Potential Implication of Residual Viremia in Patients on Effective Antiretroviral Therapy

Abstract

The current antiretroviral therapy (ART) has suppressed viremia to below the limit of detection of clinical viral load assays; however, it cannot eliminate viremia completely in the body even after prolonged treatment.

Inflammation, immune activation, and cardiovascular disease in HIV

“…Studies to date, however, have shown no significant reductions in viremia and most, but not all, studies have been unable to detect a decline in markers of inflammation [134–139]. One potential explanation is that some antiretroviral therapies may not achieve therapeutic levels at all sites with active replication [140]. Thus, intensification therapy may be ineffective in suppressing the active viral reservoir, or active replication may not be a major contributor to residual viremia and inflammation.…”

Hepatitis C virus: life cycle in cells, infection and host response, and analysis of molecular markers influencing the outcome of infection and response to therapy

“…However, even when HCV RNA is not detected with the most sensitive assay, it is possible that minute, undetected amounts of virus are still present. This ‘residual viremia’, firstly demonstrated for HIV with highly sensitive tests developed ad hoc , with enhanced sensitivity, may indicate suboptimal treatment and enhanced risk of virological failure [64]. To prevent this occurrence in HCV, ultrasensitive versions using increased input sample volume and modified calibration curve have been developed from commercial assays [65].…”

High MIP-1β Levels in Plasma Predict Long-Term Immunological Nonresponse to Suppressive Antiretroviral Therapy in HIV Infection

“…While ART generally reduces plasma viraemia to below 50 copies/mL, ultra-sensitive assays can detect residual low-level viraemia in many treated patients [235,236]. Both the cellular sources and pathogenic significance of this residual virus is unclear [237], but one study has suggested that residual viraemia is more frequent in INR [238], possibly contributing to increased immune activation and impaired immune reconstitution. However, ART intensification strategies with newer drugs such as CCR5 antagonist maraviroc and integrase inhibitor raltegravir neither reduce this residual viraemia nor significantly increase CD4 reconstitution in patients already suppressed to below 50 copies/ mL [239][240][241][242][243][244].…”