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Journal of Virology, December 2008, p. 11589-11598, Vol. 82, No. 23
0022-538X/08/$08.00+0 doi:10.1128/JVI.01596-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Complex Systems in Biology Group, Centre for Vascular Research, University of New South Wales 2052, New South Wales, Australia,1 Theoretical Biology and Biophysics, Los Alamos National Laboratory, Los Alamos, New Mexico 87545,2 Merck Research Laboratories, West Point, Pennsylvania,3 Department of Microbiology and Immunology, Uniformed Services University of Health Sciences, Bethesda, Maryland 20824,4 ImmunoTechnology Section, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 208925
Received 28 July 2008/ Accepted 8 September 2008
The dynamics of HIV infection have been studied in humans and in a variety of animal models. The standard model of infection has been used to estimate the basic reproductive ratio of the virus, calculated from the growth rate of virus in acute infection. This method has not been useful in studying the effects of vaccination, since, for the vaccines developed so far, early growth rates of virus do not differ between control and vaccinated animals. Here, we use the standard model of viral dynamics to derive the reproductive ratio from the peak viral load and nadir of target cell numbers in acute infection. We apply this method to data from studies of vaccination in SHIV and SIV infection and demonstrate that vaccination can reduce the reproductive ratio by 2.3- and 2-fold, respectively. This method allows the comparison of vaccination efficacies among different viral strains and animal models in vivo.
Published ahead of print on 17 September 2008.
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