Alfamo- and ilarviruses are characterized by the deficiency of their genomes (three messenger-sense RNAs) to start an infection cycle. The RNAs are in capsids built from a single species of protein of about 24 kD. A few dimers of this coat protein per RNA molecule are sufficient to activate the genome. Since the first description of genome activation (Bol JF, van Vloten-Doting L, Jaspars EMJ (1971) Virology 46: 73–85) three models have been proposed concerning its mechanism: the protection, the replicase and the messenger release hypotheses. The first two models make use of the fact that in these genera of RNA viruses the 3′ termini of the RNAs bind the coat protein very strongly. The resulting structure would provide protection against 3′-to 5′ exoribonucleases, or would permit correct initiation of minus-strand synthesis, respectively. However, naked inoculated RNAs of alfalfa mosaic virus appear to be quite stable in the cell, and in vitro the coat protein is inhibiting rather than stimulating initiation of minus-strand synthesis. The messenger release hypothesis states that the coat protein is needed for the release of viral messenger RNAs from membranous replication complexes throughout the whole viral replication cycle. This is supported by in vivo and in vitro observations, but as yet a detailed molecular mechanism is difficult to give.
Archives of Virology – Springer Journals
Published: May 1, 1999
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