Erik S. Barton Laboratory

Immunity during lifelong herpesvirus infection


The eight known human herpesviruses cause diseases including cold sores, blindness, chicken pox, infectious mononucleosis, and cancer. Herpesviruses are unique in their ability to persist in vivo in a non-replicating state referred to as latency, from which virus can periodically reactivate to produce infectious progeny and recurrent disease. Because of the capacity of these viruses to evade the immune response and remain with the person for life, these pathogens are the focus of intense immunologic research. However, it is still largely unclear how herpesvirus latency is maintained, and what the physiologic consequences of viral latency are for the infected cell and organism.

My lab uses the murine gammaherpesvirus 68 ( γHV68) system to address these questions and improve our understanding of the immune response to latent herpesvirus infection. γHV68 is a natural pathogen of mice and is closely related to the human herpesviruses Epstein-Barr virus (EBV, which causes mononucleosis) and Kaposi’s sarcoma herpesvirus (KSHV, which causes AIDS-associated tumors). The γHV68 model has four key advantages for studies of immunity to chronic virus infection: i) γHV68 can be easily mutated; ii) its genetic similarity to human herpesviruses has established it as a model system for exploring basic mechanisms of gammaherpesvirus infection, immunity, and cancer biology; iii) it encodes several genes that are predicted to modify cellular signaling pathways or evade the immune response; and iv) many knockout and transgenic mice with defined immune deficiencies are available, and novel mutant mice can be produced with relative ease.

My current research uses genetic and cell biological approaches to dissect mechanisms of immune function during γHV68 infection. I am specifically focused on understanding the role of interferons (a key antiviral cytokine family secreted during virus infection) in regulating latent virus infection, and the effects of prolonged interferon expression during latency on immune physiology. I seek to answer the following questions:

  • How do interferons and other immune cytokines regulate herpesvirus gene expression and reactivation during latency?
  • What host cells and cellular genes mediate the antiviral effects of interferon during herpesvirus infection in vivo?
  • What viral genetic elements allow gammaherpesviruses to replicate, persist, and reactivate in the face of the interferon response?
  • What are the long term consequences of herpesvirus latency for the host?
  • Are there beneficial effects of latent infection that might indicate a symbiotic relationship between herpesviruses and their hosts?

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Microbiology & Immunology
Wake Forest School of Medicine
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