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Journal of Virology, October 2001, p. 9328-9338, Vol. 75, No. 19
Department of Virology, Biomedical Primate
Research Centre, 2280 GH Rijswijk,1 and
Department of Immunology, Academic Hospital Dijkzigt, Erasmus
University Rotterdam, DR Rotterdam,4 The
Netherlands; Departments of Microbiology and Medicine,
Health Sciences Center, University of Washington School of
Medicine, Seattle, Washington 981952; and
Department of Virology, AIDS Collaborating Centre, National
Institute for Biological Standards and Control, Potters Bar,
Hertfordshire EN6 3QG, United Kingdom3
Received 2 January 2001/Accepted 8 June 2001
End-stage simian immunodeficiency virus (SIV)
isolates are suggested to be the most fit of the evolved
virulent variants that precipitate the progression to AIDS. To
determine if there were common characteristics of end-stage variants
which emerge from accelerated cases of AIDS, a molecular clone was
derived directly from serum following in vivo selection of a highly
virulent SIV isolate obtained by serial end-stage passage in rhesus
monkeys (Macaca mulatta). This dominant variant caused a
marked cytopathic effect and replicated to very high levels in
activated but not resting peripheral blood lymphocytes. Furthermore,
although this clone infected but did not replicate to detectable levels
in rhesus monocyte-derived macrophages, these cells were able to
transmit infection to autologous T cells upon contact. Interestingly,
although at low doses this end-stage variant did not use any of
the known coreceptors except CCR5, it was able to infect and replicate
in human peripheral blood mononuclear cells homozygous for the
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.19.9328-9338.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Characteristics of a Pathogenic Molecular Clone of an
End-Stage Serum-Derived Variant of Simian Immunodeficiency
Virus (SIVF359)
32 deletion of CCR5, suggesting the use of a novel coreceptor. It represents the first pathogenic molecular clone of SIV derived from
viral RNA in serum and provides evidence that not only the genetic but
also the biological characteristics acquired by highly fit
late-stage disease variants may be distinct in different hosts.
*
Corresponding author. Mailing address: Biomedical
Primate Research Centre (BPRC), Department of Virology, P.O. Box 3306, 2280 GH Rijswijk, The Netherlands. Phone: 31-15-284-2661. Fax:
31-15-284-3986. E-mail: heeney{at}bprc.nl.
Journal of Virology, October 2001, p. 9328-9338, Vol. 75, No. 19
0022-538X/01/$04.00+0 DOI: 10.1128/JVI.75.19.9328-9338.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
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