Single administrations of
poly C or
poly I are anti-viral against
infections of encephalomyocarditis (EMC) and Semliki Forest virus (SFV) in mice but
poly U and
poly A are not. The degree of protection is dose-dependent and mice which die do so at a later time when untreated controls even in a strain of mouse in which the time of death is not dependent on the dose of virus given. No circulating
interferon is found after treating mice with
poly C or
poly I even at
polynucleotide doses which give the same degree of protection as the
interferon inducer,
poly I:C. Several additional features distinguish the protection by
poly C and
poly I from
interferon induction: the effect is low 24h before
infection and maximal 6 h before
infection, the effect is short-lived and mice do not show hypo-reactivation to repeated treatment. Limited treatment of mice with
poly I:C,
interferon or
poly C before
infection itself results in additional protection when
poly C is also administered after
infection, indicating that
poly C has an effect after onset of virus replication. After
infection poly C and
poly I are both more effective by the intravenous route but before
infection they are most effective when administered by the same route as the virus. Quantitative comparisons of the protective effects of
poly C,
poly I and the
interferon inducer,
poly I:C, are possible from dose response curves of the
polynucleotides at different times relative to
infection and by different routes of administration. The results are considered in relation to the presence of homopolyribonucleotide tracts in the viral genomes and effects on the reticulo-endothelial system of the mice.