Special Issue "Physical Virology - Viruses at Multiple Levels of Complexity"

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

Deadline for manuscript submissions: 10 July 2023 | Viewed by 10532

Special Issue Editors

Dr. Roya Zandi
E-Mail Website
Guest Editor
Department of Physics and Astronomy, University of California, Riverside, CA, USA
Interests: statistical mechanics and condensed matter physics of virus assembly
Dr. Michael F. Hagan
E-Mail Website
Guest Editor
Physics and Biological Physics, Martin A. Fisher School of Physics, Brandeis University, Waltham, USA
Interests: physical principles controlling control assembly and dynamical organization of viruses
Heinrich Pette Institute, Leibniz Institute for Experimental Virology, CSSB and European XFEL GmbH, Hamburg, Germany
Interests: norovirus assembly and entry; coronaviral replication/transcription complexes; structural mass spectrometry; single particle imaging with X-ray free-electron lasers

Special Issue Information

Dear Colleagues,

Viral infections involve processes from atomic-scale regulation of ionic transport, to macromolecular self-assembly and membrane budding, to global epidemiology. Physical virology studies these processes as a paradigm for the intersection of fundamental physical laws and emergent biological function. Thus, diverse disciplines are relevant to physical virology, and the field is unique for its simultaneous focus on fundamental and applied aspects of virology. This Special Issue will present works by researchers with scientific expertise in virology, chemistry, material science, mathematics, physics, and engineering who share a common desire to (1) understand the biophysical mechanisms that enable and regulate viral lifecycles, (2) use this knowledge to develop and engineer novel nanotechnology platforms based on viral particles or other self-assembling structures, with applications including biomimetic materials and optoelectronics, and (3) broaden physical virology to leverage recent advances in cell biology and protein design. The COVID-19 pandemic has highlighted the need for these cross-disciplinary approaches to understand viral biology, predict their global spread and impact, and generate the fundamental knowledge that provides the foundation for the development of new treatments.

Dr. Roya Zandi
Dr. Michael F. Hagan
Dr. Charlotte Uetrecht
Guest Editors

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

  • virus assembly and disassembly
  • virus dynamics and mechanics
  • symmetry
  • biomaterials and virus-inspired designs
  • cargo encapsidation and release
  • membraneous compartments
  • interaction networks
  • immunity
  • evolution and vaccines

Published Papers (4 papers)

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Research

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Article
Novel Mode of nanoLuciferase Packaging in SARS-CoV-2 Virions and VLPs Provides Versatile Reporters for Virus Production
Viruses 2023, 15(6), 1335; https://doi.org/10.3390/v15061335 - 07 Jun 2023
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Abstract
SARS-CoV-2 is a positive-strand RNA virus in the Coronaviridae family that is responsible for morbidity and mortality worldwide. To better understand the molecular pathways leading to SARS-CoV-2 virus assembly, we examined a virus-like particle (VLP) system co-expressing all structural proteins together with an [...] Read more.
SARS-CoV-2 is a positive-strand RNA virus in the Coronaviridae family that is responsible for morbidity and mortality worldwide. To better understand the molecular pathways leading to SARS-CoV-2 virus assembly, we examined a virus-like particle (VLP) system co-expressing all structural proteins together with an mRNA reporter encoding nanoLuciferase (herein nLuc). Surprisingly, the 19 kDa nLuc protein itself was encapsidated into VLPs, providing a better reporter than nLuc mRNA itself. Strikingly, infecting nLuc-expressing cells with the SARS-CoV-2, NL63 or OC43 coronaviruses yielded virions containing packaged nLuc that served to report viral production. In contrast, infection with the flaviviruses, dengue or Zika, did not lead to nLuc packaging and secretion. A panel of reporter protein variants revealed that the packaging is size-limited and requires cytoplasmic expression, indicating that the large virion of coronaviruses can encaspidate a small cytoplasmic reporter protein. Our findings open the way for powerful new approaches to measure coronavirus particle production, egress and viral entry mechanisms. Full article
(This article belongs to the Special Issue Physical Virology - Viruses at Multiple Levels of Complexity)
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Article
Construction of a Chikungunya Virus, Replicon, and Helper Plasmids for Transfection of Mammalian Cells
Viruses 2023, 15(1), 132; https://doi.org/10.3390/v15010132 - 31 Dec 2022
Viewed by 1195
Abstract
The genome of Alphaviruses can be modified to produce self-replicating RNAs and virus-like particles, which are useful virological tools. In this work, we generated three plasmids for the transfection of mammalian cells: an infectious clone of Chikungunya virus (CHIKV), one that codes for [...] Read more.
The genome of Alphaviruses can be modified to produce self-replicating RNAs and virus-like particles, which are useful virological tools. In this work, we generated three plasmids for the transfection of mammalian cells: an infectious clone of Chikungunya virus (CHIKV), one that codes for the structural proteins (helper plasmid), and another one that codes nonstructural proteins (replicon plasmid). All of these plasmids contain a reporter gene (mKate2). The reporter gene in the replicon RNA and the infectious clone are synthesized from subgenomic RNA. Co-transfection with the helper and replicon plasmids has biotechnological/biomedical applications because they allow for the delivery of self-replicating RNA for the transient expression of one or more genes to the target cells. Full article
(This article belongs to the Special Issue Physical Virology - Viruses at Multiple Levels of Complexity)
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Article
Biophysical Modeling of SARS-CoV-2 Assembly: Genome Condensation and Budding
Viruses 2022, 14(10), 2089; https://doi.org/10.3390/v14102089 - 20 Sep 2022
Cited by 1 | Viewed by 4068
Abstract
The COVID-19 pandemic caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has spurred unprecedented and concerted worldwide research to curtail and eradicate this pathogen. SARS-CoV-2 has four structural proteins: Envelope (E), Membrane (M), Nucleocapsid (N), and Spike (S), which self-assemble along [...] Read more.
The COVID-19 pandemic caused by the Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has spurred unprecedented and concerted worldwide research to curtail and eradicate this pathogen. SARS-CoV-2 has four structural proteins: Envelope (E), Membrane (M), Nucleocapsid (N), and Spike (S), which self-assemble along with its RNA into the infectious virus by budding from intracellular lipid membranes. In this paper, we develop a model to explore the mechanisms of RNA condensation by structural proteins, protein oligomerization and cellular membrane–protein interactions that control the budding process and the ultimate virus structure. Using molecular dynamics simulations, we have deciphered how the positively charged N proteins interact and condense the very long genomic RNA resulting in its packaging by a lipid envelope decorated with structural proteins inside a host cell. Furthermore, considering the length of RNA and the size of the virus, we find that the intrinsic curvature of M proteins is essential for virus budding. While most current research has focused on the S protein, which is responsible for viral entry, and it has been motivated by the need to develop efficacious vaccines, the development of resistance through mutations in this crucial protein makes it essential to elucidate the details of the viral life cycle to identify other drug targets for future therapy. Our simulations will provide insight into the viral life cycle through the assembly of viral particles de novo and potentially identify therapeutic targets for future drug development. Full article
(This article belongs to the Special Issue Physical Virology - Viruses at Multiple Levels of Complexity)
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Review

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Review
Viral Aggregation: The Knowns and Unknowns
Viruses 2022, 14(2), 438; https://doi.org/10.3390/v14020438 - 21 Feb 2022
Cited by 8 | Viewed by 3854
Abstract
Viral aggregation is a complex and pervasive phenomenon affecting many viral families. An increasing number of studies have indicated that it can modulate critical parameters surrounding viral infections, and yet its role in viral infectivity, pathogenesis, and evolution is just beginning to be [...] Read more.
Viral aggregation is a complex and pervasive phenomenon affecting many viral families. An increasing number of studies have indicated that it can modulate critical parameters surrounding viral infections, and yet its role in viral infectivity, pathogenesis, and evolution is just beginning to be appreciated. Aggregation likely promotes viral infection by increasing the cellular multiplicity of infection (MOI), which can help overcome stochastic failures of viral infection and genetic defects and subsequently modulate their fitness, virulence, and host responses. Conversely, aggregation can limit the dispersal of viral particles and hinder the early stages of establishing a successful infection. The cost–benefit of viral aggregation seems to vary not only depending on the viral species and aggregating factors but also on the spatiotemporal context of the viral life cycle. Here, we review the knowns of viral aggregation by focusing on studies with direct observations of viral aggregation and mechanistic studies of the aggregation process. Next, we chart the unknowns and discuss the biological implications of viral aggregation in their infection cycle. We conclude with a perspective on harnessing the therapeutic potential of this phenomenon and highlight several challenging questions that warrant further research for this field to advance. Full article
(This article belongs to the Special Issue Physical Virology - Viruses at Multiple Levels of Complexity)
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