Figure 5
A model of the turnover of HIV-RNA+ cells during the viral life-cycle. The displayed cells symbolize HIV-1 infected cells of classes ILow (blue), IIMedium (blue/magenta), IIHigh (magenta/red) and IIIExtra (brown). Inserts within the circle symbolize the kinetics of each cell class during cART. Viral particles are depicted as black/yellow stars with the enclosed genomic RNA (vRNA-ex) in red. Viral proteins are shown as red/yellow diamonds, ellipses, circles and cylinders. Viral intracellular RNA is displayed as blue (UsRNA) or red (MsRNA) lines. Buckled arrows attached to viral particles signify the direct or indirect influences of activation due to ongoing viral replication and the presence of viremia on the viral life cycle [24, 43–46]. A: Immune activation can promote post-entry events in resting CD4+ T cells harboring free viral cDNA such as integration and initiation of viral transcription [25, 26, 43]. B: Nonspecific immune activation can induce transcription in latently infected cells [27, 47] and may result in a acceleration of viral replication [15, 45]. C: CD8 T-cell mediated cytoxicity (CTL) [39, 40] and humoral immunity [41], such as antibody-dependent cellular cytotoxicity (ADCC) and complement effector functions [28], are prone to attack HIV-1 infected cells expressing viral antigens. D: After initiation of cART, the viral life cycle is slowed primarily by preventing new infections but also by decreasing immune activation which results in decelerated rates of integration, detained induction of latency and reduced immune mediated HIV-specific cytotoxicity (A, B, C).