Research Projects

The COVID-19 pandemic has led to a significant lack of effective treatment regimens for viral diseases, including sARs-CoV-2 infection. The virus is primarily responsible for acute respiratory distress syndrome (ARDs) and respiratory failure, but it can also infect other organs, leading to multi-organ failure situations through direct infection or systemic inflammation. Long-term bystander damages from viral infection are a growing concern, and a comprehensive mechanistic model for chronic organ injuries is still missing. Viruses can generate a cytokine storm scenario in infected hosts, causing severe vascular and cerebrovascular damage. Hyper-inflammation caused by peripheral viral infections can trigger multiple organ failure, including neuroinflammatory anomalies in humans even after recovery and decline of viral load. These disorders are collectively termed as Post-COVID or Long COVID syndrome. Cardiovascular dysfunctions are common among COVID-19 patients, but the mechanisms behind these symptoms and vascular pathologies are poorly understood. Endothelial cells, the innermost lining of the vascular system, abundantly express Angiotensin converting enzyme 2 (ACE2), a type I membrane-localized glycoprotein. Vascular barrier function is primarily accomplished by three types of junctional proteins, which are tightly regulated for optimal immune response, metabolic exchange, and tissue repair functions in healthy situations. The proposal aims to resolve the precise role of viral genes, dysregulated host factors, and circulating signaling trails (exosomes) in host plasma, which contribute to vascular abnormalities experienced during and post sARs-CoV-2 infection.