Mathematical modeling of viral kinetics under immune control during primary HIV-1 infection

David Burg, Libin Rong, Avidan U. Neumann, Harel Dahari

Research output: Contribution to journalArticlepeer-review

78 Scopus citations

Abstract

Primary human immunodeficiency virus (HIV) infection is characterized by an initial exponential increase of viral load in peripheral blood reaching a peak, followed by a rapid decline to the viral setpoint. Although the target-cell-limited model can account for part of the viral kinetics observed early in infection [Phillips, 1996. Reduction of HIV concentration during acute infection: independence from a specific immune response. Science 271 (5248), 497-499], it frequently predicts highly oscillatory kinetics after peak viremia, which is not typically observed in clinical data. Furthermore, the target-cell-limited model is unable to predict long-term viral kinetics, unless a delayed immune effect is assumed [Stafford et al., 2000. Modeling plasma virus concentration during primary HIV infection. J. Theor. Biol. 203 (3), 285-301]. We show here that extending the target-cell-limited model, by implementing a saturation term for HIV-infected cell loss dependent upon infected cell levels, is able to reproduce the diverse observed viral kinetic patterns without the assumption of a delayed immune response. Our results suggest that the immune response may have significant effect on the control of the virus during primary infection and may support experimental observations that an anti-HIV immune response is already functional during peak viremia.

Original languageEnglish
Pages (from-to)751-759
Number of pages9
JournalJournal of Theoretical Biology
Volume259
Issue number4
DOIs
StatePublished - 21 Aug 2009

Bibliographical note

Funding Information:
DB was funded by the Bar-Ilan University President Fellowship for Excellence. HD is supported by the University of Illinois Gastrointestinal and Liver Disease (UIC GILD) Association. Portions of this work were performed under the auspices of the US Department of Energy under contract DE-AC52–06NA25396. We thank Alan S. Perelson and Ruy M. Ribeiro for their comments.

Funding

DB was funded by the Bar-Ilan University President Fellowship for Excellence. HD is supported by the University of Illinois Gastrointestinal and Liver Disease (UIC GILD) Association. Portions of this work were performed under the auspices of the US Department of Energy under contract DE-AC52–06NA25396. We thank Alan S. Perelson and Ruy M. Ribeiro for their comments.

FundersFunder number
UIC GILD) Association
US Department of EnergyDE-AC52–06NA25396
University of Illinois Gastrointestinal and Liver Disease
National Institute of General Medical SciencesP20GM103452
National Center for Research ResourcesP20RR018754

    Keywords

    • Human immunodeficiency virus (HIV)
    • Immune control
    • Primary infection
    • Viral dynamics

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