Origins of HIV and the AIDS Pandemic.

Institute of Evolutionary Biology and Centre for Immunity, Infection and Evolution, University of Edinburgh, Edinburgh EH9 3JT, United Kingdom.
Cold Spring Harbor Perspectives in Medicine (Impact Factor: 7.56). 09/2011; 1(1):a006841. DOI: 10.1101/cshperspect.a006841
Source: PubMed

ABSTRACT Acquired immunodeficiency syndrome (AIDS) of humans is caused by two lentiviruses, human immunodeficiency viruses types 1 and 2 (HIV-1 and HIV-2). Here, we describe the origins and evolution of these viruses, and the circumstances that led to the AIDS pandemic. Both HIVs are the result of multiple cross-species transmissions of simian immunodeficiency viruses (SIVs) naturally infecting African primates. Most of these transfers resulted in viruses that spread in humans to only a limited extent. However, one transmission event, involving SIVcpz from chimpanzees in southeastern Cameroon, gave rise to HIV-1 group M-the principal cause of the AIDS pandemic. We discuss how host restriction factors have shaped the emergence of new SIV zoonoses by imposing adaptive hurdles to cross-species transmission and/or secondary spread. We also show that AIDS has likely afflicted chimpanzees long before the emergence of HIV. Tracing the genetic changes that occurred as SIVs crossed from monkeys to apes and from apes to humans provides a new framework to examine the requirements of successful host switches and to gauge future zoonotic risk.

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    ABSTRACT: Some chronic medical conditions have been found to be worsened by the presence of emotional and psychological disorders which often were not given considerations or even recognized when treatment for these medical conditions are been planned. With regards to HIV/AIDS, the World Health Organization (WHO) had observed that there is a close connection between mental health and HIV/AIDS. The most prevalent mental health problems found to be mostly associated with HIV/AIDS is depression and suicide ideations. This study examined the prevalence of depression and suicide risk among HIV positive persons attending the HIV/AIDS clinic of the University of Nigeria Teaching hospital Enugu south east Nigeria. The major depressive episode and the suicidality modules of the Mini neuropsychiatric interview (MINI) were used to screen 360 persons made up of 180 HIV positive persons and 180 HIV negative blood donors (controls) attending the HIV/AIDS and the hematology clinics of the University of Nigeria Teaching hospital Ituku Ozalla, Enugu south east Nigeria for the prevalence of depression and risk of suicide. The prevalence of depression and risk of suicide was 27.8% and 7.8% respectively for the HIV positive subjects, while it was 12.8% and 2.2% respectively for the HIV negative blood donors (controls). It was concluded that there was high prevalence of depression and suicide risk among HIV positive persons than among the controls.
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    ABSTRACT: Most simian immunodeficiency viruses use their Nef protein to antagonize the host restriction factor tetherin. A deletion in human tetherin confers Nef resistance, representing a hurdle to successful zoonotic transmission. HIV-1 group M evolved to utilize the viral protein U (Vpu) to counteract tetherin. Although HIV-1 group O has spread epidemically in humans, it has not evolved a Vpu-based tetherin antagonism. Here we show that HIV-1 group O Nef targets a region adjacent to this deletion to inhibit transport of human tetherin to the cell surface, enhances virion release, and increases viral resistance to inhibition by interferon-?. The Nef protein of the inferred common ancestor of group O viruses is also active against human tetherin. Thus, Nef-mediated antagonism of human tetherin evolved prior to the spread of HIV-1 group O and likely facilitated secondary virus transmission. Our results may explain the epidemic spread of HIV-1 group O. Copyright © 2014 Elsevier Inc. All rights reserved.
    Cell Host & Microbe 11/2014; 16(5):639-650. DOI:10.1016/j.chom.2014.10.002 · 12.19 Impact Factor
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    ABSTRACT: HIV-1, the cause of AIDS, is composed of four phylogenetic lineages, groups M, N, O, and P, each of which resulted from an independent cross-species transmission event of simian immunodeficiency viruses (SIVs) infecting African apes. Although groups M and N have been traced to geographically distinct chimpanzee communities in southern Cameroon, the reservoirs of groups O and P remain unknown. Here, we screened fecal samples from western lowland (n = 2,611), eastern lowland (n = 103), and mountain (n = 218) gorillas for gorilla SIV (SIVgor) antibodies and nucleic acids. Despite testing wild troops throughout southern Cameroon (n = 14), northern Gabon (n = 16), the Democratic Republic of Congo (n = 2), and Uganda (n = 1), SIVgor was identified at only four sites in southern Cameroon, with prevalences ranging from 0.8–22%. Amplification of partial and full-length SIVgor sequences revealed extensive genetic diversity, but all SIVgor strains were derived from a single lineage within the chimpanzee SIV (SIVcpz) radiation. Two fully sequenced gorilla viruses from southwestern Cameroon were very closely related to, and likely represent the source population of, HIV-1 group P. Most of the genome of a third SIVgor strain, from central Cameroon, was very closely related to HIV-1 group O, again pointing to gorillas as the immediate source. Functional analyses identified the cytidine deaminase APOBEC3G as a barrier for chimpanzee-to-gorilla, but not gorilla-to-human, virus transmission. These data indicate that HIV-1 group O, which spreads epidemically in west central Africa and is estimated to have infected around 100,000 people, originated by cross-species transmission from western lowland gorillas.

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