Positive-strand RNA viruses [(+)RNA viruses] include many important human, animal, and plant pathogens. A highly conserved and indispensable feature of (+)RNA virus infection is that these viruses proliferate and reorganize host membranes to assemble viral replication complexes (VRCs). We show that brome mosaic virus (BMV) stimulates phosphatidylcholine (PC) synthesis at the viral replication sites. BMV recruits a host enzyme involved in PC synthesis to support proper VRC formation and genomic replication. We further show that hepatitis C virus and poliovirus also promote accumulation of PC at the viral replication sites, revealing a feature common to a group of (+)RNA viruses. This virus-specific step can be targeted to develop a broad-spectrum antiviral strategy with the least side effects on host growth.
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This is a big deal: it demonstrates a common requirement among very different (+)strand RNA viruses – picornaviruses, flaviviruses and bromoviruses – for the same lipid – phosphatidylcholine (PC) – and makes the point that inhibiting PC synthesis significantly inhibits viral replication. That means the same therapy could be used for viruses that are otherwise so different as to have no obvious similarity at all, other than genome polarity. Great stuff!