Beatrice h hahn biography of martin

Author(s): Weimin Liu, Yingying Li, Gerald H. Learn, Rebecca S. Rudicell, Joel D. Robertson, Brandon F. Keele, Jean-Bosco N. Ndjango, Crickette M. Sanz, David B. Morgan, Sabrina Locatelli, Mary K. Gonder, Philip J. Kranzusch, Peter D. Walsh, Eric Delaporte, Eitel Mpoudi-Ngole, Alexander V. Georgiev, Martin N. Muller, George M. Shaw, Martine Peeters, Paul M. Sharp, Julian C. Rayner & Beatrice H. Hahn

Publication: Nature

Publication Date: 2010

Abstract: Plasmodium falciparum is the most prevalent and lethal of the malaria parasites infecting humans, yet the origin and evolutionary history of this important pathogen remain controversial. Here we develop a single-genome amplification strategy to identify and characterize Plasmodium spp. DNA sequences in faecal samples from wild-living apes. Among nearly 3,000 specimens collected from field sites throughout central Africa, we found Plasmodium infection in chimpanzees (Pan troglodytes) and western gorillas (Gorilla gorilla), but not in eastern gorillas (Gorilla beringei) or bonobos (Pan paniscus). Ape plasmodial infections were highly prevalent, widely distributed and almost always made up of mixed parasite species. Analysis of more than 1,100 mitochondrial, apicoplast and nuclear gene sequences from chimpanzees and gorillas revealed that 99% grouped within one of six host-specific lineages representing distinct Plasmodium species within the subgenus Laverania. One of these from western gorillas comprised parasites that were nearly identical to P. falciparum. In phylogenetic analyses of full-length mitochondrial sequences, human P. falciparum formed a monophyletic lineage within the gorilla parasite radiation. These findings indicate that P. falciparum is of gorilla origin and not of chimpanzee, bonobo or ancient human origin.

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Beatrice Hahn's latest SIV sequences from Cameroonian chimps: an alternative interpretation

by Edward Hooper

If you're new to these issues, read this first.

Synopsis

a) The latest paper by Beatrice Hahn's team (B. F. Keele, B. H. Hahn et al: "Chimpanzee Reservoirs of Pandemic and Nonpandemic HIV-1") [Reference 1] features claims that they have discovered the source of pandemic HIV-1, the "AIDS virus".

b) However, on the basis of the evidence presented, this claim is unsafe. In fact, more than that, it represents a rash over-extrapolation.

c) The reasons for rejecting Hahn's claim include the following: (i) less than 1 in 200 of the chimp troops in this part of Africa have thus far been sampled for SIV; (ii) in reality, the new chimp viruses she has found fall far short of being "dead ringers" for pandemic HIV-1, as has been claimed; (iii) there are close physical and biomedical similarities between Pan troglodytes troglodytes (Ptt) chimps and Pan troglodytes schweinfurthii (Pts) chimps, which some believe should be regrouped into a single subspecies; (iv) members of some groups of Ptt cluster genetically with Pts, and vice versa; (v) despite their claims to the contrary, Hahn and co-authors have not established that Ptt (rather than Pts) represents the reservoir of pandemic HIV-1; (vi) furthermore, the closest primate virus ancestor to pandemic HIV-1 may have existed in a chimp troop that is now extinct.

d) The true reason why it is so important to Hahn's group to establish the Pan troglodytes troglodytes subspecies of chimpanzee as the reservoir of pandemic HIV-1 is that they believe that this refutes the OPV/AIDS theory, which proposes that AIDS began as a result of chimpanzee experiments conducted in Stanleyville, Belgian Congo, in the late 1950s.

e) However, their latest findings do not disprove the OPV/AIDS theory. For a long

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.

Approximately one century ago in southeastern Cameroon, cross-species transmission of SIVcpz from chimpanzees gave rise to HIV-1 group M, the principal cause of the AIDS pandemic in humans.

Acquired Immune Deficiency Syndrome (AIDS) was first recognized as a new disease in 1981 when increasing numbers of young homosexual men succumbed to unusual opportunistic infections and rare malignancies (CDC 1981; Greene 2007). A retrovirus, now termed human immunodeficiency virus type 1 (HIV-1), was subsequently identified as the causative agent of what has since become one of the most devastating infectious diseases to have emerged in recent history (Barre-Sinoussi et al. 1983; Gallo et al. 1984; Popovic et al. 1984). HIV-1 spreads by sexual, percutaneous, and perinatal routes (Hladik and McElrath 2008; Cohen et al. 2011); however, 80% of ad