Liver fibrosis progression was associated with HIV rebound, but not blips, and with increasing cumulative exposure to HIV RNA, highlighting the importance of achieving and maintaining HIV suppression in the setting of HIV/HCV coinfection.
These findings have implications for decision makers in designing safe strategies that maintain HIV-1 suppression at lower costs.
However, maintained HIV viral suppression [ 10] and improvements in drug-associated hepatotoxicity have been described in cirrhotic HCV HIV co-infected patients after switching to raltegravir [ 11].
All participants in the HAART group maintained HIV virological suppression during the study period as evidenced by follow-up plasma viral load measurements <50 copies/mL for 39 participants, and 71 and 77 copies/mL, respectively, for two additional participants, on the final date of specimen drop-off.
The fact that viral rebound was identified as a predictor of fibrosis progression despite this short period of follow-up highlights the critical role that achieving and maintaining HIV RNA suppression can play in protecting the liver from HCV-induced injury.
In a recent study, 7 DRV + r monotherapy was compared with a DRV + r triple therapy strategy to maintain HIV-1 viral load suppression through a prospective, open-label, noninferiority, randomized, 96-week trial.
28 Data from 96 weeks confirmed sustained viral suppression with 83% in the raltegravir group maintaining HIV RNA < 50 copies/mL vs 84% in the efavirenz group (Table 2).
The helper activities of antigen-specific CD4+ T cells have been shown to mediate the control of many viral infections and are critical in maintaining HIV-1 suppression[1], [3], [58].
These data support the idea that the HIV suppression mediated by unstimulated pDCs from individuals maintaining a low viral load cannot be explained by IFN-α activity, and that an important cell contact-mediated interaction occurs between pDCs and CD4+ T cells.
Suppressive factors, secreted by CTLs may also be involved in HIV suppression.
