COVID-19 and Parasitic Coinfection: A Hypothetical Link to Pulmonary Vascular Disease

Le résumé fourni par la source

Before the Coronavirus disease 2019 (COVID-19) era, the global prevalence of pulmonary arterial hypertension (PAH) was between 0.4 and 1.4 per 100,000 people. The long-term effects of protracted COVID associated with pulmonary vascular disease (PVD) risk factors such as obesity, cardiovascular disease, and some infectious diseases are expected to increase this prevalence. According to preliminary data, the exact prevalence of early estimates put the prevalence of PVD in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection at 22%, although its predictive value is unknown. PVD caused by COVID-19 co-infections is understudied and underreported during COVID-19, and its impact on the future is unknown. However, due to COVID-19/co-infection pathophysiological effects on pulmonary vascularization, PVD mortality and morbidity may be a genuine worry now and in the future. Based on reported studies, this literature looks at the potential link between COVID-19, parasitic coinfection, and PVD. This review also highlights hypothetical pathophysiological mechanisms between COVID-19 and parasitic coinfection that could trigger PVD. This review hypothesized that multiple pathways associated with schistosomiasis, human immunodeficiency virus (HIV), pulmonary tuberculosis (PTB), pulmonary aspergillosis, Wuchereria bancrofti, Clonorchis sinensis, paracoccidioidomycosis, Human Herpesvirus 8, and Scrub typhus coupled with acute or long COVID-19 may increase the burden of PVD and worsen its mortality in the future. This is due to acute and/or chronic inflammation, which contributes to endothelial dysfunctions and coagulation abnormalities in pulmonary vascularization. This review advises that PVD with a history of COVID-19/co-infections be screened systematically to enhance the epidemiology, clinical profiles, and prognostics. Further experimental studies are also needed to determine pathophysiological pathways between PVD and with history of COVID-19/co-infections.

Ce résumé expose les affirmations des auteurs. BNTIC ne l’interprète pas comme une validation indépendante des résultats.