Key result
Polycations mixed with the encephalomyocarditis virus increased viral multiplication, viremia, and fatal central nervous system disease in adult mice.
Polycations enhance the local growth and systemic dissemination of the encephalomyocarditis virus in mice, converting a nonpathogenic variant into a lethal one.
May potentiate viral disease in mice; leaves open relevance to human infections or therapies.
Pathogenicity of the encephalomyocarditis (EMC) virus for adult mice was increased when polycations of diverse type were mixed with virus and inoculated by the subcutaneous or intraperitoneal routes. Diethylaminoethyl (DEAE) dextran, hexadimethrine (polybrene), polymyxin B, polylysine, and calf thymus histone in various concentrations stimulated multiplication of virus in tissues at the injection site and enhanced entry of virus into the blood. The nonpathogenic r(+) variant of EMC which grows locally in tissues but fails to disseminate after subcutaneous and intraperitoneal inoculation was used in most experiments. This virus caused viremia and fatal central nervous system disease only when the polycations were included in the inoculum. DEAE dextran and polybrene stimulated the release of interferon in infected tissues but had no effect in the absence of virus multiplication. Histological studies of tissues from the injection site showed that polycations provoke a mononuclear cell reaction and alter the integrity of connective tissue. However, the mechanism by which the substances enhance virus growth and dissemination was not defined.
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John E. Craighead (1967) studied Encephalomyocarditis (EMC) virus infection. Polycations (DEAE dextran, hexadimethrine, polymyxin B, polylysine, calf thymus histone) vs. Virus without polycations was evaluated on Virus multiplication, viremia, and fatal central nervous system disease. Polycations mixed with the encephalomyocarditis virus increased viral multiplication, viremia, and fatal central nervous system disease in adult mice.
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