Furthermore, CVD prevention treatments will likely be most effectively implemented if they TWS119 target patients receiving ART whose risk for AIDS complications is low. Despite these potential exclusions, the difference between a low-burden of CVD risk factors and optimally managed risk factors still has substantial implications for longer-term CVD risk over a lifetime. Defining the appropriate target population that optimizes the net benefit-risk balance will be an important goal for future HIV-related CVD prevention studies. Inflammation is a key factor in the pathogenesis of cardiovascular disease and a hallmark of HIV infection that persists despite effective treatment with ART for years. The reasons for chronic immune activation and inflammation are multi-factorial, but potential drivers include residual low-level HIV replication, translocation of microbial products across damaged mucosal barriers, the presence of co-pathogens, as well as metabolic complications. In this context, antiinflammatory treatments are particularly attractive candidates for HIV-related CVD prevention, whether or not they target HIVspecific mechanisms or down-regulate inflammatory pathways more broadly. ACE-I and statins have been associated with antiinflammatory effects. We found that among persons with HIV infection, lisinopril use was associated with a decline in biomarkers of systemic inflammation. Favorable changes were evident in spite of suboptimal adherence. High-sensitivity CRP, specifically, is elevated with HIV infection and associated with risk for CVD among both HIV-infected and uninfected persons. Our findings were limited by the small sample size. Confidence intervals are wide and we may have missed important treatment effects. Low power also limited our ability to detect treatment interactions. The lack of a treatment effect of pravastatin may be due to the low potency of this statin, as we did not detect changes in cholesterol or lipoproteins. Given the approach we were studyingwe chose a starting doseto minimize risk/tolerability and our short-term follow-up duration precluded dose escalation. Other HIV studies using higher dosesor other statinshave demonstrated reductions in measures of immune activation or inflammation. In summary, our results support the feasibility of conducting further studies of similar adjunct treatments that may have multiple beneficial effects such as reducing BP and systemic inflammation among HIV positive patients. Adherence concerns with lisinopril in this context suggest other, more tolerable medications with similar effects on the renin-angiotensin-aldosterone-system, may be a more effective strategy. Ultimately, in addition to larger feasibility studies, HIV clinical outcome trials will have to performed to assess the risk/benefit of such adjunctive treatment strategies. The emergence of drug resistance is one of the major threats to successful BEZ235 antiretroviral therapy of infection with human immunodeficiency virus-1. HIV-1 cannot be eradicated with today��s antiretroviral treatment. The aim of therapy is thus to reduce morbidity and mortality by long-term inhibition of HIV-1 replication. Combination antiretroviral therapyis highly effective but viruses may start replicating if drug levels are too low, concurrent infections or recent vaccinations. In these situations drug resistance mutations can accumulate. To avoid longlasting episodes of viral replication under cART and to detect a virological failure early, it is recommended to regularly monitor plasma viral load levels. However, in resource-limited settings the technical equipment, health care infrastructure and financial capacity are often lacking.