Abstract
This article reviews the current knowledge on how viruses may utilize Extracellular Vesicle Assisted Inflammatory Load (EVAIL) to exert pathologic activities. Viruses are classically considered to exert their pathologic actions through acute or chronic infection followed by the host response. This host response causes the release of cytokines leading to vascular endothelial cell dysfunction and cardiovascular complications. However, viruses may employ an alternative pathway to soluble cytokine-induced pathologies—by initiating the release of extracellular vesicles (EVs), including exosomes. The best-understood example of this alternative pathway is human immunodeficiency virus (HIV)-elicited EVs and their propensity to harm vascular endothelial cells. Specifically, an HIV-encoded accessory protein called the “negative factor” (Nef) was demonstrated in EVs from the body fluids of HIV patients on successful combined antiretroviral therapy (ART); it was also demonstrated to be sufficient in inducing endothelial and cardiovascular dysfunction. This review will highlight HIV-Nef as an example of how HIV can produce EVs loaded with proinflammatory cargo to disseminate cardiovascular pathologies. It will further discuss whether EV production can explain SARS-CoV-2-mediated pulmonary and cardiovascular pathologies.
Highlights
For many years, acute and chronic viral infections have been associated with the development of cardiovascular disease (CVD)
While 50% of the patients (10 out of 18) displayed Nef-extracellular vesicles (EVs) positivity based on ELISA, Nef positive bronchoalveolar lavages (BAL) cells were randomly distributed between alveolar macrophages, CD4+ T cells, and CD8+ T cells
This study demonstrated that by using a specific Nef-peptide inhibitor, Nef-EV-induced disturbance of their blood-brain barrier model can be reversed [77]. These findings indicate that human immunodeficiency virus (HIV) reservoir cells in the brain can employ HIV-Nef release to contribute to HIV-associated neurocognitive diseases (HAND)
Summary
Acute and chronic viral infections have been associated with the development of cardiovascular disease (CVD). The contribution and the biology of viruses towards. After the introduction of antiretroviral therapy (ART), cardiovascular disease (CVD) became a leading cause of death in the HIV-positive population [2]. Because the HIV biology concerning cardiovascular and pulmonary diseases is so well understood, it may serve as a blueprint for studying other viruses with known impacts on CVD. This review focuses on the role of extracellular vesicles (EVs) in HIV infection and their possible CVD contribution. Using the example of the pandemic SARS-CoV-2 virus, it tries to apply what we have learned about HIV-induced EV formation to understand.
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