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.
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© 1995 Springer Science+Business Media New York
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Baric, R.S., Schaad, M.C. (1995). Evidence that MHV Subgenomic Negative Strands are Functional Templates. In: Talbot, P.J., Levy, G.A. (eds) Corona- and Related Viruses. Advances in Experimental Medicine and Biology, vol 380. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-1899-0_78
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DOI: https://doi.org/10.1007/978-1-4615-1899-0_78
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