Michael
Abecassis, MD
Associate Professor
Surgery and Microbiology/Immunology
Chief, Division of Organ Transplantation
To Contact Dr. Abecassis:
676 N St Clair St, Suite #537
phone: 312-695-8900
e-mail: mabecass@nmh.org
Dr. Abecassis's website
PubMed
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Research Interests
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.
Reactivation from
latency:
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.
Molecular mechanism
of latency:
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.