Uncovering differences between virus-specific primary and secondary effector CD4 T cells
Mice infected with the neuroattenuated rJ2.2 strain of the murine coronavirus, mouse hepatitis virus (MHV), develop acute encephalitis and acute and chronic demyelinating diseases. The pathogenesis of rJ2.2 serves as an animal model for the human disease multiple sclerosis (MS) because animals develop clinical and histopathological changes similar to those seen in patients. The immunopathological consequence of demyelination unveils the delicate balance between pro-inflammatory factors required for viral clearance and anti-inflammatory factors necessary for limiting tissue damage. Virus specific CD4 T cells are critical for viral clearance and play a role in the development of demyelination. My project seeks to understand the differences between virus-specific primary and secondary effector CD4 T cells.