Abstract
As with last year's meeting, perhaps the greatest emphasis in the basic science categories was in the area of cellular cofactors that influence HIV-1 replication either positively or negatively. A number of presentations provided detailed insight into the mechanism by which APOBEC 3G, the cellular target of Vif, effects its antiviral activity. The surprising thing is that this antiviral activity is not restricted to primate lentiviruses but is active against retroviruses and even hepatitis viruses. In the area of positive-acting cellular cofactors, the emphasis was on those cellular proteins that facilitate egress of the virus from the infected cell. It is now apparent that viruses such as HIV-1 can bud into cytoplasmic vesicles in order to establish a unique intracellular reservoir. How viruses move between cells was also the focus of several presentations at the meeting, and there were further surprises about the mechanism by which HIV-1 may establish latent infection.