Introduction: With the advent of anti-retroviral therapy (ART) patients with HIV have a life expectancy approaching the general population. However, there is a high burden of myocardial pathology, even in asymptomatic individuals. We hypothesised that chronic myocardial inflammation may partly underlie changes in cardiac function in patients with HIV. Methods: Cardiac MR (1.5Tesla) was used to assess left ventricular function, myocardial oedema (T2 STIR, native T1 mapping), fibrosis and the presence of pericardial effusions in treated patients with HIV (n=104) and compared to controls (n=92). Results: All subjects were asymptomatic without a history of cardiac disease. Groups were well matched, except a higher prevalence of smoking was noted in patients with HIV (40 vs 12%, p <0.01). Left ventricular ejection fraction, peak circumferential systolic strain and peak diastolic strain were impaired in patients with HIV, compared to controls (p<0.01). Pericardial effusions were more frequent in patients with HIV (p< 0.01). There was evidence of subclinical myocardial oedema in patients with HIV, as measured by STIR T2 and T1 mapping, using absolute values and threshold measurements (all p < 0.05). The presence of late gadolinium enhancement was more frequent in patients with HIV compared to controls (82% versus 16% %, p<0.0001, all results in Table 1). Conclusion: Frequent pericardial effusions and subclinical myocardial oedema accompany left ventricular systolic and diastolic dysfunction and myocardial fibrosis in patients with asymptomatic HIV. Chronic myocardial inflammation may therefore underlie the cardiac morbidity and mortality in patients with HIV.

Background. Rare human immunodeficiency virus type 1 (HIV-1)-infected individuals who maintain control of viremia without therapy show potent CD8+ T-cell-mediated suppression of viral replication in vitro. Whether this is a determinant of the rate of disease progression in viremic individuals is unknown.Methods. We measured CD8+ T-cell-mediated inhibition of a heterologous HIV-1 isolate in 50 HIV-1-seropositive adults with diverse progression rates. Linear mixed models were used to determine whether CD8+ T-cell function could explain variation in the rate of CD4+ T-cell decline.Results. There was a significant interaction between CD8+ T-cell antiviral activity in vitro and the rate of CD4+ T-cell decline in chronically infected individuals (P < .0001). In a second prospective analysis of recently infected subjects followed for up to 3 years, CD8+ T-cell antiviral activity strongly predicted subsequent CD4+ T-cell decline (P < .0001) and explained up to 73% of the interindividual variation in the CD4+ T-cell slope. In addition, it was inversely associated with viral load set point (r = -0.68 and P = .002).Conclusions. The antiviral inhibitory capacity of CD8+ T cells is highly predictive of CD4+ T-cell loss in early HIV-1 infection. It has potential as a benchmark of effective immunity in vaccine evaluation.