How Viruses Hijack and Modify the Secretory Transport Pathway

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.

The Transient Receptor Potential Vanilloid 2 (TRPV2) Channel Facilitates Virus Infection Through the Ca2+‐LRMDA Axis in Myeloid Cells

“…Viruses hijack the cell membrane machinery for their entry. [ 49–51 ] Interestingly, we found that the actin filament‐exerted tensile force of cell membrane that regulates the mobility of cell membrane was significantly reduced in various Lyz2 ‐Cre; Trpv2 fl/fl myeloid cells compared to the Trpv2 fl/fl counterparts. Such a process is dependent on the homeostatic Ca 2+ influx mediated by TRPV channels, as reconstitution of TRPV1 or TRPV2 but not TRPV2 E572Q or TRPV1 D646N/E648/651Q into Lyz2 ‐Cre; Trpv2 fl/fl BMDCs restored the membrane tension.…”

Discovery of host-directed modulators of virus infection by probing the SARS-CoV-2–host protein–protein interaction network

“…These network-based results also support previous studies that have shown how SARS-CoV-2 hijacks the rough endoplasmic reticulum (RER)-linked host translational machinery for its replication [ 11 ]. In addition, NIP targets were enriched for pathways related to protein export ( P = 8.99 × 10 −5 ), which also includes secretory pathways that are hijacked by the virus to carry out their essential functions, such as virus replication, assembly and egress, demonstrating that viruses evade host cellular pathways to promote their propagation [ 25 ]. These results indicate that the extended target set consisting of the top-200 NIPs identified by the RWR algorithm do not only populate similar pathways as VIPs but are also implicated in various biological processes related to viral infection.…”

Discovery of host-directed modulators of virus infection by probing the SARS-CoV-2-host protein-protein interaction network

“…These network-based results also support previous studies that have shown how SARS-CoV-2 hijacks the rough endoplasmic reticulum (RER)-linked host translational machinery for its replication (11,30). In addition, NIP proteins were enriched for pathways related to protein export (P=8.99×10 −5 ), which also includes secretory pathways that are hijacked by the virus to carry out their essential functions, such as virus replication, assembly, and egress, demonstrating that viruses evade host cellular pathways to promote their propagation (25). These results indicate that the extended target set consisting of the top-200 NIP host proteins identified by the RWR algorithm not only populate similar pathways as VIPs but are also implicated in various biological processes related to viral infection.…”