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Coronavirus Subgenomic Replicons as a Mechanism for mRNA Amplification

  • Phiroze B. Sethna
  • Shan-Ling Hung
  • David A. Brian
Conference paper
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 276)

Abstract

Assuming promoter sequences for synthesizing antigenome lie within the 3′ noncoding region on the Coronavirus genome (approximately 300 bases), and the promoter for synthesizing genome lie within the antileader sequence (approximately 80 bases) on the minus strand, we asked why do mRNAs not replicate? Coronavirus mRNAs have been shown to possess 3′ and 5′ noncoding regions in common with the genome (Brown et. al., 1984; Brown et. al., 1986; Lai et. al., 1984; Shieh et. al., 1987). If mRNA replication occurs, then we would predict the existence of (1) subgenomic (mRNA-length) minus strands, (2) subgenomic (mRNA-length) double-stranded replicative forms, and (3) subgenome mRNA replication rates that exceed that of the genome. We present evidence that suggests these three conditions are fulfilled for TGEV, and we, therefore, conclude that TGEV mRNAs undergo replication. We propose that this is a mechanism for mRNA amplification, a mechanism not yet described for any other RNA virus family having a nonsegmented genome.

Keywords

Replicative Form Minus Strand Mouse Hepatitis Virus Transmissible Gastroenteritis Virus mRNA Amplification 
These 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.

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Copyright information

© Plenum Press, New York 1990

Authors and Affiliations

  • Phiroze B. Sethna
    • 1
  • Shan-Ling Hung
    • 1
  • David A. Brian
    • 1
  1. 1.Department of MicrobiologyThe University of TennesseeKnoxvilleUSA

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