</ref>
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.
 
== Lihat pula ==
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).
* [[Tidak Terdeteksi = Tidak Menularkan|TDTM]]
* [[ARV]]
* [[Faktor NE]]
* [[Penularan kriminal HIV]]
* [[Orang HIV positif]]
* [[Tes HIV]]
* [[Post-exposure prophylaxis]]
* [[HIV+]]
 
== Referensi ==
===Viral assembly and release===
{{reflist|2}}
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.
 
== Pranala luar ==
==Signs and symptoms of HIV-1 infection==
{{col-css3-begin|2}}
[[Image:hiv-timecourse.png|right|thumbnail|500px|Graph showing HIV virus and CD4<sup>+</sup> levels over the course of an untreated infection]]
* [http://www.ericdigests.org/pre-9212/hiv.htm AIDS/HIV Education] {{Webarchive|url=https://web.archive.org/web/20060618220559/http://www.ericdigests.org/pre-9212/hiv.htm |date=2006-06-18 }}
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.
* [http://www.cmeonhiv.com Continuing medical education about HIV for healthcare providers] {{Webarchive|url=https://web.archive.org/web/20230611063516/http://cmeonhiv.com/ |date=2023-06-11 }}
 
* [http://www.un.org/ga/aids/coverage/FinalDeclarationHIVAIDS.html Declaration of Commitment on HIV/AIDS] {{Webarchive|url=https://web.archive.org/web/20190816072556/https://www.un.org/ga/aids/coverage/FinalDeclarationHIVAIDS.html |date=2019-08-16 }} UN 2001
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.
* [http://fightaidsathome.scripps.edu/ FightAIDS@Home] {{Webarchive|url=https://web.archive.org/web/20191008123857/http://fightaidsathome.scripps.edu/ |date=2019-10-08 }}
 
* [http://www.hivatis.org HIV/AIDS Treatment Information Service] {{Webarchive|url=https://web.archive.org/web/20201028003445/http://hivatis.org/ |date=2020-10-28 }}
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.
* [http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?val=NC_001802 Genome (HIV-1)] {{Webarchive|url=https://web.archive.org/web/20230812122619/https://www.ncbi.nlm.nih.gov/nuccore/NC_001802 |date=2023-08-12 }}
 
* [http://www.ncbi.nlm.nih.gov/entrez/viewer.fcgi?val=NC_001722 Genome (HIV-2)] {{Webarchive|url=https://web.archive.org/web/20230812122627/https://www.ncbi.nlm.nih.gov/nuccore/NC_001722 |date=2023-08-12 }}
* ''Stage I:'' HIV disease is asymptomatic and not categorized as AIDS
* [http://www.ericdigests.org/1997-3/hiv.html HIV/AIDS Education in Teacher Preparation Programs] {{Webarchive|url=https://web.archive.org/web/20060618083346/http://www.ericdigests.org/1997-3/hiv.html |date=2006-06-18 }}
* ''Stage II:'' include minor mucocutaneous manifestations and recurrent upper respiratory tract infections
* [http://hivinsite.org/InSite HIV InSite] {{Webarchive|url=https://web.archive.org/web/20050809233618/http://www.hivinsite.org/InSite |date=2005-08-09 }}
* ''Stage III:'' includes unexplained chronic diarrhea for longer than a month, severe bacterial infections and pulmonary tuberculosis or
* [http://health.howstuffworks.com/aids.htm How Aids Works] {{Webarchive|url=https://web.archive.org/web/20100326071544/http://health.howstuffworks.com/aids.htm |date=2010-03-26 }} (with animation)
* ''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.
* [http://www.doctorswithoutborders.org/news/hiv-aids/index.cfm Medecins Sans Frontieres/Doctors Without Borders HIV/AIDS Pages] {{Webarchive|url=https://web.archive.org/web/20060515215614/http://www.doctorswithoutborders.org/news/hiv-aids/index.cfm |date=2006-05-15 }}
 
* [http://www.niaid.nih.gov/daids/ NIH/NIAD/DAIDS] {{Webarchive|url=https://web.archive.org/web/20060414001209/http://www.niaid.nih.gov/daids/ |date=2006-04-14 }}
{{see details|WHO Disease Staging System for HIV Infection and Disease}}
* [http://www.mcld.co.uk/hiv/ "The Molecules of HIV" information resource] {{Webarchive|url=https://web.archive.org/web/20060614085651/http://www.mcld.co.uk/hiv/ |date=2006-06-14 }}
 
* [http://www.phrusa.org/campaigns/aids/release080103.html Unsafe Health Care and the HIV/AIDS Pandemic] {{Webarchive|url=https://web.archive.org/web/20060515222359/http://www.phrusa.org/campaigns/aids/release080103.html |date=2006-05-15 }} 2003
Most individuals infected with HIV will progress to [[AIDS]], but the time course that this will take depends upon a variety of factors.
* {{en}}[http://ajrccm.atsjournals.org/cgi/content/full/162/4/S1/S141 Innate Immune System Damage in Human Immunodeficiency Virus Type 1 Infection] {{Webarchive|url=https://web.archive.org/web/20081013041750/http://ajrccm.atsjournals.org/cgi/content/full/162/4/S1/S141 |date=2008-10-13 }}, Immunobiology Unit, MRC Centre for Inflammation, and Departments of Pathology and Chemistry, Edinburgh University, SARAH HOWIE, ROBERT RAMAGE, and TIM HEWSON
 
* {{en}} [http://www.nature.com/ki/journal/v42/n2/abs/ki1992298a.html Binding of serum immunoglobulins to collagens in IgA nephropathy and HIV infection] {{Webarchive|url=https://web.archive.org/web/20140223143731/http://www.nature.com/ki/journal/v42/n2/abs/ki1992298a.html |date=2014-02-23 }}
{{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 &nbsp;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] {{Webarchive|url=https://web.archive.org/web/20230812122630/https://www.nature.com/articles/17130 |date=2023-08-12 }}. ''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.
Baris 172 ⟶ 162:
* 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] {{Webarchive|url=https://web.archive.org/web/20230812123652/https://www.thelancet.com/journals/laninf/article/PIIS1473-3099(02)00343-2/fulltext |date=2023-08-12 }}. ''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
{{col-css3-end}}
 
== 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
 
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