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Viruses
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Host Cell-Virus Interaction, 4th Edition
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Host Cell-Virus Interaction, 4th Edition

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Viral Immunology, Vaccines, and Antivirals".

Deadline for manuscript submissions: 14 March 2025 | Viewed by 4906

Special Issue Editors

Dr. Parikshit Bagchi

E-Mail Website
Guest Editor
Department of Molecular Microbiology, Washington University School of Medicine in St. Louis, St. Louis, MO 63110, USA
Interests: host cell-virus interaction; intracellular trafficking of virus; membrane trafficking; non-enveloped viruses; positive sense RNA viruses
Special Issues, Collections and Topics in MDPI journals
Dr. Anupam Mukherjee

E-Mail Website
Guest Editor
Division of Virology, ICMR-National AIDS Research Institute, Pune 411026, Maharashtra, India
Interests: RNA virus; viral pathogenesis; host cell–virus interaction; RNAi; small RNA as therapeutics; targeted delivery; virus and cancer
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Activation of immune responses is the key factor for host defense against any viral infections. Yet, viruses have also adapted several strategies to escape or suppress host resistance to make a proviral environment using the cellular machineries that represent the most important components of viral pathogenicity. As an obligate parasite, viruses are eventually reliant on the host cellular components for their replication via altering the cellular signal transduction pathways and immune evasion mechanisms, including escaping recognition from intracellular sensors, suppression of IFN-α/β production, NF-kappaB, dysregulation of inflammatory responses and inflammasome activation signals, RNA interference, modulation of autophagy and programmed cell-death mechanisms, and selection of genetic variants that escape from neutralizing antibodies.

Significant research on antivirals to combat viral infections is an extensive process, which requires multidisciplinary approaches. For any antiviral agents, such as synthetic drugs, chemical inhibitors, RNAi strategies of miRNAs or siRNAs, natural compounds, phytoconstituents, herbal or Ayurvedic formulations, and metallic nanoparticles, apparently there are two different strategies of antiviral drug discovery available, which are based on targeting the viral lifecycle and/or directing the host cellular factors. The modus operandi of antivirals characterization is fundamental for identification, prediction and understanding side-effects, drug interactions and the emergence of resistance, for increasing the spectrum of activity, and for improving antiviral efficacy.

For this Special Issue, we welcome original research papers, communications and review articles that contribute to an improved understanding of the molecular details of host cell–virus interaction through viral immune evasion and host defense mechanism during any viral infection. Furthermore, understanding the mechanism of action of host-centric and/or targeting viral lifecycle antivirals could further refine our understanding of virus–host interactions and the antiviral strategies for treatment and prophylaxis, which are essential to managing any active viral infections. Hence, we invite all researchers working in the field of viral lifecycle, pathogenesis, host responses and antiviral development to submit their research to this Special Issue to highlight recent advancements and further the discussion on host–virus interactions and prospective therapeutics.

Dr. Parikshit Bagchi
Dr. Anupam Mukherjee
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
  • viral proteins
  • virus entry
  • viral replication and pathogenesis
  • virus assembly and egress
  • intracellular trafficking of virus
  • host cell
  • cellular signaling
  • interferon pathway
  • inflammasome
  • viral immune evasion
  • immune response
  • cell death
  • apoptosis
  • autophagy
  • host-virus interaction
  • anti-viral strategies
  • direct acting antivirals
  • broad-spectrum antiviral agents
  • RNAi
  • microRNAs
  • neutralizing antibodies
  • molecular mechanisms of antivirals
  • molecular mechanisms of drug-resistance

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Published Papers (4 papers)

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Research

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17 pages, 1953 KiB  
Article
Prospective and Longitudinal Analysis of Lymphocyte Subpopulations in SARS-CoV-2 Positive and Negative Pneumonia: Potential Role of Decreased Naïve CD8+ in COVID-19 Patients
by Makhabbat Bekbossynova, Lyudmila Akhmaltdinova, Kuanysh Dossybayeva, Ainur Tauekelova, Zauresh Smagulova, Tatyana Tsechoeva, Gulsimzhan Turebayeva, Aliya Sailybayeva, Zhanar Kalila, Takhmina Mirashirova, Timur Muratov and Dimitri Poddighe
Viruses 2025, 17(1), 41; https://doi.org/10.3390/v17010041 - 30 Dec 2024
Viewed by 683
Abstract
Background: During the acute phase of COVID-19, a number of immunological abnormalities have been reported, but few studies longitudinally analyzed the specific subsets of peripheral blood lymphocytes. Methods: In this observational, prospective, and longitudinal study, adult patients developing acute pneumonia during [...] Read more.
Background: During the acute phase of COVID-19, a number of immunological abnormalities have been reported, but few studies longitudinally analyzed the specific subsets of peripheral blood lymphocytes. Methods: In this observational, prospective, and longitudinal study, adult patients developing acute pneumonia during the COVID-19 pandemic have been followed up for 12 months. Peripheral blood lymphocyte subsets were assessed (with a specific focus on the memory markers) at 6 time points after the disease onset until 12 months. Results: A total of 76 patients with acute pneumonia (characterized by a prevalently interstitial pattern of lung inflammation) at the hospital admission (who completed the 12-month follow-up period) were recruited in this study. They were divided into two groups, namely positive (n = 31) and negative (n = 45) patients for the SARS-CoV-2 PCR test. In the acute phase, the general lymphocyte immunophenotyping profile was comparable for most parameters between these groups, except for B cells. When B and T cells were analyzed according to the expression of memory markers, a significant decrease in naïve CD8+ T cells was observed in the SARS-CoV-2-positive pneumonia group during the acute phase. Notably, this aspect was maintained during the follow-up period for at least 9 months. Conclusions: COVID-19 pneumonia seems to be associated with a lower number of naïve CD8+ T cells compared to pneumonia patients negative for this virus. This alteration can persist in the convalescent phase. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 4th Edition)
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30 pages, 2218 KiB  
Article
A Global Collaborative Comparison of SARS-CoV-2 Antigenicity Across 15 Laboratories
by Polina Brangel, Sina Tureli, Barbara Mühlemann, Nicole Liechti, Daniel Zysset, Olivier Engler, Isabel Hunger-Glaser, Ioana Ghiga, Giada Mattiuzzo, Isabella Eckerle, Meriem Bekliz, Annika Rössler, Melanie M. Schmitt, Ludwig Knabl, Janine Kimpel, Luis Fernando Lopez Tort, Mia Ferreira de Araujo, Any Caroline Alves de Oliveira, Braulia Costa Caetano, Marilda Mendonça Siqueira, Matthias Budt, Jean-Marc Gensch, Thorsten Wolff, Tarteel Hassan, Francis Amirtharaj Selvaraj, Tandile Hermanus, Prudence Kgagudi, Carol Crowther, Simone I. Richardson, Jinal N. Bhiman, Penny L. Moore, Samuel M. S. Cheng, John K. C. Li, Leo L. M. Poon, Malik Peiris, Victor M. Corman, Christian Drosten, Lilin Lai, Taweewun Hunsawong, Kamonthip Rungrojcharoenkit, Jindarat Lohachanakul, Alex Sigal, Khadija Khan, Volker Thiel, G. Tuba Barut, Nadine Ebert, Anna Z. Mykytyn, Irene Owusu Donkor, James Odame Aboagye, Prince Adom Nartey, Maria D. Van Kerkhove, Jane Cunningham, Bart L. Haagmans, Mehul S. Suthar, Derek Smith and Lorenzo Subissiadd Show full author list remove Hide full author list
Viruses 2024, 16(12), 1936; https://doi.org/10.3390/v16121936 - 18 Dec 2024
Viewed by 1663
Abstract
Setting up a global SARS-CoV-2 surveillance system requires an understanding of how virus isolation and propagation practices, use of animal or human sera, and different neutralisation assay platforms influence assessment of SARS-CoV-2 antigenicity. In this study, with the contribution of 15 independent laboratories [...] Read more.
Setting up a global SARS-CoV-2 surveillance system requires an understanding of how virus isolation and propagation practices, use of animal or human sera, and different neutralisation assay platforms influence assessment of SARS-CoV-2 antigenicity. In this study, with the contribution of 15 independent laboratories across all WHO regions, we carried out a controlled analysis of neutralisation assay platforms using the first WHO International Standard for antibodies to SARS-CoV-2 variants of concern (source: NIBSC). Live virus isolates (source: WHO BioHub or individual labs) or spike plasmids (individual labs) for pseudovirus production were used to perform neutralisation assays using the same serum panels. When comparing fold drops, excellent data consistency was observed across the labs using common reagents, including between pseudovirus and live virus neutralisation assays (RMSD of data from mean fold drop was 0.59). Utilising a Bayesian model, geometric mean titres and assay titre magnitudes (offsets) can describe the data efficiently. Titre magnitudes were seen to vary largely even for labs within the same assay group. We have observed that overall, live Microneutralisation assays tend to have the lowest titres, whereas Pseudovirus Neutralisation have the highest (with a mean difference of 3.2 log2 units between the two). These findings are relevant for laboratory networks, such as the WHO Coronavirus Laboratory Network (CoViNet), that seek to support a global surveillance system for evolution and antigenic characterisation of variants to support monitoring of population immunity and vaccine composition policy. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 4th Edition)
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Review

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43 pages, 3639 KiB  
Review
The ‘Oma’s of the Gammas—Cancerogenesis by γ-Herpesviruses
by Anwesha Banerjee, Debashree Dass, Soumik Mukherjee, Mollina Kaul, R. Harshithkumar, Parikshit Bagchi and Anupam Mukherjee
Viruses 2024, 16(12), 1928; https://doi.org/10.3390/v16121928 - 17 Dec 2024
Viewed by 1104
Abstract
Epstein–Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV), which are the only members of the gamma(γ) herpesviruses, are oncogenic viruses that significantly contribute to the development of various human cancers, such as Burkitt’s lymphoma, nasopharyngeal carcinoma, Hodgkin’s lymphoma, Kaposi’s sarcoma, and primary effusion [...] Read more.
Epstein–Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV), which are the only members of the gamma(γ) herpesviruses, are oncogenic viruses that significantly contribute to the development of various human cancers, such as Burkitt’s lymphoma, nasopharyngeal carcinoma, Hodgkin’s lymphoma, Kaposi’s sarcoma, and primary effusion lymphoma. Oncogenesis triggered by γ-herpesviruses involves complex interactions between viral genetics, host cellular mechanisms, and immune evasion strategies. At the genetic level, crucial viral oncogenes participate in the disruption of cell signaling, leading to uncontrolled proliferation and inhibition of apoptosis. These viral proteins can modulate several cellular pathways, including the NF-κB and JAK/STAT pathways, which play essential roles in cell survival and inflammation. Epigenetic modifications further contribute to EBV- and KSHV-mediated cancerogenesis. Both EBV and KSHV manipulate host cell DNA methylation, histone modification, and chromatin remodeling, the interplay of which contribute to the elevation of oncogene expression and the silencing of the tumor suppressor genes. Immune factors also play a pivotal role in the development of cancer. The γ-herpesviruses have evolved intricate immune evasion strategies, including the manipulation of the major histocompatibility complex (MHC) and the release of cytokines, allowing infected cells to evade immune detection and destruction. In addition, a compromised immune system, such as in HIV/AIDS patients, significantly increases the risk of cancers associated with EBV and KSHV. This review aims to provide a comprehensive overview of the genetic, epigenetic, and immune mechanisms by which γ-herpesviruses drive cancerogenesis, highlighting key molecular pathways and potential therapeutic targets. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 4th Edition)
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20 pages, 3007 KiB  
Review
Host-Driven Ubiquitination Events in Vector-Transmitted RNA Virus Infections as Options for Broad-Spectrum Therapeutic Intervention Strategies
by Sanskruthi Sreepangi, Haseebullah Baha, Lorreta Aboagyewa Opoku, Naomi X. Jones, Maame Konadu, Farhang Alem, Michael D. Barrera and Aarthi Narayanan
Viruses 2024, 16(11), 1727; https://doi.org/10.3390/v16111727 - 31 Oct 2024
Viewed by 1132
Abstract
Many vector-borne viruses are re-emerging as public health threats, yet our understanding of the virus–host interactions critical for productive infection remains limited. The ubiquitination of proteins, including host- and pathogen-derived proteins is a highly prominent and consistent post-translational modification that regulates protein function [...] Read more.
Many vector-borne viruses are re-emerging as public health threats, yet our understanding of the virus–host interactions critical for productive infection remains limited. The ubiquitination of proteins, including host- and pathogen-derived proteins is a highly prominent and consistent post-translational modification that regulates protein function through signaling and degradation. Viral proteins are documented to hijack the host ubiquitination machinery to modulate multiple host processes including antiviral defense mechanisms. The engagement of the host ubiquitination machinery in the post-translational modification of viral proteins to support aspects of the viral life cycle including assembly and egress is also well documented. Exploring the role ubiquitination plays in the life cycle of vector-transmitted viral pathogens will increase the knowledge base pertinent to the impact of host-enabled ubiquitination of viral and host proteins and the consequences on viral pathogenesis. In this review, we explore E3 ligase-regulated ubiquitination pathways functioning as proviral and viral restriction factors in the context of acutely infectious, vector-transmitted viral pathogens and the potential for therapeutically targeting them for countermeasures development. Full article
(This article belongs to the Special Issue Host Cell-Virus Interaction, 4th Edition)
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