Back MIV Afrikaans HIV ALS ኤችአይቪ Amharic فيروس العوز المناعي البشري Arabic ايتش آى ڤى ARZ এইচ.আই.ভি. Assamese Virus d'Inmunodeficiencia Humana AST İnsanın immunçatışmazlığı virusu Azerbaijani HIV BCL Вірус імунадэфіцыту чалавека Byelorussian

HIV

This article is about the virus. For the infection caused by the virus, see HIV/AIDS. For other uses, see HIV (disambiguation).
"AIDS virus" redirects here. For the computer virus, see AIDS (computer virus).

Human immunodeficiency viruses
Scanning electron micrograph of HIV-1 (in green) budding from cultured lymphocyte. Multiple round bumps on cell surface represent sites of assembly and budding of virions.
Scanning electron micrograph of HIV-1 (in green) budding from cultured lymphocyte. Multiple round bumps on cell surface represent sites of assembly and budding of virions.
Scientific classificationEdit this classification
(unranked): Virus
Realm: Riboviria
Kingdom: Pararnavirae
Phylum: Artverviricota
Class: Revtraviricetes
Order: Ortervirales
Family: Retroviridae
Subfamily: Orthoretrovirinae
Genus: Lentivirus
Groups included
Other lentiviruses

The human immunodeficiency viruses (HIV) are two species of Lentivirus (a subgroup of retrovirus) that infect humans. Over time, they cause acquired immunodeficiency syndrome (AIDS),[1][2] a condition in which progressive failure of the immune system allows life-threatening opportunistic infections and cancers to thrive.[3] Without treatment, the average survival time after infection with HIV is estimated to be 9 to 11 years, depending on the HIV subtype.[4]

In most cases, HIV is a sexually transmitted infection and occurs by contact with or transfer of blood, pre-ejaculate, semen, and vaginal fluids.[5][6] Non-sexual transmission can occur from an infected mother to her infant during pregnancy, during childbirth by exposure to her blood or vaginal fluid, and through breast milk.[7][8][9][10] Within these bodily fluids, HIV is present as both free virus particles and virus within infected immune cells. Research has shown (for both same-sex and opposite-sex couples) that HIV is not contagious during sexual intercourse without a condom if the HIV-positive partner has a consistently undetectable viral load.[5][6]

HIV infects vital cells in the human immune system, such as helper T cells (specifically CD4+ T cells), macrophages, and dendritic cells.[11] HIV infection leads to low levels of CD4+ T cells through a number of mechanisms, including pyroptosis of abortively infected T cells,[12] apoptosis of uninfected bystander cells,[13] direct viral killing of infected cells, and killing of infected CD4+ T cells by CD8+ cytotoxic lymphocytes that recognize infected cells.[14] When CD4+ T cell numbers decline below a critical level, cell-mediated immunity is lost, and the body becomes progressively more susceptible to opportunistic infections, leading to the development of AIDS.

  1. ^ Weiss RA (May 1993). "How does HIV cause AIDS?". Science. 260 (5112): 1273–9. Bibcode:1993Sci...260.1273W. doi:10.1126/science.8493571. PMID 8493571.
  2. ^ Douek DC, Roederer M, Koup RA (2009). "Emerging Concepts in the Immunopathogenesis of AIDS". Annual Review of Medicine. 60: 471–84. doi:10.1146/annurev.med.60.041807.123549. PMC 2716400. PMID 18947296.
  3. ^ Powell MK, Benková K, Selinger P, Dogoši M, Kinkorová Luňáčková I, Koutníková H, Laštíková J, Roubíčková A, Špůrková Z, Laclová L, Eis V, Šach J, Heneberg P (2016). "Opportunistic Infections in HIV-Infected Patients Differ Strongly in Frequencies and Spectra between Patients with Low CD4+ Cell Counts Examined Postmortem and Compensated Patients Examined Antemortem Irrespective of the HAART Era". PLOS ONE. 11 (9): e0162704. Bibcode:2016PLoSO..1162704P. doi:10.1371/journal.pone.0162704. PMC 5017746. PMID 27611681.
  4. ^ UNAIDS, WHO (December 2007). "2007 AIDS epidemic update" (PDF). p. 16.
  5. ^ a b Rodger AJ, Cambiano V, Bruun T, Vernazza P, Collins S, Degen O, et al. (June 2019). "Risk of HIV transmission through condomless sex in serodifferent gay couples with the HIV-positive partner taking suppressive antiretroviral therapy (PARTNER): final results of a multicentre, prospective, observational study". Lancet. 393 (10189): 2428–2438. doi:10.1016/S0140-6736(19)30418-0. PMC 6584382. PMID 31056293.
  6. ^ a b Eisinger RW, Dieffenbach CW, Fauci AS (February 2019). "HIV Viral Load and Transmissibility of HIV Infection: Undetectable Equals Untransmittable". JAMA. 321 (5): 451–452. doi:10.1001/jama.2018.21167. PMID 30629090. S2CID 58599661.
  7. ^ Mabuka J, Nduati R, Odem-Davis K, Peterson D, Overbaugh J (2012). Desrosiers RC (ed.). "HIV-Specific Antibodies Capable of ADCC Are Common in Breastmilk and Are Associated with Reduced Risk of Transmission in Women with High Viral Loads". PLOS Pathogens. 8 (6): e1002739. doi:10.1371/journal.ppat.1002739. PMC 3375288. PMID 22719248.
  8. ^ Hahn RA, Inhorn MC, eds. (2009). Anthropology and public health : bridging differences in culture and society (2nd ed.). Oxford: Oxford University Press. p. 449. ISBN 978-0-19-537464-3. OCLC 192042314.
  9. ^ Mead MN (2008). "Contaminants in human milk: weighing the risks against the benefits of breastfeeding". Environmental Health Perspectives. 116 (10): A426–34. doi:10.1289/ehp.116-a426. PMC 2569122. PMID 18941560. Archived from the original on 6 November 2008.
  10. ^ Public Domain This article incorporates text from this source, which is in the public domain: "Preventing Mother-to-Child Transmission of HIV". HIV.gov. May 15, 2017. Retrieved December 8, 2017.
  11. ^ Cunningham AL, Donaghy H, Harman AN, Kim M, Turville SG (August 2010). "Manipulation of dendritic cell function by viruses". Current Opinion in Microbiology. 13 (4): 524–9. doi:10.1016/j.mib.2010.06.002. PMID 20598938.
  12. ^ Doitsh G, Galloway NL, Geng X, Yang Z, Monroe KM, Zepeda O, et al. (January 2014). "Cell death by pyroptosis drives CD4 T-cell depletion in HIV-1 infection". Nature. 505 (7484): 509–14. Bibcode:2014Natur.505..509D. doi:10.1038/nature12940. PMC 4047036. PMID 24356306.
  13. ^ Garg H, Mohl J, Joshi A (November 2012). "HIV-1 induced bystander apoptosis". Viruses. 4 (11): 3020–43. doi:10.3390/v4113020. PMC 3509682. PMID 23202514.
  14. ^ Kumar V (2012). Robbins Basic Pathology (9th ed.). Elsevier Health Sciences. p. 147. ISBN 978-1-4557-3787-1.
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