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Insights into Viral Pathogenesis: Host Antiviral Responses and Viral Countermeasures
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Insights into Viral Pathogenesis: Host Antiviral Responses and Viral Countermeasures

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: 20 February 2025 | Viewed by 6809

Special Issue Editor

Dr. Don Gammon

E-Mail Website
Guest Editor
Department of Microbiology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA
Interests: DNA virus; RNA virus; innate immunity; viral pathogenesis; immune evasion
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

As obligate intracellular parasites, there is extraordinary selective pressure on viruses to exhibit mastery at manipulating, usurping, and/or inhibiting cellular functions to efficiently replicate. Thus, it is not surprising that studies of viruses have, in turn, led to key discoveries regarding the many cellular processes and factors they target. For example, mRNA processing, cellular oncogenes, and an inhibitor of apoptosis proteins were revealed by studying viruses. Given the incredible number of molecular virus–host interactions that occur at all stages of the viral life cycle, the basic cellular functions and processes that can be revealed by studying viruses are virtually limitless.

Virus–host coevolution has resulted in remarkable diversity in both host antiviral responses and viral countermeasures to overcome such host defenses. For example, the critical role of the interferon response in mammalian antiviral immunity is underscored by the finding of viral immune evasion factors encoded by disparate viruses that function to inhibit this response. In contrast, insects, which lack interferon responses, appear to predominantly employ antiviral RNA interference (RNAi) response pathways to combat virus infection. However, insect viruses, in turn, use both common and unique mechanisms to target RNAi responses. Identifying and characterizing virus–host interactions within this evolutionary “arms race” is critical for understanding how the outcomes of these interactions favor either productive viral replication or abortive infection. Moreover, the identification of virus-encoded immune evasion proteins can allow for their exploitation as molecular tools to discover and probe the host antiviral machinery they target.

For this Special Issue, original research articles, review articles, and short communications are welcome. Research areas of interest include (but are not limited to): host innate and adaptive antiviral immune responses, mechanisms of viral evasion of innate or adaptive immune responses, and animal model studies investigating antiviral host immune responses and/or viral pathogenesis/virulence. Translational studies that apply basic concepts in virus–host interactions to new therapeutic strategies (e.g., oncolytic virotherapy, gene therapy, etc.) are also welcome.

Dr. Don Gammon
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • RNA virus
  • DNA virus
  • innate immunity
  • adaptive immunity
  • immune evasion
  • viral pathogenesis
  • virus–host interactions

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Published Papers (5 papers)

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Research

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17 pages, 5127 KiB  
Article
Identifying the HIV-Resistance-Related Factors and Regulatory Network via Multi-Omics Analyses
by Xueyan Long, Gexin Liu, Xinyi Liu, Chunlin Zhang, Lei Shi and Zhenglin Zhu
Int. J. Mol. Sci. 2024, 25(21), 11757; https://doi.org/10.3390/ijms252111757 - 1 Nov 2024
Viewed by 663
Abstract
For research on HIV/AIDS, it is important to elucidate the complex viral–host interaction, host dependency factors (HDFs), and restriction factors. However, the regulatory network of HIV-resistance-related factors remains not well understood. Therefore, we integrated four publicly available HIV-related transcriptome datasets, along with three [...] Read more.
For research on HIV/AIDS, it is important to elucidate the complex viral–host interaction, host dependency factors (HDFs), and restriction factors. However, the regulatory network of HIV-resistance-related factors remains not well understood. Therefore, we integrated four publicly available HIV-related transcriptome datasets, along with three datasets on HIV-infection-related DNA methylation, miRNA, and ChIP-seq, to predict the factors influencing HIV resistance and infection. Our approach involved differential analysis, functional annotation, and protein–protein interaction network analysis. Through comprehensive analyses, we identified 25 potential HIV-resistance-related genes (including shared EGF) and 24 HIV-infection-related hub genes (including shared JUN). Additionally, we pinpointed five key differentially methylated genes, five crucial differentially expressed microRNAs, and five significant pathways associated with HIV resistance. We mapped the potential regulatory pathways involving these HIV-resistance-related factors. Among the predicted factors, RHOA, RAD51, GATA1, IRF4, and CXCL8 have been validated as HDFs or restriction factors. The identified factors, such as JUN, EGF, and PLEK, are potential HDFs or restriction factors. This study uncovers the gene signatures and regulatory networks associated with HIV-1 resistance, suggesting potential targets for the development of new therapies against HIV/AIDS. Full article
(This article belongs to the Special Issue Insights into Viral Pathogenesis: Host Antiviral Responses and Viral Countermeasures)
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22 pages, 7934 KiB  
Article
Conserved Functions of Orthohepadnavirus X Proteins to Inhibit Type-I Interferon Signaling
by Amonrat Choonnasard, Maya Shofa, Tamaki Okabayashi and Akatsuki Saito
Int. J. Mol. Sci. 2024, 25(7), 3753; https://doi.org/10.3390/ijms25073753 - 28 Mar 2024
Cited by 2 | Viewed by 1238
Abstract
Orthohepadnavirus causes chronic hepatitis in a broad range of mammals, including primates, cats, woodchucks, and bats. Hepatitis B virus (HBV) X protein inhibits type-I interferon (IFN) signaling, thereby promoting HBV escape from the human innate immune system and establishing persistent infection. However, whether [...] Read more.
Orthohepadnavirus causes chronic hepatitis in a broad range of mammals, including primates, cats, woodchucks, and bats. Hepatitis B virus (HBV) X protein inhibits type-I interferon (IFN) signaling, thereby promoting HBV escape from the human innate immune system and establishing persistent infection. However, whether X proteins of Orthohepadnavirus viruses in other species display a similar inhibitory activity remains unknown. Here, we investigated the anti-IFN activity of 17 Orthohepadnavirus X proteins derived from various hosts. We observed conserved activity of Orthohepadnavirus X proteins in inhibiting TIR-domain-containing adaptor protein inducing IFN-β (TRIF)-mediated IFN-β signaling pathway through TRIF degradation. X proteins from domestic cat hepadnavirus (DCH), a novel member of Orthohepadnavirus, inhibited mitochondrial antiviral signaling protein (MAVS)-mediated IFNβ signaling pathway comparable with HBV X. These results indicate that inhibition of IFN signaling is conserved in Orthohepadnavirus X proteins. Full article
(This article belongs to the Special Issue Insights into Viral Pathogenesis: Host Antiviral Responses and Viral Countermeasures)
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Review

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38 pages, 1853 KiB  
Review
Interactions of SARS-CoV-2 with Human Target Cells—A Metabolic View
by Wolfgang Eisenreich, Julian Leberfing, Thomas Rudel, Jürgen Heesemann and Werner Goebel
Int. J. Mol. Sci. 2024, 25(18), 9977; https://doi.org/10.3390/ijms25189977 - 16 Sep 2024
Viewed by 1348
Abstract
Viruses are obligate intracellular parasites, and they exploit the cellular pathways and resources of their respective host cells to survive and successfully multiply. The strategies of viruses concerning how to take advantage of the metabolic capabilities of host cells for their own replication [...] Read more.
Viruses are obligate intracellular parasites, and they exploit the cellular pathways and resources of their respective host cells to survive and successfully multiply. The strategies of viruses concerning how to take advantage of the metabolic capabilities of host cells for their own replication can vary considerably. The most common metabolic alterations triggered by viruses affect the central carbon metabolism of infected host cells, in particular glycolysis, the pentose phosphate pathway, and the tricarboxylic acid cycle. The upregulation of these processes is aimed to increase the supply of nucleotides, amino acids, and lipids since these metabolic products are crucial for efficient viral proliferation. In detail, however, this manipulation may affect multiple sites and regulatory mechanisms of host-cell metabolism, depending not only on the specific viruses but also on the type of infected host cells. In this review, we report metabolic situations and reprogramming in different human host cells, tissues, and organs that are favorable for acute and persistent SARS-CoV-2 infection. This knowledge may be fundamental for the development of host-directed therapies. Full article
(This article belongs to the Special Issue Insights into Viral Pathogenesis: Host Antiviral Responses and Viral Countermeasures)
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20 pages, 3831 KiB  
Review
Triggering Degradation of Host Cellular Proteins for Robust Propagation of Influenza Viruses
by Chuan Xia, Ting Wang and Bumsuk Hahm
Int. J. Mol. Sci. 2024, 25(9), 4677; https://doi.org/10.3390/ijms25094677 - 25 Apr 2024
Viewed by 1298
Abstract
Following infection, influenza viruses strive to establish a new host cellular environment optimized for efficient viral replication and propagation. Influenza viruses use or hijack numerous host factors and machinery not only to fulfill their own replication process but also to constantly evade the [...] Read more.
Following infection, influenza viruses strive to establish a new host cellular environment optimized for efficient viral replication and propagation. Influenza viruses use or hijack numerous host factors and machinery not only to fulfill their own replication process but also to constantly evade the host’s antiviral and immune response. For this purpose, influenza viruses appear to have formulated diverse strategies to manipulate the host proteins or signaling pathways. One of the most effective tactics is to specifically induce the degradation of the cellular proteins that are detrimental to the virus life cycle. Here, we summarize the cellular factors that are deemed to have been purposefully degraded by influenza virus infection. The focus is laid on the mechanisms for the protein ubiquitination and degradation in association with facilitated viral amplification. The fate of influenza viral infection of hosts is heavily reliant on the outcomes of the interplay between the virus and the host antiviral immunity. Understanding the processes of how influenza viruses instigate the protein destruction pathways could provide a foundation for the development of advanced therapeutics to target host proteins and conquer influenza. Full article
(This article belongs to the Special Issue Insights into Viral Pathogenesis: Host Antiviral Responses and Viral Countermeasures)
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19 pages, 804 KiB  
Review
Meeting the Challenge of Controlling Viral Immunopathology
by Engin Berber, Sachin Mulik and Barry T. Rouse
Int. J. Mol. Sci. 2024, 25(7), 3935; https://doi.org/10.3390/ijms25073935 - 1 Apr 2024
Viewed by 1567
Abstract
The mission of this review is to identify immune-damaging participants involved in antiviral immunoinflammatory lesions. We argue these could be targeted and their activity changed selectively by maneuvers that, at the same time, may not diminish the impact of components that help resolve [...] Read more.
The mission of this review is to identify immune-damaging participants involved in antiviral immunoinflammatory lesions. We argue these could be targeted and their activity changed selectively by maneuvers that, at the same time, may not diminish the impact of components that help resolve lesions. Ideally, we need to identify therapeutic approaches that can reverse ongoing lesions that lack unwanted side effects and are affordable to use. By understanding the delicate balance between immune responses that cause tissue damage and those that aid in resolution, novel strategies can be developed to target detrimental immune components while preserving the beneficial ones. Some strategies involve rebalancing the participation of immune components using various approaches, such as removing or blocking proinflammatory T cell products, expanding regulatory cells, restoring lost protective cell function, using monoclonal antibodies (moAb) to counteract inhibitory molecules, and exploiting metabolic differences between inflammatory and immuno-protective responses. These strategies can help reverse ongoing viral infections. We explain various approaches, from model studies and some clinical evidence, that achieve innate and adaptive immune rebalancing, offering insights into potential applications for controlling chronic viral-induced lesions. Full article
(This article belongs to the Special Issue Insights into Viral Pathogenesis: Host Antiviral Responses and Viral Countermeasures)
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