Maternal deaths emanating from preeclampsia remain a public health challenge in low- and middle-income countries. However, the pathophysiological mechanisms of preeclampsia (PE) still remain unclear. Placental maladaptation and consequent oxidative stress and ischemia/hypoxia results in the discharge of bioactive factors that cause widespread systemic endothelial dysfunction. Several mechanisms such as impaired endothelial nitric oxide (NO) synthase (eNOS) and vascular adhesion molecules contribute to an imbalance in the bioavailability of endothelium-derived factors. Moreover, HIV-1 accessory proteins such as Tat, Gp120 and Nef predispose to endothelial injury. The tat protein mimics vascular endothelial growth factor and impairs angiogenesis. While immune reconstitution occurs with antiretroviral therapy (protease inhibitors, HAART and nucleoside reverse transcriptase), endothelial damage persists with HIV infection and PE. SARS-CoV-2 also induces endothelial dysfunction and hypertension via angiotensin-converting enzyme 2 (ACE 2). Elevated ACE 2 levels during pregnancy may be a potential risk factor for SARS-CoV-2 infection and subsequently PE development. Unravelling the etiology of PE, either alone or more importantly during the HIV-COVID-19 pandemic, is relevant to understanding cellular and molecular vascular changes.
Thajasvarie Naicker and Nalini Govender
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