Abstract

SARS-coronavirus (SARS-CoV) replication and transcription are mediated by a replication/transcription complex (RTC) of which virus-encoded, non-structural proteins (nsps) are the primary constituents. The 16 SARS-CoV nsps are produced by autoprocessing of two large precursor polyproteins. The RTC is believed to be associated with characteristic virus-induced double-membrane structures in the cytoplasm of SARS-CoV-infected cells. To investigate the link between these structures and viral RNA synthesis, and to dissect RTC organization and function, we isolated active RTCs from infected cells and used them to develop the first robust assay for their in vitro activity. The synthesis of genomic RNA and all eight subgenomic mRNAs was faithfully reproduced by the RTC in this in vitro system. Mainly positive-strand RNAs were synthesized and protein synthesis was not required for RTC activity in vitro. All RTC activity, enzymatic and putative membrane-spanning nsps, and viral RNA cosedimented with heavy membrane structures. Furthermore, the pelleted RTC required the addition of a cytoplasmic host factor for reconstitution of its in vitro activity. Newly synthesized subgenomic RNA appeared to be released, while genomic RNA remained predominantly associated with the RTC-containing fraction. RTC activity was destroyed by detergent treatment, suggesting an important role for membranes. The RTC appeared to be protected by membranes, as newly synthesized viral RNA and several replicase/transcriptase subunits were protease- and nuclease-resistant and became susceptible to degradation only upon addition of a non-ionic detergent. Our data establish a vital functional dependence of SARS-CoV RNA synthesis on virus-induced membrane structures.

Highlights

  • Following infection and genome translation, positive-strand RNA (+RNA) viruses establish a cytoplasmic enzyme complex that directs the amplification and expression of their genome

  • Virus-encoded enzymes form the core of this replication/transcription complex’ (RTC), which is believed to be associated with characteristic virus-induced membrane structures derived from modified host cell membranes

  • RTC activity was destroyed by detergent treatment, suggesting a critical role for membranes that appeared to protect the complex against protease and nuclease digestion

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Summary

Introduction

Following infection and genome translation, positive-strand RNA (+RNA) viruses establish a cytoplasmic enzyme complex that directs the amplification and expression of their genome. It has become clear that +RNA virus RTCs are invariably associated with virus-induced membrane structures, which are poorly characterized but presumably provide a framework for RNA synthesis by facilitating the concentration and cooperation of viral macromolecules on a dedicated membrane surface. They may protect the viral RNA from nucleases in the cytoplasm of the host cell, aid in shielding the double-stranded RNA intermediates of virus replication from the host cell’s innate immune system, or contribute to the coordination of the viral life cycle in time and space. Unraveling their structure and function will be critical to understand the biochemistry of +RNA virus replication and develop novel antiviral control strategies

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