Protection of Mice Against Infection with Wild-type Mengo Virus and an Interferon Sensitive Mutant (IS-1) by Polynucleotides and Interferons

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Abstract
Single-stranded polynucleotide preparations [tRNA, poly(rI) plus poly(ho5C)-copolymer] which protect mice against picornavirus infections without inducing interferon, protected mice equally against infection with an interferon-sensitive mutant (IS-1) of Mengo virus and with wild-type virus (IS+). Poly(rI) .cntdot. poly(rC) and mouse macrophage interferon [i.e., serum from mice treated with poly(rI) .cntdot. poly(rC)] protected mice equally against infections with the 2 viruses, but fibroblast interferon protected better against infection with the interferon-sensitive mutant than with the wild-type virus. These and other results indicate that: Mengo virus has a genetic locus affecting sensitivity to fibroblast but not macrophage interferon; these 2 types of interferon have different mechanisms of action against Mengo virus infections in mice; Mengo virus genes controlling sensitivity to fibroblast interferon may modulate disease since infection in vivo induces only fibroblast interferon; the antiviral activity of the single-stranded polynucleotides is unlikely to be mediated by induction of macrophage or fibroblast interferon.