Dr. Xuebin Qin discusses the development and characterization of new models of SARS-CoV-2 and HIV, and how his lab uses these models to study cardiovascular injury associated with infection.

Despite ongoing research around the world to better understand the pathogenesis of SARS-CoV-2, the ways in which it 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, Dr. Xuebin Qin will discuss his lab’s development and characterization of new rodent models of COVID-19, and how they use these models to study endothelial dysfunction and injury resulting from immune activation. Dr. Qin will also discuss why HIV infection is associated with increased risk of CVD. He will provide an overview of the cellular and molecular mechanisms underlying HIV-1-associated CVD, and the mouse and NHP models he has worked with to elucidate them.

Key Topics Include:

  • Cellular mechanisms by which SARS-CoV-2 and HIV contribute to cardiovascular disease
  • Development, characterization and analysis of Mouse and NHP models for the study of COVID-19- or HIV-associated CVD
  • Potential targets for therapeutic vaccine testing and pathogenesis studies

Presenters

Professor of Medicine
Tulane National Primate Research Center

Dr. Xuebin Qin's research focuses on defining the role of innate immunity including complement system and monocyte activation in the pathogenesis of human diseases, such as HIV infection, HIV-associated cardiovascular diseases, and on developing a novel cell ablation research tool for broad scientific applications. He has extensive expertise in immunology, monocyte & macrophage biology, complement, HIV-1 therapy, atherosclerosis, and cancer biology. One of Dr. Qin's research focuses has been to identify novel approach targeting complement system for HIV-1 therapy. Another portion of his research is to investigate HIV-associated cardiovascular diseases, such as atherosclerosis. His major contributions to the fields include: 1) generation a novel and potent anti-MAC regulator CD59 inhibitor, a potential therapeutic candidate for control HIV-1 infections. 2) generation of the novel mouse model for HIV-associated atherosclerossi, 3) establishment of the causative role of MAC in atherosclerosis, 4) documentation of the inhibition of MAC with a targeted complement inhibitor as a potential novel approach for the treatment of atherosclerosis-associated complications, and 5) generation of a human CD59 mediated novel cell ablation for dissecting immune cell functionality and differentiation.

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