We transfected cells with either a 1:1 or a 4:1 ratio of SG3deltaEnv to envelope plasmid and purified the pseudovirions. We analyzed similar quantities of pelleted virus for envelope, p24 incorporation and single round infectivity. Envelope incorporation was not altered by modulation of the ratio of transfected DNA. The discrepancy in envelope incorporation between signature and non-signature pseudovirions was similar at both transfection ratios. In contrast, p24 incorporation was reduced by four to five fold at a transfection ratio of 1:1 in comparison to a transfection ratio of 4:1. This was true for both signature and non-signature pseudovirions. These results suggest that envelopes with the position 12 signature were incorporated at higher density into virions. One intuitively straightforward hypothesis regarding why a signature that associates with infectivity of HIV in vitro may be selected for during early NSC 136476 infection is that it is important during initial expansion of the virus upon infection, and lost during chronic infection, when other factors may play a stronger selective role. It is possible that during chronic infection a steady-state develops in viral replication and target cell populations. At this steady-state, limitations on target cell numbers and immune susceptibility may play a more important role in viral WY 14643 propagation than do elements that marginally augment viral infectivity. To investigate this hypothesis, we used mathematical models to explore the relationship of viral infectivity to viral load during early and late infection. Similar ideas of trade offs during the life history of a population have been developed in ecology as first proposed by MacArthur and Wilson and are called r/K selection theory, where r denotes the growth rate of a population and K denotes the carrying capacity of the environment. Mathematical models can be used to evaluate the plausibility of hypotheses about the relationships between different viral and host characteristics and clinical consequences of infection. Previously published models derived by Nowak et al. and by Stafford et al. have been used to approximate the dynamics of in vivo SIV and HIV viral load after infection and prior to the exertion of substantial immunologic pressure. We used a previously studied data set of viral loads from ten acutely infected individuals to validate our hypothesis that viral load increases exponentially with viral infectivity. Using equation with empirically derived values for the viral production rate, the viral and infected cell decay rates, and varying the viral infectivity, we demonstrated that as infectivity increases, the exponent governing the rate of viral expansion also increases linearly.