Mechanisms of viral escape from host immunity

Monday, March 21, 2011 - 3:00pm
Event Type: 

Gold Room, Hilton Garden Inn, 1325 Dickenson Avenue, Ames

Gaya Amarasinghe , Department of Biochemistry, Biophysics and Molecular Biology

ABSTRACT: Emerging and remerging viral diseases, such as the Ebola and Marburg hemorrhagic fevers, are a significant threat to human health and are potential agents of bioterrorism. Ebola viral (EBOV) infections simultaneously suppress the host innate and adaptive immune systems, which lead to severe viral hemorrhagic fever and high fatality rates in humans. However, no approved vaccines or treatments are currently available to counter these infections, in part due to the paucity of knowledge on viral components. Multifunctional filoviral protein 35 (VP35) has emerged as a critical viral component important for infection, immune evasion, and pathogenesis. Using a combination of structural, biochemical and cell biological studies, we have recently delineated mechanisms by which pathogenic viruses such as the ebolavirus evade host immunity. These studies as well as recent results of structure-based diagnostic and therapeutic development will be discussed. This work was supported in part by grants from Midwestern Research Center for Excellence for Biodefense and Emerging Infectious Diseases Research/NIAID, Northeast Biodefense Center/NIAID, NIH and the Roy J. Carver Trust.