The objective of this thesis was to examine the role of ps20 in virus infections. We provide evidence that MHV-1 infection resulted in increased lung viral titers in ps20-/- mice. These data highlight an antiviral role for ps20 in MHV-1 infection. We also observed an increase in the percentage of GR1+ neutrophils infiltrating the BAL and in the lung draining lymph node of ps20-/- mice, on day 2 post-infection. In vitro, gene expression analysis identified an increase in expression of CXCL1 and CXCL2 in MHV-1 infected ps20-/- fibroblasts. These data suggest a role for ps20 in regulating neutrophil chemotactic factors, and migration. Next, we examined influenza A/WSN/33, and provide evidence that ps20 functions as a proviral factor. In vivo, ps20-/- mice infected with influenza A/WSN/33 exhibited decreased lung viral titers. These data suggest that ps20 functions as either a proviral or antiviral agent, dependent on the infecting virus.

The objective of this thesis was to examine the role of ps20 in virus infections. We provide evidence that MHV-1 infection resulted in increased lung viral titers in ps20-/- mice. These data highlight an antiviral role for ps20 in MHV-1 infection. We also observed an increase in the percentage of GR1+ neutrophils infiltrating the BAL and in the lung draining lymph node of ps20-/- mice, on day 2 post-infection. In vitro, gene expression analysis identified an increase in expression of CXCL1 and CXCL2 in MHV-1 infected ps20-/- fibroblasts. These data suggest a role for ps20 in regulating neutrophil chemotactic factors, and migration. Next, we examined influenza A/WSN/33, and provide evidence that ps20 functions as a proviral factor. In vivo, ps20-/- mice infected with influenza A/WSN/33 exhibited decreased lung viral titers. These data suggest that ps20 functions as either a proviral or antiviral agent, dependent on the infecting virus.