Estimation of the Initial Viral Growth Rate and Basic Reproductive Number during Acute HIV-1 Infection▿
- Ruy M. Ribeiro1,†,
- Li Qin2,†,
- Leslie L. Chavez1,†,
- Dongfeng Li3,
- Steven G. Self2 and
- Alan S. Perelson1,*
- 1Theoretical Biology and Biophysics Group, Los Alamos National Laboratory, Los Alamos, New Mexico 87545
- 2 Statistical Center for HIV/AIDS Research and Prevention (SCHARP), Vaccine and Infectious Disease Institute, Fred Hutchinson Cancer Research Center, 1100 Fairview Avenue N., LE-400, Seattle, Washington 98109, and Department of Biostatistics, University of Washington, Seattle, Washington 98105
- 3Department of Probability and Statistics, School of Mathematical Sciences, Peking University, Beijing 100871, China
ABSTRACT
During primary infection, the number of HIV-1 particles in plasma increases rapidly, reaches a peak, and then declines until it reaches a set point level. Understanding the kinetics of primary infection, and its effect on the establishment of chronic infection, is important in defining the early pathogenesis of HIV. We studied the viral dynamics of very early HIV-1 infection in 47 subjects identified through plasma donation screening. We calculated how fast the viral load increases and how variable this parameter is among individuals. We also estimated the basic reproductive ratio, the number of new infected cells generated by an infectious cell at the start of infection when target cells are not limiting. The initial viral doubling time had a median of 0.65 days with an interquartile range of 0.56 to 0.91 days. The median basic reproductive ratio was 8.0 with an interquartile range of 4.9 to 11. In 15 patients, we also observed the postpeak decay of plasma virus and found that the virus decay occurred at a median rate of 0.60 day−1, corresponding to a half-life of 1.2 days. The median peak viral load was 5.8 log10 HIV-1 RNA copies/ml, and it was reached 14 days after the virus was quantifiable with an assay, with a lower limit of detection of 50 copies/ml. These results characterize the early plasma viral dynamics in acute HIV infection better than it has been possible thus far. They also better define the challenge that the immune response (or therapeutic intervention) has to overcome to defeat HIV at this early stage.
FOOTNOTES
- Received 20 January 2010.
- Accepted 21 March 2010.
- ↵*Corresponding author. Mailing address: Theoretical Biology and Biophysics Group, MS K710, Los Alamos National Laboratory, Los Alamos, NM 87545. Phone: (505) 667-6829. Fax: (505) 665-3493. E-mail: asp{at}lanl.gov
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↵† These authors contributed equally to this paper.
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↵▿ Published ahead of print on 31 March 2010.
- American Society for Microbiology











