About us

A hallmark of herpesviruses is the establishment of a life-long persistent infection in the host called latency.  During this period of time, viral genomes are maintained in the absence of virus production; however, the virus retains the ability to reactivate its replication in response to stress or immune deficiency or other host cues. Our laboratory studies human cytomegalovirus (HCMV), a prototypical beta-herpesviruses that infects a majority of the world’s population. Although most HCMV infections are asymptomatic in healthy individuals, the virus is the leading cause of congenital abnormalities following fetal infection and is a significant cause of morbidity and mortality following hematopoietic stem cell transplant and solid organ transplant. 

In patients, CD34⁺ Hematopoietic Progenitor Cells (HPCs) represent a critical reservoir of latent HCMV, thereby providing a source of virus for dissemination to visceral organs. Reactivation in vivo is initiated when infected HPCs exit the bone marrow in response to cytokine/growth factor signaling, traffic to the periphery, and differentiate first into monocytes and ultimately into tissue macrophages that support lytic replication. The viral and cellular gene products required for all aspects of latency/reactivation remain an understudied area of HCMV biology.

Our long-term objective is to understand the mechanisms by which HCMV persist in myeloid cells to identify new potential targets for therapeutic intervention. We are interested in finding viral genes involved in the latency/reactivation process as well as the host pathways modulated by these viral factors. We use in vitro and in vivo models that take advantage of the latest innovations in stem cell culture and genetically engineered mouse strains to study the intricate and balanced relationship between HCMV and its host.