Figure 8

A model for the interplay of Cav-1 with Nef that counters Nef induced impairment of cholesterol efflux by apoA-l and contribution to persistent infection. Upon HIV infection, Nef protein interacts with ABCA-1 and down-regulates and/or redistributes ABCA-1 expression which results in cholesterol efflux impairment. This creates a micro-environment in which HIV can replicate efficiently. On the other hand, in cells which express Cav-1, such as macrophages, Tat induces an up-regulation of Cav-1. The overabundance of Cav-1 then leads to both its binding to Nef and ability to activate cholesterol efflux. This, therefore, leads to less cholesterol accumulation which in turn reduces the amount that can be incorporated into viral particles and thereby reducing HIV infectivity.