Abstract
DA and other TO subgroup strains of Theiler's murine encephalomyelitis virus synthesize a protein called L* which interferes with DA virus clearance from the central nervous system of susceptible SJL mice, thereby fostering virus persistence and a late demyelinating disease. By using CD4 (-/-) and CD8 (-/-) mice as well as adoptive transfer studies we demonstrate that susceptible mouse strains are capable of clearing DA virus through a CD4+ T cell-dependent activity that is inhibited by L*.
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