Abstract Mice infected with the JHM strain mouse hepatitis virus (JHMV) develop a fatal encephalomyelitis with evidence of demyelination. It has previously been shown that the adoptive transfer of 5 × 107 nylon wool adherent (NWA) spleen cells from immunized donors to lethally infected recipients clears virus from the central nervous system (CNS) and prevents demyelination. Adoptive transfer of a smaller number (1 × 107) of NWA spleen cells from immunized donors also protects from death but does not significantly alter virus replication in the CNS during the acute phase of the infection. Moreover, these mice develop a transient non-fatal encephalomyelitis which occurs approximately 3 weeks post-infection. This delayed encephalomyelitis is associated with a mononuclear cell infiltration into the CNS but little or no evidence of virus replication or increased viral antigen. A virus-specific delayed-type hypersensitivity (DTH) response precedes this delayed onset of disease by 24 to 48 h. Resolution of disease correlates with a selective and permanent suppression of the JHMV-specific DTH reactivity. In addition, no virus-specific DTH is detected following adoptive transfer of viral-specific DTH effectors derived from immunized donors. In contrast, these mice respond to a heterologous antigen, KLH, suggesting that the resolution of the encephalitis is accompanied by a profound suppression in viral-specific DTH response.
Relapsing encephalomyelitis following transfer of partial immunity to JHM virus