CELLULAR IMMUNE RESPONSE TO RIFT VALLEY FEVER VIRUS MP-12 INFECTION

Kimberly K. Gray¹, M. Holbrook Ph.D.²

¹Department Microbiology and Immunology, ²Department of Pathology, UTMB

Background: RVFV is a very important human pathogen and it is listed as a Category A agent on the NIAID list of priority pathogens. During outbreaks, this virus infects humans and in some cases results in severe disease and, potentially, death in the form of encephalitis or hemorrhagic fever. RVFV is also a significant agricultural risk as the virus causes severe disease in ruminants. There is very little published data pertaining to the effect of RVFV infection on the host cellular immune response. Objective: To characterize the cellular immune response to RVFV MP12 infection in an effort to identify specific mechanisms associated with disease pathogenesis. Methods: Cells were infected with RVFV MP12 and then cell supernatants (for cytokines) and lysates (for phosphoproteins) were analyzed using a Bio-plex system or western blots. Results: Preliminary efforts to characterize the effect of MP-12 infection on cellular immunity in mice have found that the MP-12 vaccine strain can significantly inhibit Th1 associated cytokines including interferon and Th1 associated pro-inflammatory cytokines (RANTES, MCP, and MIP). I have also found that there is a difference between infected and uninfected cells in regards to the pro-apoptotic proteins (JNK, STATs, p53, and p38-MAPK) that have been examined to date. Conclusions: There is a noticeable difference in cytokine induction and phosphoprotein expression between cells infected with MP-12 and uninfected cells. At the present time, these differences can be correlated with disease pathogenesis, but a definitive link cannot be made. Supported by the Department of Pathology, UTMB.