A major focus of our laboratory is human cytomegalovirus (HCMV), a herpes virus, which is the leading cause of congenital viral infection, occurring in approximately 1% of all live births. Congenital HCMV infection results in central nervous system damage in the majority of symptomatic newborns. HCMV infection also poses a serious health risk to immunosuppressed individuals, increasing morbidity in the elderly and in patients receiving immunosuppressive chemotherapy, including cancer patients, transplant recipients, and AIDS patients.
The majority of the projects in our lab study the interfaces between viruses and the host cell that determine the outcome of infection. Specifically, we focus on how viruses usurp cellular metabolic controls and subvert cellular anti-viral signaling to support productive infection. The goal of our laboratory is to increase our mechanistic understanding of these processes to identify novel avenues for therapeutic intervention that could prevent virally-associated pathogenesis.
The global SARS-CoV-2 pandemic is responsible for hundreds of thousands of deaths globally. Anti-viral therapeutic strategies are desperately needed to attenuate SARS-CoV-2-associated disease. We have initiated a high-throughput pharmacologic screen of a unique metabolism-focused compound library to identify drugs that limit coronavirus infection in pulmonary human fibroblasts. Our preliminary data has identified several compounds that substantially inhibit coronavirus infection. Our laboratory is in the process of validating the anti-viral activity of these compounds against SARS-CoV-2. In addition, we are elucidating how coronaviruses modulate cellular metabolism to support productive infection in an attempt to identify viral metabolic vulnerabilities that might be targeted for further therapeutic development.