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Viruses
Special Issues
Chaperones and Viral-Host Interactions
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Chaperones and Viral-Host Interactions

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Animal Viruses".

Deadline for manuscript submissions: closed (30 September 2021) | Viewed by 12107

Special Issue Editor

Prof. Dr. Jaquelin P. Dudley

E-Mail Website
Guest Editor
Department of Molecular Biosciences, University of Texas at Austin, Austin, TX, USA
Interests: APOBECs; cytidine deaminase; AID; viral antagonists; viral hypermutation; innate immunity; viral selection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Viruses are obligate intracellular parasites that are dependent on host factors for their propagation and survival. Interactions between viral and host proteins have continued to co-evolve to shape and maximize virus transmission. Study of virus-host interactions is important for determining the final outcome of viral infections. Chaperones are critical host proteins that promote multiple aspects of viral replication.  For example, one host protein that plays multiple roles in different stages of the viral life cycle is valosin-containing protein (VCP), also known as p97 in mammals or Cdc48 in yeast. This highly conserved AAA ATPase participates in virtually every stage of virus replication from entry, trafficking, nucleic acid replication, and maturation.  Furthermore, viral proteins, such as SV40 T antigen, have their own chaperone activities.  Both RNA-containing and DNA-containing viruses use chaperone functions for multiple aspects of their life cycles. Better understanding of the molecular details of viral and host chaperones will provide important information about normal cellular processes and how viruses manipulate them.  Continued studies are predicted to have clinical importance for the design of antiviral and vaccine strategies.

Prof. Dr. Jaquelin Dudley
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Viruses is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • chaperones
  • p97
  • valosin-containing protein
  • protein folding
  • ATPase
  • ERAD
  • viral replication
  • trafficking
  • viral entry
  • transcription
  • subcellular localization
  • proteostasis
  • assembly
  • viral-host interactions

Published Papers (3 papers)

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Research

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19 pages, 5996 KiB  
Article
The Biogenesis of Dengue Virus Replication Organelles Requires the ATPase Activity of Valosin-Containing Protein
by Clément Mazeaud, Anaïs Anton, Felix Pahmeier, Aïssatou Aïcha Sow, Berati Cerikan, Wesley Freppel, Mirko Cortese, Ralf Bartenschlager and Laurent Chatel-Chaix
Viruses 2021, 13(10), 2092; https://doi.org/10.3390/v13102092 - 18 Oct 2021
Cited by 9 | Viewed by 3346
Abstract
The dengue virus (DENV) causes the most prevalent arthropod-borne viral disease worldwide. While its incidence is increasing in many countries, there is no approved antiviral therapy currently available. In infected cells, the DENV induces extensive morphological alterations of the endoplasmic reticulum (ER) to [...] Read more.
The dengue virus (DENV) causes the most prevalent arthropod-borne viral disease worldwide. While its incidence is increasing in many countries, there is no approved antiviral therapy currently available. In infected cells, the DENV induces extensive morphological alterations of the endoplasmic reticulum (ER) to generate viral replication organelles (vRO), which include convoluted membranes (CM) and vesicle packets (VP) hosting viral RNA replication. The viral non-structural protein NS4B localizes to vROs and is absolutely required for viral replication through poorly defined mechanisms, which might involve cellular protein partners. Previous interactomic studies identified the ATPase valosin-containing protein (VCP) as a DENV NS4B-interacting host factor in infected cells. Using both pharmacological and dominant-negative inhibition approaches, we show, in this study, that VCP ATPase activity is required for efficient DENV replication. VCP associates with NS4B when expressed in the absence of other viral proteins while in infected cells, both proteins colocalize within large DENV-induced cytoplasmic structures previously demonstrated to be CMs. Consistently, VCP inhibition dramatically reduces the abundance of DENV CMs in infected cells. Most importantly, using a recently reported replication-independent plasmid-based vRO induction system, we show that de novo VP biogenesis is dependent on VCP ATPase activity. Overall, our data demonstrate that VCP ATPase activity is required for vRO morphogenesis and/or stability. Considering that VCP was shown to be required for the replication of other flaviviruses, our results argue that VCP is a pan-flaviviral host dependency factor. Given that new generation VCP-targeting drugs are currently evaluated in clinical trials for cancer treatment, VCP may constitute an attractive broad-spectrum antiviral target in drug repurposing approaches. Full article
(This article belongs to the Special Issue Chaperones and Viral-Host Interactions)
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Review

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20 pages, 2560 KiB  
Review
How Viruses Use the VCP/p97 ATPase Molecular Machine
by Poulami Das and Jaquelin P. Dudley
Viruses 2021, 13(9), 1881; https://doi.org/10.3390/v13091881 - 21 Sep 2021
Cited by 11 | Viewed by 4398
Abstract
Viruses are obligate intracellular parasites that are dependent on host factors for their replication. One such host protein, p97 or the valosin-containing protein (VCP), is a highly conserved AAA ATPase that facilitates replication of diverse RNA- and DNA-containing viruses. The wide range of [...] Read more.
Viruses are obligate intracellular parasites that are dependent on host factors for their replication. One such host protein, p97 or the valosin-containing protein (VCP), is a highly conserved AAA ATPase that facilitates replication of diverse RNA- and DNA-containing viruses. The wide range of cellular functions attributed to this ATPase is consistent with its participation in multiple steps of the virus life cycle from entry and uncoating to viral egress. Studies of VCP/p97 interactions with viruses will provide important information about host processes and cell biology, but also viral strategies that take advantage of these host functions. The critical role of p97 in viral replication might be exploited as a target for development of pan-antiviral drugs that exceed the capability of virus-specific vaccines or therapeutics. Full article
(This article belongs to the Special Issue Chaperones and Viral-Host Interactions)
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15 pages, 1646 KiB  
Review
How DNA and RNA Viruses Exploit Host Chaperones to Promote Infection
by Kaitlyn Speckhart, Jeffrey M. Williams and Billy Tsai
Viruses 2021, 13(6), 958; https://doi.org/10.3390/v13060958 - 21 May 2021
Cited by 5 | Viewed by 3594
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Chaperones and Viral-Host Interactions)
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