title: How viruses use the endoplasmic reticulum for entry, replication, and assembly.
abstract: To cause infection, a virus enters a host cell, replicates, and assembles, with the resulting new viral progeny typically released into the extracellular environment to initiate a new infection round. Virus entry, replication, and assembly are dynamic and coordinated processes that require precise interactions with host components, often within and surrounding a defined subcellular compartment. Accumulating evidence pinpoints the endoplasmic reticulum (ER) as a crucial organelle supporting viral entry, replication, and assembly. This review focuses on the molecular mechanism by which different viruses co-opt the ER to accomplish these crucial infection steps. Certain bacterial toxins also hijack the ER for entry. An interdisciplinary approach, using rigorous biochemical and cell biological assays coupled with advanced microscopy strategies, will push to the next level our understanding of the virus-ER interaction during infection.
authors.affiliation: Department of Cell and Developmental Biology, University of Michigan Medical School, Ann Arbor, MI 48103, USA.
authors.forename: Takamasa
authors.initials: T
authors.lastname: Inoue
authors.forename: Billy
authors.initials: B
authors.lastname: Tsai
mesh_terms: D002772:Cholera Toxin / Q000378:metabolism; D004721:Endoplasmic Reticulum / Q000378:metabolism / Q000502:physiology*; D054884:Host-Pathogen Interactions; D057131:Immune Evasion; D008954:Models, Biological; D011120:Polyomavirus / Q000502:physiology*; D019065:Virus Assembly / Q000502:physiology*; D053586:Virus Internalization; D014779:Virus Replication / Q000502:physiology*
chemical_list: D002772:Cholera Toxin