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Jason Weinberg

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Primary Appointment: Pediatrics-Infectious Diseases
Primary PIBS Dept.: Microbiology and Immunology
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  Research in the Weinberg Laboratory is focused on understanding interactions between adenoviruses and host immune responses. 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 (BMT) recipients, can be particularly devastating, often resulting in rapidly disseminated infection and death. Emerging evidence suggests a role for persistent adenovirus infection in chronic lung diseases such as chronic obstructive lung disease (COPD) and asthma. 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 (MAV-1), to study the pathogenesis of an adenovirus in its natural host.

Our research seeks to define mechanisms by which host inflammatory responses are induced by viral infection and the contributions that specific components of these host responses make to the control of acute viral infection. Trainees in the laboratory will have the opportunity to participate in a variety of projects related to this work. Prostaglandin E2 (PGE2) is a lipid-derived mediator that influences host immune function in many ways. A central goal of our research program is to characterize ways in which PGE2 modulates the pathogenesis of MAV-1 respiratory infection. Specifically, we use MAV-1 to study the effects of PGE2 on viral replication and virus-induced inflammation in a normal host, in PGE2-deficient and PGE2-unresponsive hosts, and in a BMT model in which PGE2 is aberrantly overexpressed. A second major goal of our research is to characterize the contributions of specific cytokines and immune cells to the clearance of MAV-1 during acute infection. We define ways in which these immune responses to MAV-1 differ between neonates and adults. In related work, we are interested in learning how these different responses in neonates lead to increased susceptibility to infection and to long-term effects on lung physiology, such as increased airway hyperreactivity. We anticipate that information derived from our work will enhance the understanding of the adenovirus pathogenesis. Ultimately, we hope that our work will identify novel virus- and host-specific targets to exploit for the treatment of adenovirus infections and adenovirus-associated lung disease.