HIV/AIDS Warning: You are not logged in. Your IP address will be publicly visible if you make any edits. If you log in or create an account, your edits will be attributed to your username, along with other benefits.Anti-spam check. Do not fill this in! == Virology == {{Main|HIV}} [[File:HI-virion-structure en.svg|thumb|alt=diagram of microscopic viron structure|Diagram of an HIV virion structure]] [[File:HIV-budding-Color.jpg|thumb|alt=A large round blue object with a smaller red object attached to it. Multiple small green spots are speckled over both.|[[Scanning electron micrograph]] of HIV-1, colored green, budding from a cultured [[lymphocyte]]]] [[HIV]] is the cause of the spectrum of disease known as HIV/AIDS. HIV is a [[retrovirus]] that primarily infects components of the human [[immune system]] such as CD4<SUP>+</SUP> T cells, [[macrophage]]s and [[dendritic cell]]s. It directly and indirectly destroys CD4<SUP>+</SUP> T cells.<ref name=Alimonti>{{cite journal | vauthors = Alimonti JB, Ball TB, Fowke KR | title = Mechanisms of CD4+ T lymphocyte cell death in human immunodeficiency virus infection and AIDS | journal = The Journal of General Virology | volume = 84 | issue = Pt 7 | pages = 1649–61 | date = July 2003 | pmid = 12810858 | doi = 10.1099/vir.0.19110-0 | doi-access = free }}</ref> HIV is a member of the [[genus]] ''[[Lentivirus]]'',<ref name=ICTV61.0.6>{{cite web | author=International Committee on Taxonomy of Viruses| author-link=International Committee on Taxonomy of Viruses | publisher=[[National Institutes of Health]] | year=2002 | url=https://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/61060000.htm |archive-url=https://web.archive.org/web/20060418135608/http://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/61060000.htm | title=61.0.6. Lentivirus | newspaper=Men's Journal | access-date=June 25, 2012 |archive-date=April 18, 2006}}</ref> part of the family ''[[Retroviridae]]''.<ref name=ICTV61.>{{cite web | author=International Committee on Taxonomy of Viruses | publisher=National Institutes of Health | year=2002 | url=https://www.ncbi.nlm.nih.gov/ICTVdb/ICTVdB/61000000.htm | title=61. Retroviridae | newspaper=Men's Journal | archive-url=http://webarchive.loc.gov/all/20011217155644/http%3A//www%2Encbi%2Enlm%2Enih%2Egov/ictvdb/ictvdb/61000000%2Ehtm | access-date=June 25, 2012 | archive-date= December 17, 2001}}</ref> Lentiviruses share many [[morphology (biology)|morphological]] and [[biology|biological]] characteristics. Many species of mammals are infected by lentiviruses, which are characteristically responsible for long-duration illnesses with a long [[incubation period]].<ref name=Levy>{{cite journal | vauthors = Levy JA | title = HIV pathogenesis and long-term survival | journal = AIDS | volume = 7 | issue = 11 | pages = 1401–10 | date = November 1993 | pmid = 8280406 | doi = 10.1097/00002030-199311000-00001 }}</ref> Lentiviruses are transmitted as single-stranded, positive-[[Sense (molecular biology)|sense]], enveloped [[RNA virus]]es. Upon entry into the target cell, the viral [[RNA]] [[genome]] is converted (reverse transcribed) into double-stranded [[DNA]] by a virally encoded [[reverse transcriptase]] that is transported along with the viral genome in the virus particle. The resulting viral DNA is then imported into the cell nucleus and integrated into the cellular DNA by a virally encoded [[integrase]] and host co-factors.<ref name="JASmith">{{cite journal | vauthors = Smith JA, Daniel R | title = Following the path of the virus: the exploitation of host DNA repair mechanisms by retroviruses | journal = ACS Chemical Biology | volume = 1 | issue = 4 | pages = 217–26 | date = May 2006 | pmid = 17163676 | doi = 10.1021/cb600131q }}</ref> Once integrated, the virus may become [[Incubation period|latent]], allowing the virus and its host cell to avoid detection by the immune system.<ref>{{cite book|veditors=Martínez MA|title=RNA interference and viruses : current innovations and future trends|year=2010|publisher=Caister Academic Press|location=Norfolk|isbn=978-1-904455-56-1|page=73|url=https://books.google.com/books?id=C5TY8W74scIC&pg=PA73|access-date=June 27, 2015|archive-url=https://web.archive.org/web/20150911042839/https://books.google.com/books?id=C5TY8W74scIC&pg=PA73|archive-date=September 11, 2015|url-status=live}}</ref> Alternatively, the virus may be [[Transcription (genetics)|transcribed]], producing new RNA genomes and viral proteins that are packaged and released from the cell as new virus particles that begin the replication cycle anew.<ref>{{cite book|editor=Gerald B. Pier|title=Immunology, infection, and immunity|year=2004|publisher=ASM Press|location=Washington, DC|isbn=978-1-55581-246-1|page=550|url=https://books.google.com/books?id=kBb-wYsMHEAC&pg=PA550|access-date=June 27, 2015|archive-url=https://web.archive.org/web/20160509095319/https://books.google.com/books?id=kBb-wYsMHEAC&pg=PA550|archive-date=May 9, 2016|url-status=live}}</ref> HIV is now known to spread between CD4<SUP>+</SUP> T cells by two parallel routes: cell-free spread and cell-to-cell spread, i.e. it employs hybrid spreading mechanisms.<ref name=Zhang>{{cite journal | vauthors = Zhang C, Zhou S, Groppelli E, Pellegrino P, Williams I, Borrow P, Chain BM, Jolly C | title = Hybrid spreading mechanisms and T cell activation shape the dynamics of HIV-1 infection | journal = PLOS Computational Biology | volume = 11 | issue = 4 | page= e1004179 | date = April 2015 | pmid = 25837979 | pmc = 4383537 | doi = 10.1371/journal.pcbi.1004179 | arxiv = 1503.08992 | bibcode = 2015PLSCB..11E4179Z | doi-access = free }}</ref> In the cell-free spread, virus particles bud from an infected T cell, enter the blood/extracellular fluid and then infect another T cell following a chance encounter.<ref name="Zhang"/> HIV can also disseminate by direct transmission from one cell to another by a process of cell-to-cell spread.<ref name=Jolly>{{cite journal | vauthors = Jolly C, Kashefi K, Hollinshead M, Sattentau QJ | title = HIV-1 cell to cell transfer across an Env-induced, actin-dependent synapse | journal = [[The Journal of Experimental Medicine]] | volume = 199 | issue = 2 | pages = 283–93 | date = January 2004 | pmid = 14734528 | pmc = 2211771 | doi = 10.1084/jem.20030648 }}</ref><ref name=Sattentau>{{cite journal | vauthors = Sattentau Q | title = Avoiding the void: cell-to-cell spread of human viruses | journal = Nature Reviews. Microbiology | volume = 6 | issue = 11 | pages = 815–26 | date = November 2008 | pmid = 18923409 | doi = 10.1038/nrmicro1972 | s2cid = 20991705 | doi-access = free }}</ref> The hybrid spreading mechanisms of HIV contribute to the virus' ongoing replication against antiretroviral therapies.<ref name="Zhang"/><ref name=Sigal>{{cite journal | vauthors = Sigal A, Kim JT, Balazs AB, Dekel E, Mayo A, Milo R, Baltimore D | title = Cell-to-cell spread of HIV permits ongoing replication despite antiretroviral therapy | journal = [[Nature (journal)|Nature]] | volume = 477 | issue = 7362 | pages = 95–98 | date = August 2011 | pmid = 21849975 | doi = 10.1038/nature10347 | bibcode = 2011Natur.477...95S | s2cid = 4409389 | url = https://authors.library.caltech.edu/102808/2/41586_2011_BFnature10347_MOESM271_ESM.pdf }}</ref> Two [[Subtypes of HIV|types of HIV]] have been characterized: HIV-1 and HIV-2. HIV-1 is the virus that was originally discovered (and initially referred to also as LAV or HTLV-III). It is more [[virulent]], more [[infectivity|infective]],<ref>{{cite journal | vauthors = Gilbert PB, McKeague IW, Eisen G, Mullins C, Guéye-NDiaye A, Mboup S, Kanki PJ | title = Comparison of HIV-1 and HIV-2 infectivity from a prospective cohort study in Senegal | journal = Statistics in Medicine | volume = 22 | issue = 4 | pages = 573–93 | date = February 2003 | pmid = 12590415 | doi = 10.1002/sim.1342 | s2cid = 28523977 }}</ref> and is the cause of the majority of HIV infections globally. The lower infectivity of HIV-2 as compared with HIV-1 implies that fewer people exposed to HIV-2 will be infected per exposure. Because of its relatively poor capacity for transmission, HIV-2 is largely confined to [[West Africa]].<ref name="Reeves">{{cite journal | vauthors = Reeves JD, Doms RW | title = Human immunodeficiency virus type 2 | journal = The Journal of General Virology | volume = 83 | issue = Pt 6 | pages = 1253–65 | date = June 2002 | pmid = 12029140 | doi = 10.1099/0022-1317-83-6-1253 | doi-access = free }}</ref> Summary: Please note that all contributions to Christianpedia may be edited, altered, or removed by other contributors. If you do not want your writing to be edited mercilessly, then do not submit it here. You are also promising us that you wrote this yourself, or copied it from a public domain or similar free resource (see Christianpedia:Copyrights for details). Do not submit copyrighted work without permission! Cancel Editing help (opens in new window) Discuss this page