Evidence that MHV subgenomic negative strands are functional templates.

Abstract

The genome of mouse hepatitis virus (MHV) is transcribed into a full length (~32 kb) and 6–8 subgenomic length mRNAs upon entry into susceptible cells1. Several discontinuous transcription models have been proposed to explain the presence of leader RNAs on positive-stranded mRNAs and antileader RNAs on full-length and subgenomic-length negative-stranded RNAs. One model proposes that subgenomic mRNAs are initially synthesized from a full-length negative-stranded RNA template by a leader-priming mechanism followed by mRNA amplification through subgenomic negative-stranded RNA intermediates2,3. Alternative models propose that subgenomic-length negative strands are synthesized directly from the genomic template by either a looping-out or transcription attenuation, or are functionally unimportant dead-end transcriptional products5. In this study, we demonstrate that the MHV group C1 mutants regulate negative strand synthesis and that the subgenomic length negative-stranded RNAs are the predominant template for mRNA synthesis late in infection.KeywordsmRNA SynthesisMouse Hepatitis VirusNegative StrandGenomic TemplateSubgenomic mRNAsThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.