Mechanisms of HIV non-progression; robust and sustained CD4+ T-cell proliferative responses to p24 antigen correlate with control of viraemia and lack of disease progression after long-term transfusion-acquired HIV-1 infection

Dyer, Wayne B; Zaunders, John J; Yuan, Fang Fang; Wang, Bin; Learmont, Jennifer C; Geczy, Andrew F; Saksena, Nitin K; McPhee, Dale A; Gorry, Paul R; Sullivan, John S

To determine why immunodominant B27-restricted CTL initially contributed to reduced viral replication in C13 and C122, but not in C117, sequencing of plasma and PBMC derived virus spanning the period before and after signs of disease progression was carried out to determine if viral escape mutants had emerged in this region of Gag (Figure 7) . With the exception of one sample in 1996, a well characterised escape mutant [34] was detected from the earliest time point in C117. This escape mutant was not detected in C13 or C122, and hence was not the cause for the loss of control of viraemia in C122, nor was it detected in the latest time point from C13 when viraemia first increased above 1000 copies/ml. This suggests that immune escape at this B27 Gag epitope was not a major cause of disease progression in very long term infected Dynamics of immune responses during an episode of increased viral replication in SBBC patient C18 Figure 3 Dynamics of immune responses during an episode of increased viral replication in SBBC patient C18. individuals. The sole common factor was a decline in p24specific proliferative responses.