Infectivity of mengovirus replicative form. IV. Intracellular conversion into replicative intermediate

Abstract

The replicative form (RF) of mengovirus was previously shown to be infectious, and the infectivity of this virus-induced, double-stranded RNA, to depend on the host-cell macromolecular synthesis. Analysis of the 3H-labeled RNAs recovered from the cytoplasm of 3H-RF-infected cells revealed that the parental RF molecules sedimented faster in neutral sucrose density gradients as the infectious cycle proceeded. When 3H-RF-infected cells were pulse-labeled with [ 14C]uridine at 3 hr after infection most of the [ 14C]RNA was found in a rapidly sedimenting structure derived from (or tightly associated with) the parental 3H-RF. This structure had all the characteristics of the replicative intermediate (RI). Treatment of the host cell with interferon abolished the infectivity of RF, but did not prevent the intracellular conversion of RIP into RI. By contrast, exposure of the cultures to actinomycin D suppressed both the infectivity of RF and its transition to RI. The role of a host cell factor in the mechanism of infectivity of picornavirus RF is discussed.