Jason B Weinberg, MD

Dr. Weinberg obtained his A.B. in Psychology from Princeton University and his M.D. at Duke University. He completed a residency in Pediatrics and served as Chief Resident at the Children’s Hospital/ University of Colorado Health Sciences Center in Denver Colorado. He then completed a fellowship in Pediatric Infectious Diseases at the University of Michigan. He is active in patient care and research, and he teaches graduate students, medical students, residents in Pediatrics, and fellows in Pediatric Infectious Diseases.

When he is not at work, Dr. Weinberg enjoys spending time outside with his family and dog in Ann Arbor. He is an avid cyclist and can often be found on a bike on pavement, gravel, or singletrack in the area.

The Weinberg Laboratory is focused on understanding interactions between viruses and host immune responses. The overarching goals of our work are to define specific components of the immune system contribute to appropriate control of viral replication, to characterize virus-induced inflammatory responses that contribute to tissue damage and disease, and to define mechanisms by which persistent viral infections modulate host responses to subsequent unrelated challenges. We use mouse models and mouse pathogens to study viral pathogenesis, but our work has its roots in clinically relevant scenarios, such as defining differences in pathogenesis that are based on age or immunocompromise following bone marrow transplantation and considering effects of virus persistence on bacterial sepsis.

We have a longstanding research program involving studies of adenovirus pathogenesis. Respiratory infection with a human adenovirus can present with varying severity, ranging from mild upper respiratory tract infections to more severe pneumonia and destructive lung disease. Adenovirus infection of immunocompromised patients, particularly bone marrow transplant recipients, can be particularly devastating, often resulting in rapidly disseminated infection and death. We use mouse adenovirus type 1 (MAdV-1) to study the pathogenesis of an adenovirus in its natural host. Our research has recently focused on contributions of the immunoproteasome, a host function that makes essential contributions to protein homeostasis, innate and adaptive immune function, and downstream inflammatory responses. We also use a mouse coronavirus, murine hepatitis virus strain 1 (MHV-1), to define contributions of the immunoproteasome to coronavirus pathogenesis, comparing the role of the immunoproteasome in the pathogenesis of key representative RNA and DNA viruses.

Adenoviruses and other DNA viruses, such as cytomegalovirus, Epstein-Barr virus, and other herpesviruses, establish long-term persistence in their host following the resolution of acute infection. DNA virus persistence and reactivation from persistence can be associated with a variety of disease states, and in some cases virus persistence is likely to have long-term effects on host immune function and inflammatory responses. With translational work directly related to our basic science program focused on virus persistence, we are working to define mechanisms by which virus persistence and reactivation affect outcomes of unrelated clinical conditions, such as bacterial sepsis.