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Journal of Virology, November 2001, p. 10187-10199, Vol. 75, No. 21
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.21.10187-10199.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Role of CD8+ Lymphocytes in Control of Simian Immunodeficiency Virus Infection and Resistance to Rechallenge after Transient Early Antiretroviral Treatment†

Jeffrey D. Lifson,1,* Jeffrey L. Rossio,1 Michael Piatak Jr.,1 Thomas Parks,1 Li Li,1 Rebecca Kiser,2 Vicky Coalter,2 Brad Fisher,3 Bernard M. Flynn,3 Susan Czajak,4 Vanessa M. Hirsch,5 Keith A. Reimann,6 Joern E. Schmitz,6 John Ghrayeb,7 Norbert Bischofberger,8 Martin A. Nowak,9 Ronald C. Desrosiers,4 and Dominik Wodarz9

Retroviral Pathogenesis Laboratory1 and Vaccine Support Laboratory,2 AIDS Vaccine Program, SAIC Frederick, National Cancer Institute at Frederick, Frederick, Maryland 21702; Animal Sciences Branch, National Cancer Institute, Bethesda, Maryland 208923; New England Regional Primate Research Center, Harvard Medical School, Southborough, Massachusetts 017724; Laboratory of Molecular Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Rockville, Maryland 208525; Division of Viral Pathogenesis, Beth Israel Deaconess Medical Center, Boston, Massachusetts 022156; Centocor, Inc., Malvern, Pennsylvania 193557; Gilead Sciences, Inc., Foster City, California 944048; and Program in Theoretical Biology, Institute of Advanced Study, Princeton, New Jersey 085409

Received 26 March 2001/Accepted 30 July 2001

Transient antiretroviral treatment with tenofovir, (R)-9-(2-phosphonylmethoxypropyl)adenine, begun shortly after inoculation of rhesus macaques with the highly pathogenic simian immunodeficiency virus (SIV) isolate SIVsmE660, facilitated the development of SIV-specific lymphoproliferative responses and sustained effective control of the infection following drug discontinuation. Animals that controlled plasma viremia following transient postinoculation treatment showed substantial resistance to subsequent intravenous rechallenge with homologous (SIVsmE660) and highly heterologous (SIVmac239) SIV isolates, up to more than 1 year later, despite the absence of measurable neutralizing antibody. In some instances, resistance to rechallenge was observed despite the absence of detectable SIV-specific binding antibody and in the face of SIV lymphoproliferative responses that were low or undetectable at the time of challenge. In vivo monoclonal antibody depletion experiments demonstrated a critical role for CD8+ lymphocytes in the control of viral replication; plasma viremia rose by as much as five log units after depletion of CD8+ cells and returned to predepletion levels (as low as <100 copy Eq/ml) as circulating CD8+ cells were restored. The extent of host control of replication of highly pathogenic SIV strains and the level of resistance to heterologous rechallenge achieved following transient postinoculation treatment compared favorably to the results seen after SIVsmE660 and SIVmac239 challenge with many vaccine strategies. This impressive control of viral replication was observed despite comparatively modest measured immune responses, less than those often achieved with vaccination regimens. The results help establish the underlying feasibility of efforts to develop vaccines for the prevention of AIDS, although the exact nature of the protective host responses involved remains to be elucidated.

* Corresponding author. Mailing address: Retroviral Pathogenesis Laboratory, AIDS Vaccine Program, SAIC Frederick, National Cancer Institute at Frederick, Building 535, Fifth Floor, Frederick, MD 21702. Phone: (301) 846-5019. Fax: (301) 846-5588. E-mail: lifson{at}avpaxpl.ncifcrf.gov.

dagger Dedicated to the memory of our colleague Kalachar Suryanarayana.

Journal of Virology, November 2001, p. 10187-10199, Vol. 75, No. 21
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.21.10187-10199.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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