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© The Rockefeller University Press, 0022-1007/1999/9/841/ $5.00
The Journal of Experimental Medicine, Volume 190, Number 6, September 20, 1999 841-850

Original Article

Viral Dynamics of Acute HIV-1 Infection

Susan J. Littlea, Angela R. McLeanb, Celsa A. Spinac,d, Douglas D. Richmana,c,d, and Diane V. Havlira

a Department of Medicine, University of California San Diego, San Diego, California 92103
b Institute for Animal Health, Compton, Newbury RG20 7NN, United Kingdom
c Department of Pathology, University of California San Diego, La Jolla, California 92093
d Department of Veterans Affairs Medical Center, San Diego, California 92161
UCSD Treatment Center, 2760 5th Ave., Suite 300, San Diego, CA 92103.619-298-0177619-543-8080

slittle{at}ucsd.edu

Viral dynamics were intensively investigated in eight patients with acute HIV infection to define the earliest rates of change in plasma HIV RNA before and after the start of antiretroviral therapy. We report the first estimates of the basic reproductive number (R0), the number of cells infected by the progeny of an infected cell during its lifetime when target cells are not depleted. The mean initial viral doubling time was 10 h, and the peak of viremia occurred 21 d after reported HIV exposure. The spontaneous rate of decline ({alpha}) was highly variable among individuals. The phase 1 viral decay rate ({delta}I = 0.3/day) in subjects initiating potent antiretroviral therapy during acute HIV infection was similar to estimates from treated subjects with chronic HIV infection. The doubling time in two subjects who discontinued antiretroviral therapy was almost five times slower than during acute infection. The mean basic reproductive number (R0) of 19.3 during the logarithmic growth phase of primary HIV infection suggested that a vaccine or postexposure prophylaxis of at least 95% efficacy would be needed to extinguish productive viral infection in the absence of drug resistance or viral latency. These measurements provide a basis for comparison of vaccine and other strategies and support the validity of the simian immunodeficiency virus macaque model of acute HIV infection.

Key Words: basic reproductive number • viral decay • primary HIV • lymphocyte dynamics • modeling

1used in this paper: PID, patient identification number; SIV, simian immunodeficiency virus

© 1999 The Rockefeller University Press


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