Michael Abecassis, MD, MBA
J Roscoe Miller Distinguished Professor of Surgery and Microbiology/Immunology
Chief, Division of Organ Transplantation
Founding Director, Comprehensive Transplant Center
Feinberg School of Medicine
Director, Liver Transplant Program, Ann & Robert H. Lurie Children's Hospital of Chicago
Cytomegalovirus (CMV) is a herpes virus which infects the majority of adults and is able to establish a lifelong latent infection. Reactivation of the virus is frequently observed in transplant recipients, and is associated with serious morbidity and occasionally with mortality. CMV infection can be transmitted from the mother to the fetus during pregnancy and can be associated with severe congenital abnormalities or death of the fetus.The laboratory of Dr. Michael Abecassis studies the molecular mechanism by which CMV establishes latent infection and reactivates from latency. These studies may suggest strategies for developing drugs which prevent reactivation and its associated sequelae.
Mice latently infected with murine CMV are used in transplants to investigate the hypothesis that reactivation is triggered by the allogeneic response to the transplanted organ. The inflammatory cytokine TNF and the transcription factor NF_B are particular targets of investigation. Transplanted organs are analyzed for RNA expression and activation of transcription factors known to be involved in regulating viral gene expression. Transgenic and knock-out mice are used to identify cellular genes involved in reactivation of the virus. Gene therapy vectors and pharmacological agents are used to investigate new potential therapeutic agents.
The mechanism by which CMV is able to hide in a quiescent state in latently infected cells and avoid elimination by the host immune response is unknown. Studies to investigate potential epigenetic mechanisms of transcriptional silencing, including DNA methylation and histone modifications are being explored to investigate viral latency.