AIDS origin: Difference between revisions
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SIVs in non-human primates tend to cause non-fatal disease. Comparison of the gene sequence of SIV with HIV should therefore give us information about the factors necessary to cause disease in humans. The factors that determine the virulence of HIV as compared to most SIVs are only now being elucidated. Non-human SIVs contain a ''nef'' gene that down-regulates [[CD3]], [[CD4]], and [[MHC class I]] expression; most non-human SIV's therefore do not induce immunodeficiency; the HIV ''nef'' gene however has lost its ability to down-regulate CD3, which results in the immune activation and apoptosis that is characteristic of chronic HIV infection.<ref>{{Cite journal | author=Schindler M, Münch J, Kutsch O, ''et al.'' | title=Nef-mediated suppression of T cell activation was lost in a lentiviral lineage that gave rise to HIV-1 | journal=Cell | year=2006 | volume=125 | pages=1055–67 | doi=10.1016/j.cell.2006.04.033 }}</ref> | SIVs in non-human primates tend to cause non-fatal disease. Comparison of the gene sequence of SIV with HIV should therefore give us information about the factors necessary to cause disease in humans. The factors that determine the virulence of HIV as compared to most SIVs are only now being elucidated. Non-human SIVs contain a ''nef'' gene that down-regulates [[CD3]], [[CD4]], and [[MHC class I]] expression; most non-human SIV's therefore do not induce immunodeficiency; the HIV ''nef'' gene however has lost its ability to down-regulate CD3, which results in the immune activation and apoptosis that is characteristic of chronic HIV infection.<ref>{{Cite journal | author=Schindler M, Münch J, Kutsch O, ''et al.'' | title=Nef-mediated suppression of T cell activation was lost in a lentiviral lineage that gave rise to HIV-1 | journal=Cell | year=2006 | volume=125 | pages=1055–67 | doi=10.1016/j.cell.2006.04.033 }}</ref> | ||
== Identification of the virus == | == Identification of the virus == | ||
Revision as of 16:28, 2 June 2012
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AIDS origin On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
HIV, the infectious agent of AIDS, is thought to have originated in non-human primates in sub-Saharan Africa and transferred to humans during the 20th century. The epidemic officially began on 5 June 1981.
Two species of HIV infect humans: HIV-1 and HIV-2. HIV-2 may have originated from the Sooty Mangabey (Cercocebus atys), an Old World monkey of Guinea-Bissau, Gabon, and Cameroon.[1] HIV-1 is more virulent. It is easily transmitted and is the cause of the majority of HIV infections globally. HIV-2 is less transmittable and is largely confined to West Africa. HIV-1 is the species described below.
Likely spread from animal to human populations
A variety of theories exist explaining the transfer of HIV to humans, but no single hypothesis is unanimously accepted, and the topic remains controversial.
From Cameroon chimpanzees? (Contested)
The most widely accepted theory is so called 'Hunter' Theory according to which transference from ape to human most likely occurred when a human was bitten by an ape or was cut while butchering one, and the human became infected.[2] Researchers announced in May 2006 that HIV most likely originated in wild chimpanzees in the southeastern rain forests of Cameroon (modern East Province) [3] [4] rather than in Kinshasa, Democratic Republic of Congo (formerly Zaire), as had previously been believed. Seven years of research and 1,300 chimpanzee genetic samples led Dr. Beatrice Hahn of the University of Alabama, Birmingham, to identify chimpanzee communities near Cameroon's Sanaga River as the most likely originators. Presumably, someone in rural Cameroon was bitten by a chimp or was cut while butchering one and became infected with the ape virus. That person passed it to someone else. [5]
Calculating based on a fixed mutation rate, the jump from chimpanzee to human likely occurred during the French colonial period (1919–1960). Comparative primatologist Jim Moore suggests that this may have been the result of colonial practices of forced labour, which could have suppressed the immune system of the initial hunter enough to allow the virus to infect and take hold. Likewise, forced immunisations (using one needle on many patients) may have sped the virus's spread through Cameroon and beyond.[6]
The Times published an article in 1987 stating that WHO suspected some kind of connection with its vaccine program and AIDS-epidemic. The story was almost entirely based on statements given by one unnamed WHO advisor. The theory was supported only by weak circumstantial evidence and is now disproven by unraveling the genetic code of the virus and finding out that the virus dates back to the 1930s.[7]
From Congo macaques via OPV? (Contested)
Freelance journalist Tom Curtis discussed one controversial possibility for the origin of HIV/AIDS in a 1992 Rolling Stone magazine article. He put forward what is now known as the OPV AIDS hypothesis, which suggests that AIDS was inadvertently caused in the late 1950s in the Belgian Congo by Hilary Koprowski's research into a polio vaccine.[8] Although subsequently retracted due to libel issues surrounding its claims, the Rolling Stone article motivated another freelance journalist, Edward Hooper, to probe more deeply into this subject. Hooper's research resulted in his publishing a 1999 book, The River, in which he alleged that an experimental oral polio vaccine prepared using chimpanzee kidney tissue was the route through which simian immunodeficiency virus (SIV) crossed into humans to become HIV, thus starting the human AIDS pandemic.[9]
This theory is contradicted by an analysis of genetic mutation in primate lentivirus strains that estimates the origin of the HIV-1 strain to be around 1930, with 95% certainty of it lying between 1910 and 1950.[10]
In February 2000 one of the original developers of the polio vaccine, Philadelphia based Wistar Institute found from its stores a vial of the original vaccine used in the vaccination program. It was analyzed in April 2001 and no traces of either HIV-1 or SIV were found in the sample.[11] A second analysis showed that only macaque monkey kidney cells, which cannot be infected with SIV or HIV, were used to produce the vaccine.[12] While the analysis was done on only one vial of vaccine, some scientists have concluded that the polio vaccine theory of the origins of HIV is not possible. [2] [8]
However the sample tested was never used in the Congo nor was it ever claimed by Hooper that the original vaccines were contaminated, the OPV hypothesis claims instead that HIV was introduced in the Congo at the Stanlyvile laboratory as the local administers amplified the original vaccine using infected Chimp kidneys (local amplification was widely practiced at the time) for the 1 million to whom it was forcefully administered. As such there is no hard evidence to dismiss the OPV hypothesis.[13]
Edward Hooper rejects the dates calculated using a fixed mutation rate on the basis that phylogenetic dating of "the most recombinogenic organisms known to medical science", immunodeficiency viruses, is "inherently incapable of making any allowance for recombination". [14][9]
Method of spread
After the initial transfer of HIV from a non-human primate to humans, the virus ultimately spread via contact among humans to the rest of the world. Since a cross species jump is most likely the origin of HIV, and since HIV became a true epidemic, transmissible from human to human, then the following conditions were needed:
- A large human population,
- A large nearby population of the appropriate host animal,
- An infectious pathogen in the host animal, that eventually produces a mutation that can spread from animal to human,
- Interaction between the species to transmit enough of it to humans to establish a human foothold, which may take millions of individual exposures,
- A mutation of same pathogen that can spread from human to human,
- Some method that allows the pathogen to disperse widely. This prevents the infection from "burning out" by either killing off its human hosts or provoking immunity in a local population of humans.
Such requirements existed in the remote past with smallpox, and also with the 20th century Spanish Flu, despite Spanish Flu's New World origin at Fort Riley, Kansas (there the animal reservoir seems to have been two species, chickens and pigs, which were of Old World origin.)
Two species of HIV infect humans: HIV-1 and HIV-2. HIV-1 is more virulent and more easily transmitted. HIV-1 is the source of the majority of HIV infections throughout the world, while HIV-2 is less easily transmitted and is largely confined to West Africa.[15]
Both species of the virus (HIV-1 and HIV-2) are believed to have originated in West-Central Africa and jumped species (zoonosis) from a non-human primate to humans. HIV-1 evolved from a Simian Immunodeficiency Virus (SIVcpz) found in the chimpanzee subspecies Pan troglodytes troglodytes.[16] DNA sequencing indicates that HIV-1 (group M) entered the human population in the early 20th century, probably sometime between 1915 and 1941.[17][18] HIV-2 crossed species from a different strain of SIV, this one found in sooty mangabeys (an Old World monkey) of Guinea-Bissau.[19]
SIVs in non-human primates tend to cause non-fatal disease. Comparison of the gene sequence of SIV with HIV should therefore give us information about the factors necessary to cause disease in humans. The factors that determine the virulence of HIV as compared to most SIVs are only now being elucidated. Non-human SIVs contain a nef gene that down-regulates CD3, CD4, and MHC class I expression; most non-human SIV's therefore do not induce immunodeficiency; the HIV nef gene however has lost its ability to down-regulate CD3, which results in the immune activation and apoptosis that is characteristic of chronic HIV infection.[20]
Identification of the virus
May 1983: LAV
In May 1983, doctors from Dr. Luc Montagnier's team at the Pasteur Institute in France, reported that they had isolated a new retrovirus from lymphoid ganglions that they believed was the cause of AIDS. [21] The virus was later named lymphadenopathy-associated virus (LAV) and a sample was sent to the U.S. Centers for Disease Control, which was later passed to the National Cancer Institute (NCI).[22] [23]
May 1984: HTLV-III
In May 1984 a team led by Robert Gallo of the United States confirmed the discovery of the virus, but they renamed it human T lymphotropic virus type III (HTLV-III).[24] [25] The dual discovery led to considerable scientific disagreement, and it was not until President Mitterrand of France and President Reagan of the USA met that the major issues were resolved.
Jan 1985: both found to be the same
In January 1985 a number of more detailed reports were published concerning LAV and HTLV-III, and by March it was clear that the viruses were the same, from the same source, and was the etiological agent of AIDS [26] [27]
May 1986: the name HIV
In May 1986, the International Committee on Taxonomy of Viruses ruled that both names should be dropped and a new name, HIV (Human Immunodeficiency Virus), be used. [28]
Also see
Reference
- ↑ Reeves, J. D. and Doms, R. W (2002). "Human Immunodeficiency Virus Type 2". J. Gen. Virol. 83 (Pt 6): 1253–1265. PMID 12029140.
- ↑ 2.0 2.1 Annabel Kanabus & Sarah Allen. Updated by Bonita de Boer (2007). "The Origins of HIV & the First Cases of AIDS". AVERT (an international HIV and AIDS charity based in the UK). Retrieved 2007-02-28.
- ↑ 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). "Origin of HIV-1 in the Chimpanzee Pan troglodytes troglodytes". Nature. 397 (6718): 436–441. doi:10.1038/17130. PMID 9989410.
- ↑ Keele, B. F., van Heuverswyn, F., Li, Y. Y., Bailes, E., Takehisa, J., Santiago, M. L., Bibollet-Ruche, F., Chen, Y., Wain, L. V., Liegois, F., Loul, S., Mpoudi Ngole, E., Bienvenue, Y., Delaporte, E., Brookfield, J. F. Y., Sharp, P. M., Shaw, G. M., Peeters, M., and Hahn, B. H. (2006). "Chimpanzee Reservoirs of Pandemic and Nonpandemic HIV-1". Science. Online 2006-05-25. doi:10.1126/science.1126531.
- ↑ http://www.usatoday.com/news/health/2006-05-25-hiv-cameroon_x.htm
- ↑ http://www.npr.org/templates/story/story.php?storyId=5450391
- ↑ The Times, frontpage, 1987/5/11,
Glenn Garvin Ana Lense-Larrauri, Monika Leal And Megan
Walters, Miami Herald Staff (2006). "25 YEARS OF AIDS/HIV AIDS Showed The Media At Their Best, Worst And Everywhere In Between". Media Awareness Project. Retrieved 2007-02-27. line feed character in
|author=at position 55 (help) - ↑ 8.0 8.1 Curtis, T. (1992). "The origin of AIDS". Rolling Stone (626): 54–59, 61, 106, 108.
- ↑ 9.0 9.1 Hooper, E. (1999). The River : A Journey to the Source of HIV and AIDS (1st ed.). Boston, MA: Little Brown & Co. pp. 1–1070. ISBN 0-316-37261-7.
- ↑ Korber B, Muldoon M, Theiler J; et al. (January 30 – February 2, 2000). "Timing the origin of the HIV-1 pandemic". Programs and abstracts of the 7th Conference on Retroviruses and Opportunistic Infections. Abstract L5. (Online version at United States National Library of Medicine)
- ↑ Blancou, P. et al. "Polio vaccine samples not linked to AIDS" Nature: 410, p. 1045-1046 (2001)
- ↑ Blancou, P. et al. "Polio vaccine samples not linked to AIDS" Nature: 410, p. 1045-1046 (2001)
- ↑ Template:Cite documentary
- ↑ Ed Hooper Beatrice Hahn. A Portrait of Scientific Certainty. Retrieved December 6, 2006.
- ↑ http://www.socgenmicrobiol.org.uk/JGVDirect/18253/18253ft.htm
- ↑ http://www.nature.com/nature/journal/v397/n6718/abs/397436a0_fs.html
- ↑ http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10846155&dopt=Abstract
- ↑ http://evolve.zoo.ox.ac.uk/papers/Lemey%20et%20al%20(2004)%20Genetics.pdf
- ↑ http://evolve.zoo.ox.ac.uk/publications.html?id=132
- ↑ Schindler M, Münch J, Kutsch O; et al. (2006). "Nef-mediated suppression of T cell activation was lost in a lentiviral lineage that gave rise to HIV-1". Cell. 125: 1055&ndash, 67. doi:10.1016/j.cell.2006.04.033.
- ↑ Barre-Sinoussi et al., 1983
- ↑ Connor and Kingman, 1988 (ISBN 0-14-011397-5)
- ↑ 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 (4599): 868–871. PMID 6189183.
- ↑ 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 (4648): 497–500. PMID 6200935.
- ↑ Popovic et al., 1984
- ↑ Marx, 1985
- ↑ Chang et al., 1993
- ↑ Coffin et al., 1986