Key result
Influenza A virus synthesizes both mRNA and cRNA early in infection, suggesting nascent cRNA is degraded by host nucleases unless stabilized by newly synthesized viral RNA polymerase and NP.
The study proposes a model where influenza virus replication is regulated by the stabilization of replicative intermediates rather than a switch mechanism for RNA synthesis initiation.
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Challenges switch model for influenza RNA synthesis; leaves open cRNA stabilization as primary regulator in vivo.
The RNA-dependent RNA polymerase of influenza A virus is responsible for both transcription and replication of negative-sense viral RNA. It is thought that a “switching” mechanism regulates the transition between these activities. We demonstrate that, in the presence of preexisting viral RNA polymerase and nucleoprotein (NP), influenza A virus synthesizes both mRNA (transcription) and cRNA (replication) early in infection. We suggest that there may be no switch regulating the initiation of RNA synthesis and present a model suggesting that nascent cRNA is degraded by host cell nucleases unless it is stabilized by newly synthesized viral RNA polymerase and NP.
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Vreede et al. (2004) studied Influenza A virus infection. Influenza A virus synthesizes both mRNA and cRNA early in infection, suggesting nascent cRNA is degraded by host nucleases unless stabilized by newly synthesized viral RNA polymerase and NP.
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