Our lab is interested in how HCMV manipulates cellular signaling to establish, maintain, and reactivate from latency in CD34+ hematopoietic progenitor cells. We also collaborate on ongoing projects to understand the molecular basis of unconventional T-cell responses elicited by CMV vaccines. Current research projects in the lab include:

HCMV miRNAs and viral latency and reactivation

HCMV encodes 22 miRNAs from the viral genome, and many of these miRNAs can be detected in latently-infected CD34+ hematopoietic progenitor cells (HPCs). miRNAs downregulate expression of both viral and cellular proteins, and we have shown that HCMV miRNAs can manipulate entire signaling pathways to regulate the viral life cycle. We have several projects focusing on the roles of some of these miRNAs to regulate signaling including PI3K, TGFb, and Wnt pathways.

HCMV proteins that regulate latency

We collaborate with labs at VGTI as well as across the country to understand the interaction between viral miRNAs and viral proteins during HCMV latency and reactivation. In addition, we have ongoing projects investigating the roles of HCMV proteins that are nonessential for lytic replication, but may be important for viral latency.

CMV as a vaccine vector

VGTI has been instrumental in understanding the unique immune responses elicited by Rhesus CMV (RhCMV)-based vaccine vectors, and our lab contributes to studying the molecular basis of this mechanism of vaccine responses. Because CMV has a broad cell tropism, we have used miRNA targeting to understand which cell types are important for eliciting protective T-cell responses. Moreover, we have projects investigating the role of CMV miRNAs in regulating the trafficking and cell surface expression of HLA-E following vaccination.