Neuropathology and Neurovirulence of Canine Distemper Virus Plaque Isolates in the Hamster

Abstract

The relationship between neuropathological abnormalities, antibody response and neurovirulence of plaque isolates has been studied in an experimental model of canine distemper in the hamster. Genetic virus variance influenced neurovirulence and the experimental evidence supports the hypothesis that the mechanism of this effect may be through the modulating effect of circulating antibody. Large plaque virus (LPV) produced severe encephalitis with little early antibody response and a high degree of pathological abnormality. Small plaque virus (SPV) produced mild chronic encephalitis and early antibody response. Microscopically, histological abnormalities in this group were qualitatively similar to those seen with LPV but generally of lesser degree. Immunosuppression in SPV infected animals increased the severity of the encephalitis, reflected by the increase in inflammation and inclusion formation. Combined SPV and LPV infection produced high antibody levels and less severe disease than LPV infection alone with an intermediate pattern of histological abnormality.

Rapid identification of antigenic T‐cell epitopes by extracellular acidification rate signals

“…Major histocompatibility complex (MHC) class II (DR) molecules are heterodimers on the surface of antigen-processing/presenting cells (APCs), which bind and present autoantigenic peptides to autoreactive CD4 ϩ T cells. In demyelinating disease, such as MS, MBP, proteolipid protein, and myelin oligodendrocyte antigen peptides complexed with disease-associated MHC class II (DR2) heterodimers on APCs stimulate autoreactive T cells [Buss et al, 1987;Allen et al, 1987]. These activated cells induce cellular and humoral effector mechanisms, leading to the destruction of the myelin sheath in MS patients [Todd et al, 1988;Spielman et al, 1982;Olerup et al, 1989].…”