How DNA and RNA Viruses Exploit Host Chaperones to Promote Infection.

Kaitlyn Speckhart,Jeffrey M Williams,Billy Tsai

doi:10.3390/v13060958

Abstract

To initiate infection, a virus enters a host cell typically via receptor-dependent endocytosis. It then penetrates a subcellular membrane, reaching a destination that supports transcription, translation, and replication of the viral genome. These steps lead to assembly and morphogenesis of the new viral progeny. The mature virus finally exits the host cell to begin the next infection cycle. Strikingly, viruses hijack host molecular chaperones to accomplish these distinct entry steps. Here we highlight how DNA viruses, including polyomavirus and the human papillomavirus, exploit soluble and membrane-associated chaperones to enter a cell, penetrating and escaping an intracellular membrane en route for infection. We also describe the mechanism by which RNA viruses—including flavivirus and coronavirus—co-opt cytosolic and organelle-selective chaperones to promote viral endocytosis, protein biosynthesis, replication, and assembly. These examples underscore the importance of host chaperones during virus infection, potentially revealing novel antiviral strategies to combat virus-induced diseases.

Highlights

To cause infection, an incoming viral particle engages a receptor that is expressed on the plasma membrane of the host cell [1]
We describe how viruses across different families exploit the activities of soluble, membrane-bound, and organelle-specific host chaperones to accomplish the select entry steps required for successful infection
Exploiting host chaperones is a common strategy used during the entry of many viruses

Summary

Background

An incoming viral particle engages a receptor that is expressed on the plasma membrane of the host cell [1]. Because NS4A and NS4B exert critical roles in generating the aforementioned flavivirus replication compartments (Figure 3, step 4) [80,81,82], EMC supports virus replication, albeit indirectly Another ERresident chaperone called BiP was posited to regulate flavivirus infection [83], the molecular basis of the BiP’s action during viral entry is not entirely obvious. Viruses 2021, 13, x FOR PEER REVIEW exert critical roles in generating the aforementioned flavivirus replication compartments (Figure 3, step 4) [80,81,82], EMC supports virus replication, albeit indirectly.7Aofn other ER-resident chaperone called BiP was posited to regulate flavivirus infection [83], the molecular basis of the BiP’s action during viral entry is not entirely obvious.

Commandeering ER-Associated Chaperones during Coronavirus Entry

Conclusions