Abstract
Eukaryotic cells contain dynamic membrane-bound organelles that are constantly remodeled in response to physiological and environmental cues. Key organelles are the endoplasmic reticulum, the Golgi apparatus and the plasma membrane, which are interconnected by vesicular traffic through the secretory transport route. Numerous viruses, especially enveloped viruses, use and modify compartments of the secretory pathway to promote their replication, assembly and cell egression by hijacking the host cell machinery. In some cases, the subversion mechanism has been uncovered. In this review, we summarize our current understanding of how the secretory pathway is subverted and exploited by viruses belonging to Picornaviridae, Coronaviridae, Flaviviridae, Poxviridae, Parvoviridae and Herpesviridae families.
Highlights
Eukaryotic cells have numerous compartments to carry out specialized functions
Through its ability to dimerize in its GTP-bound form and recruit actin, cortactin and dynamin 2, ARF1 is a key player in the biogenesis and budding of both complex I (COPI)-coated vesicles and clathrin-mediated fission at the trans-Golgi network (TGN) [20]
When autophagy is altered by inhibiting the acidification of cellular compartments, poliovirus maturation is affected by up to 90%, leading to a decrease in the production of infectious virus particles [103]. Both poliovirus and coxsackievirus B3 (CVB3) assembly vesicles are believed to be double-membrane vesicles (DMVs) derived from single-membrane vesicles (SMVs), which are redistributed near the cis-Golgi when the infection progresses [8,81,98]
Summary
Eukaryotic cells have numerous compartments to carry out specialized functions. These subcellular organelles are separated from each other, and from the cell’s cytoplasm, by membranes. In addition to the genes that encode for viral structural components, viruses express proteins that are not incorporated into the progeny virions but are essential for the viral life cycle [7] These proteins modify intracellular compartments to generate new membranous structures to carry essential functions, such as virus replication, assembly and egression. Class III PI4K is a Golgi lipid kinase important for Golgi structure and function, and it activates lipid kinases [18,19] Viruses usurp this pathway for a supply of essential lipid to the viral replication platforms; this in turn depletes lipid from the host cell [19]. Vesicle fusion with the acceptor compartments requires tethering factors, RAB GTPases and SNAREs (image created in Biorender)
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