Key result
Positive-strand RNA viruses utilize transmembrane viroporins to regulate redox dependencies and activate viral RNA capping, presenting a potential target for broad-spectrum antivirals.
Shared principles in transmembrane redox regulation of positive-strand RNA virus genome replication could spur development of broad-spectrum antivirals.
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Identifies shared redox and membrane features in viral replication; leaves open targeted antiviral strategies for flaviviruses.
Positive-strand RNA virus genome replication takes place on intracellular membranes that separate the reduced cytosol from the oxidized extracellular/luminal milieu. Ongoing studies of these membrane-bounded genome replication complexes have revealed underlying common principles in their structure, assembly and functionalization, including transmembrane features and redox dependencies. Among these, members of the alphavirus, flavivirus, and picornavirus supergroups all encode membrane-permeabilizing viroporins required for efficient RNA replication. For flaviviruses and particularly alphavirus supergroup members, these viroporins are linked to activating viral RNA capping and potentially other later-stage RNA replication functions, and to local transmembrane release of oxidizing potential to trigger these changes in cytoplasmic RNA replication complexes. Further exploration of these emerging shared principles could spur development of broad-spectrum antivirals.
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Nishikiori et al. (2020) conducted a review in Positive-strand RNA virus infection. Positive-strand RNA viruses utilize transmembrane viroporins to regulate redox dependencies and activate viral RNA capping, presenting a potential target for broad-spectrum antivirals.
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