WEBINAR SERIES—Inflammation and Immunophysiology: An Exploration of Pathophysiology—Cardiovascular Disease Associated With SARS-CoV-2 and HIV Infections

September 9, 2021
11 a.m. EDT

Despite the ongoing research to better characterize the effects and pathogenesis of COVID-19, the ways in which it interacts with or exacerbates cardiovascular disease (CVD) are not fully understood. While it is well accepted that SARS-CoV-2 infects lung epithelial cells, whether it can also infect endothelial cells is less clear.

In this webinar, Xuebin Qin, MD, PhD, professor at Tulane University School of Medicine in New Orleans, will discuss his lab's development and characterization of new rodent models of COVID-19 and how his lab uses these models to study endothelial dysfunction and injury resulting from immune activation. Qin will also discuss why HIV infection is associated with increased risk of CVD, give an overview of the cellular and molecular mechanisms underlying HIV-1-associated CVD, and discuss the mouse and nonhuman primate models he has worked with to elucidate these mechanisms.

Key discussion topics will include:

• cellular mechanisms by which SARS-CoV-2 and HIV contribute to cardiovascular disease;
• development, characterization and analysis of mouse and nonhuman primate models for the study CVD associated with COVID-19 or HIV; and
• potential targets for therapeutic vaccine testing and pathogenesis studies.

Presenter

Xuebin Qin, MD, PhD, focuses on defining the role of innate immunity, including complement system and monocyte activation, in the pathogenesis of human diseases, such as HIV infection and HIV-associated cardiovascular diseases. His research explores developing a novel cell ablation research tool for broad scientific applications. He has extensive expertise in immunology, monocyte and macrophage biology, HIV-1 therapy, atherosclerosis and cancer biology. Qin’s major contributions to the field include:

• generation of a novel and potent that is a potential therapeutic candidate for control HIV-1 infections (anti-MAC regulator CD59 inhibitor);
• development of the novel mouse model for HIV-associated atherosclerosis;
• establishment of the causative role of MAC in atherosclerosis;
• documentation of the inhibition of MAC with a targeted complement inhibitor as a potential novel approach for the treatment of atherosclerosis-associated complications; and
• generation of a human CD59 mediated novel cell ablation for dissecting immune cell functionality and differentiation.