HIV

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 untransmittable through condomless sexual intercourse 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 Cite error: The named reference PARTNER2-2019 was invoked but never defined (see the help page).
  6. ^ a b Cite error: The named reference Fauci-JAMA was invoked but never defined (see the help page).
  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.