Abstract

Background: Variations in immune phenotype are increasingly recognized as drivers of cardiovascular disease (CVD). For example, the inflammatory effect of HIV-infection is associated with a 2-fold higher risk of CVD. Conversely, schistosome infection induces an anti-inflammatory immune response, which may counter CVD pathways related to inflammation. Whether the immune regulatory effect of schistosome infection is sufficient to suppress the contrasting stimulatory effect of another disease such as HIV remains unknown and may provide critical insight into the immunologic basis of non-communicable diseases. Methods: In this prospective cohort study, we enrolled 1,000 HIV-infected and uninfected adults at a referral HIV clinic in a schistosome endemic area in Mwanza, Tanzania. Standardized history, echocardiography and serum were obtained. Blood pressure was monitored over two years. Regression models adjusted for age and sex were used to quantify associations. Results: We enrolled 503 schistosome infected and 497 uninfected adults with a median age of 36 [28- 43]. Schistosome infection was significantly associated with a lower prevalence of hypertension (39.6% vs 46.7%, p=0.016), myocardial diastolic dysfunction (8.1% vs 13.4%, p=0.015) and total-to-high density lipoprotein ratio (1.77 vs 1.82, p<0.0001) as compared to uninfected participants. Additionally, schistosome-infection was associated with significantly improved change in blood pressure over time (0.67 vs 3.35 mmHg increase, p=0.005). When stratified by concurrent HIV-infection, schistosome infection was associated with lower prevalence of diastolic dysfunction and total-to-HDL ratio in HIV- infected adults but lower prevalence of hypertension in those without HIV-infection. Conclusions: We provide the first evidence that schistosome infection may directly impact cardiac function and slow the age-related increase in blood pressure over time. Further, associations between schistosome and CVD differ by HIV status, implying that immune mediated interactions may have important physiologic ramifications for CVD. The patterns of these interactions may provide insight into the immunologic mechanisms of cardiovascular diseases.

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