David Knipe (Harvard Medical School)

David Knipe (Harvard Medical School)

Butler Seminar Series

Event Date/Location

November 20, 2017 - 12:00 pm
Thomas Laboratory 003


  • David Knipe

    Department of Microbiology and Molecular Genetics
    Harvard Medical School

    David M. Knipe, PhD, is the Higgins Professor of Microbiology and Molecular Genetics and Interim Co-Chair in the Department of Microbiology and Immunobiology at Harvard Medical School.  Dr. Knipe received his PhD degree in cell biology from MIT in 1976 for his thesis research on vesicular stomatitis virus assembly with Drs. David Baltimore and Harvey Lodish.  He did postdoctoral work on herpesvirus molecular genetics with Dr. Bernard Roizman at the University of Chicago.  He serves as a member of the Harvard Medical School Center for AIDS Research executive committee, an editor for the journal Virology, and co-chief editor of Fields Virology, the leading virology reference book.  He has been the program director for the Mechanisms of Viral Infection Training program since 1986.  He has received an American Cancer Society Faculty Research Award, an NIH MERIT Award, and he served as chair of the NIH Virology Study Section from 1998 to 2000.

    Dr. Knipe’s laboratory investigates the molecular and cellular biology of herpes simplex virus infection during productive and latent infection and the host immune responses to viral infection.  His work has defined the nuclear remodeling events that take place during productive infection that allow the virus to take over the host cell nucleus for replication.  This research is now defining the mechanisms by which HSV blocks the innate immunity signaling pathways through modifications of the host cell.  His research has developed a replication-defective HSV-2 mutant virus as a candidate genital herpes vaccine, which is now in a phase I clinical trial.


Epigenetic Regulation of DNA Virus Lytic and Latent Infection

Abstract:  Viruses have evolved to commandeer their host cells to optimize their infections, and host organisms have evolved many mechanisms to resist them.  Foreign or non-self DNA is a threat, and all cells have mechanisms to resist them.  For eukaryotic cells, this involves epigenetic silencing of the invading viral genome.  The herpesviruses contain no histones associated with their virion DNA genomes, and when the viral DNA genomes enter the nucleus, cellular mechanisms load heterochromatin on viral genes to silence them.  I will discuss the mechanisms that HSV gene products use to reverse the epigenetic silencing of their genome during lytic infection and to further silence their genome during latent infection.  These studies also reveal that mammalian cells use normal epigenetic mechanisms for sensing and silencing foreign DNA such as viral and plasmid DNA.


Free and open to the university community and the public.


Ileana Cristea, Department of Molecular Biology