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Virus Infection and Infectious Diseases: Unraveling Mechanisms, Innovations, and Therapeutic Strategies

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 June 2024 | Viewed by 2424

Special Issue Editor

Dr. Jung-Hyun Lee

E-Mail Website
Guest Editor
Department of Life Science, University of Seoul, Seoul 02504, Republic of Korea
Interests: virus infection; extracellular vesicles; virus-host interactions; immune responses; immune sensors

Special Issue Information

Dear Colleagues,

Viruses constitute an abundant, highly diverse and economically significant group of pathogens affecting plants, animals and humans. Despite their minuscule size, viruses initiate extensive pathological changes or modifications in various host cells to ensure their survival.

The forthcoming Special Issue will publish a collection of the latest original research articles, short communications and reviews concerning recent progress in virus–host interaction research and therapeutic approaches for infectious diseases. The Special Issue aims to furnish a comprehensive platform for the exchange of knowledge and contributions, enriching the evolving landscape in this field.

Dr. Jung-Hyun Lee
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

  • mechanism of virus infection
  • host immune responses
  • innovations in diagnostics and surveillance
  • therapeutic strategies
  • epidemiology and global health
  • data science for infectious disease
  • zoonotic transmission
  • virus evolution

Published Papers (3 papers)

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Research

12 pages, 1341 KiB  
Article
The Diverse Nature of the Molecular Interactions That Govern the COV-2 Variants’ Cell Receptor Affinity Ranking and Its Experimental Variability
by Fredy Sussman and Daniel S. Villaverde
Int. J. Mol. Sci. 2024, 25(5), 2585; https://doi.org/10.3390/ijms25052585 - 23 Feb 2024
Viewed by 475
Abstract
A critical determinant of infectivity and virulence of the most infectious and or lethal variants of concern (VOCs): Wild Type, Delta and Omicron is related to the binding interactions between the receptor-binding domain of the spike and its host receptor, the initial step [...] Read more.
A critical determinant of infectivity and virulence of the most infectious and or lethal variants of concern (VOCs): Wild Type, Delta and Omicron is related to the binding interactions between the receptor-binding domain of the spike and its host receptor, the initial step in cell infection. It is of the utmost importance to understand how mutations of a viral strain, especially those that are in the viral spike, affect the resulting infectivity of the emerging VOC, knowledge that could help us understand the variant virulence and inform the therapies applied or the vaccines developed. For this sake, we have applied a battery of computational protocols of increasing complexity to the calculation of the spike binding affinity for three variants of concern to the ACE2 cell receptor. The results clearly illustrate that the attachment of the spikes of the Delta and Omicron variants to the receptor originates through different molecular interaction mechanisms. All our protocols unanimously predict that the Delta variant has the highest receptor-binding affinity, while the Omicron variant displays a substantial variability in the binding affinity of the spike that relates to the structural plasticity of the Omicron spike–receptor complex. We suggest that the latter result could explain (at least in part) the variability of the in vitro binding results for this VOC and has led us to suggest a reason for the lower virulence of the Omicron variant as compared to earlier strains. Several hypotheses have been developed around this subject. Full article
(This article belongs to the Special Issue Virus Infection and Infectious Diseases: Unraveling Mechanisms, Innovations, and Therapeutic Strategies)
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24 pages, 3582 KiB  
Article
The African Swine Fever Virus Virulence Determinant DP96R Suppresses Type I IFN Production Targeting IRF3
by Niranjan Dodantenna, Ji-Won Cha, Kiramage Chathuranga, W. A. Gayan Chathuranga, Asela Weerawardhana, Lakmal Ranathunga, Yongkwan Kim, Weonhwa Jheong and Jong-Soo Lee
Int. J. Mol. Sci. 2024, 25(4), 2099; https://doi.org/10.3390/ijms25042099 - 08 Feb 2024
Cited by 1 | Viewed by 880
Abstract
DP96R of African swine fever virus (ASFV), also known as uridine kinase (UK), encodes a virulence-associated protein. Previous studies have examined DP96R along with other genes in an effort to create live attenuated vaccines. While experiments in pigs have explored the [...] Read more.
DP96R of African swine fever virus (ASFV), also known as uridine kinase (UK), encodes a virulence-associated protein. Previous studies have examined DP96R along with other genes in an effort to create live attenuated vaccines. While experiments in pigs have explored the impact of DP96R on the pathogenicity of ASFV, the precise molecular mechanism underlying this phenomenon remains unknown. Here, we describe a novel molecular mechanism by which DP96R suppresses interferon regulator factor-3 (IRF3)-mediated antiviral immune responses. DP96R interacts with a crucial karyopherin (KPNA) binding site within IRF3, disrupting the KPNA-IRF3 interaction and consequently impeding the translocation of IRF3 to the nucleus. Under this mechanistic basis, the ectopic expression of DP96R enhances the replication of DNA and RNA viruses by inhibiting the production of IFNs, whereas DP96R knock-down resulted in higher IFNs and IFN-stimulated gene (ISG) transcription during ASFV infection. Collectively, these findings underscore the pivotal role of DP96R in inhibiting IFN responses and increase our understanding of the relationship between DP96R and the virulence of ASFV. Full article
(This article belongs to the Special Issue Virus Infection and Infectious Diseases: Unraveling Mechanisms, Innovations, and Therapeutic Strategies)
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13 pages, 5571 KiB  
Article
Chicken Interferon-Alpha and -Lambda Exhibit Antiviral Effects against Fowl Adenovirus Serotype 4 in Leghorn Male Hepatocellular Cells
by Jinyu Lai, Xingchen He, Rongjie Zhang, Limei Zhang, Libin Chen, Fengping He, Lei Li, Liangyu Yang, Tao Ren and Bin Xiang
Int. J. Mol. Sci. 2024, 25(3), 1681; https://doi.org/10.3390/ijms25031681 - 30 Jan 2024
Viewed by 736
Abstract
Hydropericardium hepatitis syndrome (HHS) is primarily caused by fowl adenovirus serotype 4 (FAdV-4), causing high mortality in chickens. Although vaccination strategies against FAdV-4 have been adopted, HHS still occurs sporadically. Furthermore, no effective drugs are available for controlling FAdV-4 infection. However, type I [...] Read more.
Hydropericardium hepatitis syndrome (HHS) is primarily caused by fowl adenovirus serotype 4 (FAdV-4), causing high mortality in chickens. Although vaccination strategies against FAdV-4 have been adopted, HHS still occurs sporadically. Furthermore, no effective drugs are available for controlling FAdV-4 infection. However, type I and III interferon (IFN) are crucial therapeutic agents against viral infection. The following experiments were conducted to investigate the inhibitory effect of chicken IFN against FadV-4. We expressed recombinant chicken type I IFN-α (ChIFN-α) and type III IFN-λ (ChIFN-λ) in Escherichia coli and systemically investigated their antiviral activity against FAdV-4 infection in Leghorn male hepatocellular (LMH) cells. ChIFN-α and ChIFN-λ dose dependently inhibited FAdV-4 replication in LMH cells. Compared with ChIFN-λ, ChIFN-α more significantly inhibited viral genome transcription but less significantly suppressed FAdV-4 release. ChIFN-α- and ChIFN-λ-induced IFN-stimulated gene (ISG) expression, such as PKR, ZAP, IRF7, MX1, Viperin, IFIT5, OASL, and IFI6, in LMH cells; however, ChIFN-α induced a stronger expression level than ChIFN-λ. Thus, our data revealed that ChIFN-α and ChIFN-λ might trigger different ISG expression levels, inhibiting FAdV-4 replication via different steps of the FAdV-4 lifecycle, which furthers the potential applications of IFN antiviral drugs in chickens. Full article
(This article belongs to the Special Issue Virus Infection and Infectious Diseases: Unraveling Mechanisms, Innovations, and Therapeutic Strategies)
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