title: Nuclear proteins hijacked by mammalian cytoplasmic plus strand RNA viruses.
abstract: Plus strand RNA viruses that replicate in the cytoplasm face challenges in supporting the numerous biosynthetic functions required for replication and propagation. Most of these viruses are genetically simple and rely heavily on co-opting cellular proteins, particularly cellular RNA-binding proteins, into new roles for support of virus infection at the level of virus-specific translation, and building RNA replication complexes. In the course of infectious cycles many nuclear-cytoplasmic shuttling proteins of mostly nuclear distribution are detained in the cytoplasm by viruses and re-purposed for their own gain. Many mammalian viruses hijack a common group of the same factors. This review summarizes recent gains in our knowledge of how cytoplasmic RNA viruses use these co-opted host nuclear factors in new functional roles supporting virus translation and virus RNA replication and common themes employed between different virus groups.
authors.affiliation: Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, TX 77030, United States. Electronic address: rlloyd@bcm.edu.
authors.forename: Richard E
authors.initials: RE
authors.lastname: Lloyd
mesh_terms: D003593:Cytoplasm / Q000821:virology*; D054884:Host-Pathogen Interactions; D009687:Nuclear Proteins / Q000378:metabolism*; D014176:Protein Biosynthesis; D012328:RNA Viruses / Q000502:physiology*; D014779:Virus Replication
chemical_list: D009687:Nuclear Proteins
keywords: Coronavirus; Enterovirus; Flavivirus; G3BP1; Hepatitis C virus; La protein; NSAP; Norovirus; PCBP2; PTB; Poliovirus; RNA helicase A; RNA virus; SRp20; Tia1/TIAR; UNR; hnRNP A1; hnRNP C; hnRNP K; hnRNP M
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