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Journal of Virology, July 2006, p. 7208-7218, Vol. 80, No. 14
0022-538X/06/$08.00+0     doi:10.1128/JVI.00382-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.

Transmission of Simian Immunodeficiency Virus SIVcpz and the Evolution of Infection in the Presence and Absence of Concurrent Human Immunodeficiency Virus Type 1 Infection in Chimpanzees

Jonathan L. Heeney,1* Erik Rutjens,1 Ernst J. Verschoor,1 Henk Niphuis,1 Peter ten Haaft,1 Scott Rouse,2 Hazel McClure,2 Sunita Balla-Jhagjhoorsingh,1 Willy Bogers,1 Mary Salas,2 Kathy Cobb,2 Luc Kestens,3 David Davis,1 Guido van der Groen,3 Valerie Courgnaud,4 Martine Peeters,4 and Krishna K. Murthy2

Department of Virology, Biomedical Primate Research Centre, Rijswijk, The Netherlands,1 Department of Virology and Immunology, Southwest Foundation for Biomedical Research, San Antonio, Texas,2 Prins Leopold Instituut voor Tropische Geneeskunde, Antwerp, Belgium,3 Laboratoire Retrovirus UMR 145, Institut de Recherche pour le Développement, and University of Montpellier, Montpellier, France4

Received 23 February 2006/ Accepted 24 April 2006

Current data suggest that the human immunodeficiency virus type 1 (HIV-1) epidemic arose by transmission of simian immunodeficiency virus (SIV) SIVcpz from a subspecies of common chimpanzees (Pan troglodytes troglodytes) to humans. SIVcpz of chimpanzees is itself a molecular chimera of SIVs from two or more different monkey species, suggesting that recombination was made possible by coinfection of one individual animal with different lentiviruses. However, very little is known about SIVcpz transmission and the susceptibility to lentivirus coinfection of its natural host, the chimpanzee. Here, it is revealed that either infected plasma or peripheral blood mononuclear cells readily confer infection when exposure occurs by the intravenous or mucosal route. Importantly, the presence of preexisting HIV-1 infection did not modify the kinetics of SIVcpz infection once it was established by different routes. Although humoral responses appeared as early as 4 weeks postinfection, neutralization to SIVcpz-ANT varied markedly between animals. Analysis of the SIVcpz env sequence over time revealed the emergence of genetic viral variants and persistent SIVcpz RNA levels of between 104 and 105 copies/ml plasma regardless of the presence or absence of concurrent HIV-1 infection. These unique data provide important insight into possible routes of transmission, the kinetics of acute SIVcpz infection, and how readily coinfection with SIVcpz and other lentiviruses may be established as necessary preconditions for potential recombination.

* Corresponding author. Mailing address: Dept. of Virology, Biomedical Primate Research Centre, Lange Kleiweg 139, P.O. Box 3306, 2280 GH Rijswijk, The Netherlands. Phone: 31 15 284 2661. Fax: 31 15 284 2601. E-mail: heeney{at}bprc.nl.

Journal of Virology, July 2006, p. 7208-7218, Vol. 80, No. 14
0022-538X/06/$08.00+0     doi:10.1128/JVI.00382-06
Copyright © 2006, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Heeney, J. L., Dalgleish, A. G., Weiss, R. A. (2006). Origins of HIV and the evolution of resistance to AIDS.. Science 313: 462-466 [Abstract] [Full Text]  


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