Chronic viral infection of hematopoietic stem cells provides a reservoir for the maintenance of infection and results in dramatically altered patterns of hematopoiesis and effects on downstream immune function. While recent research has begun to describe some viral gene products involved in latency and reactivation, much remains to be understood about how
these, and other viral genes, cooperate and manipulate the host cell system. A main focus of the lab is in determining how HCMV (human cytomegalovirus, a common human herpesvirus) exploits cellular traits to establish latency, maintain a viral reservoir, control reactivation, and manipulate hematopoiesis which will help develop novel targeted
treatments, a more detailed understanding of hematopoietic mechanisms, and an improved understanding of immune cell fate during viral infection. Other projects look at specific mechanisms of viral genes (i.e. HCMV RL11 region), other beta-herpesviruses (HHV-6a and 6b), and overarching commonalities with other chronic latency-establishing viruses to
understand viral manipulation of the hematopoietic system via the interconnected mechanisms of cellular hematopoietic control and viral latency. These projects combine biochemistry, virology, immunology, and stem cell biology approaches to address questions in viral pathogenesis, herpesvirus latency and reactivation, hematopoietic stem cell fate, and
immune system differentiation.