Cellular RNA and protein synthesis are required both for interferon synthesis (Heller, 1963; Wagner, 1963) and the expression of the antivirus activity of interferon (Taylor, 1964). The suppression of the antivirus activity of interferon by metabolic inhibitors has been interpreted to mean that interferon acts as a de-repressor for the synthesis of a cellular antivirus protein. While direct proof for the interferon-induced antivirus protein is still lacking, recent circumstantial evidence supports this interpretation (Dianzani, Buckler & Baron, 1968; Stewart & Lockart, 1970).

In a recent publication, Kjeldsberg & Flikke (1971) reported that polyinosinic-polycytidylic acid (poly I:C) inhibited poliovirus RNA synthesis in cells whose DNA-dependent RNA synthesis had been suppressed by actinomycin D. They suggested that, rather than acting through interferon induction, low concentrations of poly I:C may directly interfere with virus replication by binding to the virus-specific RNA polymerase.


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