Yu Lab Research

My laboratory studies the molecular mechanisms of human cytomegalovirus (HCMV) replication and pathogenesis. HCMV is a beta-herpesvirus, contains a 250-kb double-stranded DNA genome and encodes ~166 annotated viral genes. HCMV is a ubiquitous pathogen that establishes a life-long latent infection and recurrent reactivation in the human host. HCMV is the leading viral cause of birth defects in the United States and a major cause of disease in immuno-compromised hosts, including cancer patients, patients with HIV infection, and recipients of bone marrow and solid organ transplants. In addition, HCMV has also been associated with various vascular diseases such as atherosclerosis and restenosis.

We have developed the infectious bacterial artificial chromosome (BAC)-based reverse genetic system for HCMV, and we have defined the entire set of HCMV genes into 3 functional categories (98 non-essential genes, 41 essential genes, and 27 important genes). Our current research focuses on the interface of virus-host interactions. In particular, we are interested in understanding how the host controls HCMV replication (e.g., apoptosis, interferon), how HCMV evades anti-viral responses, and how the virus modulates host processes (e.g., cellular gene expression, cell cycle control) to create a favorable environment needed for its replication. We use cellular and virological approaches to study HCMV biology in multiple cell culture systems and we also use mouse cytomegalovirus (MCMV) as the surrogate model for studying roles of the conserved CMV genes in viral pathogenesis in vivo.

We have recently identified the functions of several viral proteins that are important in HCMV infection. For instance, we found that the HCMV protein pUL38 functions as an inhibitor to block endoplasmic reticulum-induced cell death and that the viral protein pUL117 modulates the architecture of replicating viral DNA to promote HCMV replication. Our other research efforts focus on viral proteins regulating host cell cycle control, modulating DNA damage responses, suppressing interferon signaling pathways, and promoting virus replication in various cultured human cells that are natural targets of HCMV in vivo.

Home | About Us | Faculty & Research | Research Facilities | Education | Seminars & Events | Links