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Journal of Virology, June 1999, p. 4829-4839, Vol. 73, No. 6
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Simian Immunodeficiency Virus Disease Course Is Predicted by the Extent of Virus Replication during Primary Infection

Silvija I. Staprans,1,2,dagger Peter J. Dailey,3 Ann Rosenthal,4 Chris Horton,1 Robert M. Grant,2 Nicholas Lerche,4 and Mark B. Feinberg5,*

Department of Medicine---AIDS Program, University of California, San Francisco, San Francisco, California 941101; Gladstone Institute of Virology and Immunology, San Francisco, California 94141-91002; Nucleic Acid Diagnostics, Chiron Diagnostics (D-200), Emeryville, California 946083; California Regional Primate Research Center, University of California, Davis, California 956164; and Departments of Medicine and Microbiology and Immunology, Emory University School of Medicine, Atlanta, Georgia 303225

Received 23 December 1998/Accepted 10 March 1999

To elucidate the relationship between early viral infection events and immunodeficiency virus disease progression, quantitative-competitive and branched-DNA methods of simian immunodeficiency virus (SIV) RNA quantitation were cross-validated and used to measure viremia following infection of rhesus macaques with the pathogenic SIVmac251 virus isolate. Excellent correlation between the methods suggests that both accurately approximate SIV copy number. Plasma viremia was evident 4 days postinfection, and rapid viral expansion led to peak viremia levels of 107 to 109 SIV RNA copies/ml by days 8 to 17. Limited resolution of primary viremia was accompanied by relatively short, though variable, times to the development of AIDS (81 to 630 days). The persistent high-level viremia observed following intravenous inoculation of SIVmac251 explains the aggressive disease course in this model. Survival analyses demonstrated that the disease course is established 8 to 17 days postinfection, when peak viremia is observed. The most significant predictor of disease progression was the extent of viral decline following peak viremia; larger decrements in viremia were associated with both lower steady-state viremia (P = 0.0005) and a reduced hazard of AIDS (P = 0.004). The data also unexpectedly suggested that following SIVmac251 infection, animals with the highest peak viremia were better able to control virus replication rather than more rapidly developing disease. Analysis of early viral replication dynamics should help define host responses that protect from disease progression and should provide quantitative measures to assess the extent to which protective responses may be induced by prophylactic vaccination.

* Corresponding author. Mailing address: Departments of Medicine and Microbiology and Immunology, Emory University School of Medicine, 1518 Clifton Rd., NE, Atlanta, GA 30322. Phone: (404) 727-4374. Fax: (404) 727-9853. E-mail: mbf{at}sph.emory.edu.

dagger Present address: Departments of Medicine and Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA 30322.

Journal of Virology, June 1999, p. 4829-4839, Vol. 73, No. 6
0022-538X/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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