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: 9.47). 09/2011; 1(1):a006841. DOI: 10.1101/cshperspect.a006841
Source: PubMed


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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Available from: Paul M Sharp, Jul 30, 2014
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    • "The nonhuman primate HBVs share the consensus PreS1 sequence that allows binding to the NTCP receptor on human hepatocytes (Ni et al. 2014). Thus, drawing from the evolutionary history of HIV-1 and HIV-2 that were initiated from cross-species transmission of simian immunodeficiency virus (SIV) from infected chimpanzees, gorillas, and macaques into humans (Sharp and Hahn 2011), a similar scenario may have occurred between the nonhuman and human primate hepadnaviruses. Determination of the timing of these events could provide important insights into HBV origins and subsequent evolution. "
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    ABSTRACT: Members of the family Hepadnaviridae fall into two subgroups: mammalian and avian. The detection of endogenous avian hepadnavirus DNA integrated into the genomes of zebra finches has revealed a deep evolutionary origin of hepadnaviruses that was not previously recognized, dating back at least 40 million and possibly >80 million years ago. The nonprimate mammalian members of the Hepadnaviridae include the woodchuck hepatitis virus (WHV), the ground squirrel hepatitis virus, and arctic squirrel hepatitis virus, as well as a number of members of the recently described bat hepatitis virus. The identification of hepatitis B viruses (HBVs) in higher primates, such as chimpanzee, gorilla, orangutan, and gibbons that cluster with the human HBV, aswell as a number of recombinant forms between humans and primates, further implies a more complex origin of this virus. We discuss the current theories of the origin and evolution of HBVand propose a model that includes crossspecies transmissions and subsequent recombination events on a genetic backbone of genotype C HBV infection. The hepatitis delta virus (HDV) is a defective RNAvirus requiring the presence of the HBV for the completion of its life cycle. The origins of this virus remain unknown, although some recent studies have suggested an ancient African radiation. The age of the association between HDV and HBV is also unknown.
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    • "An intriguing possibility is that non-canonical cofactors act to increase the evolvability of their Vif partner, enabling Vif proteins to retain activity with otherwise lethal mutations during transitions to more-fit states. Restriction factors are a major barrier to zoonosis (Sharp and Hahn, 2011), and a Vif protein able to adapt more quickly to a new host's A3 proteins should grant the lentivirus a competitive advantage in zoonotic transmission, as well as in populations with diverse restriction factor haplotypes (Binka et al., 2012; Ooms et al., 2013). Whether gaining an interaction partner makes a viral protein more robust to mutation is debatable, as the benefits of stabilization via the interaction may be outweighed by the mutational constrains imposed by the interaction itself. "
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    • "The most prevalent of these (HIV-1, group M) was transmitted into humans approximately 100 years ago and is responsible for well over 90% of global HIV infections (Worobey et al., 2008). HIV- 2 also causes AIDS but is associated with lower viral loads and reduced person-to-person transmission rates, and has not spread substantially from West Africa (Reeves and Doms, 2002; Sharp and Hahn, 2011). Overall, approximately 35 million people are currently infected with HIV and a similar number have already died of AIDS (UNAIDS, 2013). "
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