Figure 3.

MFNLPs compensate for RBEIII mutations, by maintaining functional coupling, of Nef and RBF-2. In this schematic representation four states are considered. In A & B, normal progressive disease with high viral titer would develop. In C & D, difficult-to-revert-mutations to Nef or the RBEIII site, would result in LTNP, and deletions of both RBEIII LTR sequences and Nef sequences. This is because, in our model, Nef can activate the MAPK pathway, and exert its effects through RBEIII.