Samuel H. Speck, Ph.D.
Herpesviruses are hard to fight against because they’re sneaky.
They enter the body, deposit some genetic code in lymphocyte cells, then lie in wait, hiding from the immune system. They don’t proliferate or cause symptoms. But even in this latent state, they continue to pose a risk for the development of lymphoma, lupus, multiple sclerosis and some cancers.
Samuel Speck wants to know how herpesviruses establish latency, and how this dormant state protects them from how the body’s immune system responds to other viral antigens. He also wants to know how a latent virus eventually reactivates to produce additional viral cells and infect other hosts.
So far, Speck has identified several proteins that the virus releases to modify the host’s immune response. The more he learns about how the virus works, the greater the chances of finding a weakness that could be targeted with antiviral therapy.
Supported by grants from the NIH, Speck’s research is focused on Epstein-Barr virus and murine gamma herpesvirus 68 – a similar virus that is easier to study in animal models. Epstein-Barr virus is linked to Burkitt's lymphoma, nasopharyngeal carcinoma and Hodgkin's disease, and is the cause of half of the lymphomas that arise in people with suppressed immune systems.
- Pathogenesis of gamma-herpesviruses and development of lymphoma and other cancers
- The role of B cells in murine gamma HV-68
- Function of the gamma HV-68 M2 antigen
Dr. Speck was drawn to Georgia because of the outstanding research faculty and commitment to basic science research at Emory University and the support of the Georgia Research Alliance.