Impeding Neonatal Immunity, Causing Birth Defects

Many persistent viral infections are transmitted early in life and are responsible for long-term morbidity and mortality. Cytomegalovirus (CMV) is the most common congenital infection and the leading cause of birth defects in children in the United States. While the urgent need for a vaccine against congenital CMV is widely recognized, the underlying mechanisms responsible for the poor generation and inadequate maintenance of immunity remain undefined.

Brian Rudd, Microbiology and Immunology, is working to identify both the mechanisms and consequences of failing to control CMV in early life. Since immune control of CMV is largely dependent upon CD8+ T cells, Rudd is focusing on understanding why CD8+ T cells in early life fail to control congenital CMV infection. Based on earlier studies and new results, he hypothesizes that neonatal CD8+ T cells have an inherent propensity to become functionally exhausted during CMV infection, leading to prolonged viral shedding and the altered development of the CD8+ T cell compartment.

Rudd is working toward understanding why neonatal CD8+ T cells fail to control CMV during the acute stage of infection and attempting to revive immune functionality by blocking inhibitory receptors. He is also examining CD8+ T cells made after infection and looking at why they fail to control ongoing viral replication during the latent stage of infection. Work from these studies is expected to pave the way for the development of vital preventative and therapeutic strategies against congenital CMV disease.

NIH Award Number: 2R01AI105265-06A1

Cornell Researchers

Funding Received

$2.17 Million spanning 5 years