title: Viral and Cellular mRNA Translation in Coronavirus-Infected Cells.
abstract: Coronaviruses have large positive-strand RNA genomes that are 5' capped and 3' polyadenylated. The 5'-terminal two-thirds of the genome contain two open reading frames (ORFs), 1a and 1b, that together make up the viral replicase gene and encode two large polyproteins that are processed by viral proteases into 15-16 nonstructural proteins, most of them being involved in viral RNA synthesis. ORFs located in the 3'-terminal one-third of the genome encode structural and accessory proteins and are expressed from a set of 5' leader-containing subgenomic mRNAs that are synthesized by a process called discontinuous transcription. Coronavirus protein synthesis not only involves cap-dependent translation mechanisms but also employs regulatory mechanisms, such as ribosomal frameshifting. Coronavirus replication is known to affect cellular translation, involving activation of stress-induced signaling pathways, and employing viral proteins that affect cellular mRNA translation and RNA stability. This chapter describes our current understanding of the mechanisms involved in coronavirus mRNA translation and changes in host mRNA translation observed in coronavirus-infected cells.
authors.affiliation: The University of Texas Medical Branch, Galveston, TX, United States.
authors.forename: K
authors.initials: K
authors.lastname: Nakagawa
authors.affiliation: The University of Texas Medical Branch, Galveston, TX, United States.
authors.forename: K G
authors.initials: KG
authors.lastname: Lokugamage
authors.affiliation: The University of Texas Medical Branch, Galveston, TX, United States; Center for Biodefense and Emerging Infectious Diseases, The University of Texas Medical Branch, Galveston, TX, United States; UTMB Center for Tropical Diseases, The University of Texas Medical Branch, Galveston, TX, United States; Sealy Center for Vaccine Development, The University of Texas Medical Branch, Galveston, TX, United States; Institute for Human Infections and Immunity, The University of Texas Medical Branch, Galveston, TX, United States. Electronic address: shmakino@utmb.edu.
authors.forename: S
authors.initials: S
authors.lastname: Makino
mesh_terms: D000818:Animals; D017934:Coronavirus / Q000235:genetics* / Q000378:metabolism; D018352:Coronavirus Infections / Q000378:metabolism / Q000821:virology; D004847:Epithelial Cells / Q000378:metabolism / Q000821:virology; D016679:Genome, Viral; D054884:Host-Pathogen Interactions; D006801:Humans; D009713:Nucleotidyltransferases / Q000235:genetics / Q000378:metabolism; D016366:Open Reading Frames; D014176:Protein Biosynthesis; D012333:RNA, Messenger / Q000235:genetics* / Q000378:metabolism; D012367:RNA, Viral / Q000235:genetics* / Q000378:metabolism; D012270:Ribosomes / Q000737:chemistry / Q000378:metabolism; D015678:Viral Structural Proteins / Q000235:genetics* / Q000378:metabolism
chemical_list: D012333:RNA, Messenger; D012367:RNA, Viral; D015678:Viral Structural Proteins; D009713:Nucleotidyltransferases
keywords: Coronaviruses; Host gene expression; Host shutoff; Ribosomal frameshift; Stress response; Translation; Viral gene expression