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 goal of our work is to define ways in which specific components of the immune system contribute to appropriate control of viral replication but also induce inflammation that contributes to tissue damage and disease. 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 (BMT).

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. Persistent adenovirus infection has been linked to chronic lung and heart disease. The strict species specificity of the human adenoviruses precludes a complete study of their pathogenesis. Instead, we use a mouse pathogen, mouse adenovirus type 1 (MAdV-1), to study the pathogenesis of an adenovirus in its natural host. Using this mouse model, we have been working to define mechanisms of adenovirus persistence and ways in which adenovirus persistence might alter host responses to subsequent challenges.

We have also used the MAdV-1 model to study, the immunoproteasome, a host function that makes essential contributions to protein homeostasis, innate and adaptive immune function, and downstream inflammatory responses. Newer research in the Weinberg Laboratory, which was spurred on by the COVID-19 pandemic, capitalizes on the use of mouse models with a mouse coronavirus, murine hepatitis virus strain 1 (MHV-1), to define contributions of the immunoproteasome to coronavirus pathogenesis. We hope that increased knowledge about how the immunoproteasome affects immune control of infection and inflammatory responses triggered by infection will aid in the development of targeted anti-inflammatory therapies and novel vaccine strategies.