Immunopathology resulting from lack of early control of influenza virus infection by interferon-induced Mx proteins: causes and consequences

Project Summary

The project characterizes the molecular events that facilitate influenza A virus escape from MxA restriction and evaluates whether escape from MxA restriction is also possible by acquiring adaptive mutations in viral proteins other than the viral nucleoprotein NP. Furthermore, the role of MxA in restricting viral infections in lung epithelial cells through inflammasome activation will be studied. It is planned to search for evidence that MxA activates the inflammasome effector protein caspase-1 in IAV-infected mice as well as human airway cell culture systems, and to study the MxA-dependent downstream signaling pathway, resulting in the activation of the inflammasome.