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.Human immunodeficiency virus (HIV) infects approximately 0.5% of the world population and is a major cause of morbidity and mortality worldwide. A vaccine for HIV is urgently required, and a variety of vaccine modalities have been tested in animal models of infection. A number of these studies have shown protection in monkey models of infection, although the ability of the vaccine to protect appears to vary with the viral strain and animal model used (8). The recent failure of a large vaccine study in humans (1) suggests that further understanding of the basic dynamics of infection and the impact of vaccination are required in order to understand the variable efficacies of vaccination in different infections.The initial ability of HIV to propagate within the host is determined by the abundance of target cells (e.g., CD4ϩ T lymphocytes) the virus can infect in order to produce progeny, by the replicative capacity of the virus, and by how cytopathic it is to infected cells. At later stages of the disease, in addition to changes in the target cell availability, there may also be changes in virus-specific properties, such as the ability of the virus to reproduce and the survival of productively infected cells as a result of changes in immune pressure and viral evolution. These parameters may be variable among individuals and within one individual over time and affect the impact of vaccination. In order to compare the efficacies of vaccination strategies, we need a quantitative measure of the factors that influence virus replication.In this work, we focus on the basic reproductive ratio (R 0 ) as a measure of vaccine efficacy in the acute phase of infection. In epidemiology, R 0 measures the potential for the spread of an epidemic and is defined as the average number of people infected by one infected individual in a susceptible population. If this number is below 1, the disease will not spread in a population. Therefore, the knowledge of R 0 allows one to estimate the fraction of a population that needs to be vaccinated in order to eradicate the disease. Analogously, in hostpathogen dynamics, the basic reproductive ratio i...