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Viruses
Special Issues
Viral Infections and Immune Dysregulation 2024
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Viral Infections and Immune Dysregulation 2024

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

Deadline for manuscript submissions: 25 November 2024 | Viewed by 3248

Special Issue Editors

Dr. Ester Ballana Guix

E-Mail Website
Guest Editor
AIDS Research Institute-IrsiCaixa and Health Research Institute Germans Trias i Pujol (IGTP), Hospital Germans Trias i Pujol, 08916 Badalona, Spain
Interests: HIV; retroviruses; virus restriction; virus–host interactions; antiviral drug development; antiviral screening; innate immunity
Special Issues, Collections and Topics in MDPI journals
Dr. Ifeanyi Jude Ezeonwumelu

E-Mail Website
Guest Editor
Gladstone Institute of Virology, University of California San Francisco, 1650 Owens Street, San Francisco, CA 94158, USA
Interests: HIV-1; virus–host interactions; immune responses to viruses; antiviral screening

Special Issue Information

Dear Colleagues,

The ability of our immune system to effectively control viral infections relies heavily on the interplay between innate and adaptive immunity. However, despite these protective mechanisms, many viruses have developed immune evasion strategies to counter or hijack immune responses for their own benefit, compromising the efficacy of available vaccine and therapeutic regimens. Therefore, understanding the interactions between the immune system and viral pathogens is crucial for the development of effective treatments.

This Special Issue focuses on exploring the complex interactions between innate and adaptive immunity to viral infections, mechanisms of viral immune evasion and host countermeasures, sex-specific differences in immune response to viral infections, virus-induced autoimmunity and autoimmune disorders. We also invite contributions that discuss recent advances in overcoming virus-induced immune dysregulation, such as the development of immunomodulators, vaccines, and antiviral therapies.

In this Special Issue, original research articles, reviews, perspectives, communications, and case reports are welcome.

Dr. Ester Ballana Guix
Dr. Ifeanyi Jude Ezeonwumelu
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

  • immune responses
  • immune dysregulation
  • autoimmunity
  • viral infections
  • immunomodulation

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Published Papers (2 papers)

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14 pages, 4336 KiB  
Article
Histone H1.2 Inhibited EMCV Replication through Enhancing MDA5-Mediated IFN-β Signaling Pathway
by Yangran Song, Huixia Li, Ruiya Lian, Xueer Dou, Shasha Li, Jingying Xie, Xiangrong Li, Ruofei Feng and Zhiqiang Li
Viruses 2024, 16(2), 174; https://doi.org/10.3390/v16020174 - 24 Jan 2024
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Abstract
Histone H1.2 is a member of the linker histone family, which plays extensive and crucial roles not only in the regulation of chromatin dynamics, cell cycle, and cell apoptosis, but also in viral diseases and innate immunity response. Recently, it was discovered that [...] Read more.
Histone H1.2 is a member of the linker histone family, which plays extensive and crucial roles not only in the regulation of chromatin dynamics, cell cycle, and cell apoptosis, but also in viral diseases and innate immunity response. Recently, it was discovered that H1.2 regulates interferon-β and inhibits influenza virus replication, whereas its role in other viral infections is poorly reported. Here, we first found the up-regulation of H1.2 during Encephalomyocarditis virus (EMCV) infection, implying that H1.2 was involved in EMCV infection. Overexpression of H1.2 inhibited EMCV proliferation, whereas knockdown of H1.2 showed a significant promotion of virus infection in HEK293T cells. Moreover, we demonstrated that overexpression of H1.2 remarkably enhanced the production of EMCV-induced type I interferon, which may be the crucial factor for H1.2 proliferation–inhibitory effects. We further found that H1.2 up-regulated the expression of the proteins of the MDA5 signaling pathway and interacted with MDA5 and IRF3 in EMCV infection. Further, we demonstrated that H1.2 facilitated EMCV-induced phosphorylation and nuclear translocation of IRF3. Briefly, our research uncovers the mechanism of H1.2 negatively regulating EMCV replication and provides new insight into antiviral targets for EMCV. Full article
(This article belongs to the Special Issue Viral Infections and Immune Dysregulation 2024)
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Review

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25 pages, 2482 KiB  
Review
The Immune Escape Strategy of Rabies Virus and Its Pathogenicity Mechanisms
by Abraha Bahlbi Kiflu
Viruses 2024, 16(11), 1774; https://doi.org/10.3390/v16111774 - 14 Nov 2024
Viewed by 1086
Abstract
In contrast to most other rhabdoviruses, which spread by insect vectors, the rabies virus (RABV) is a very unusual member of the Rhabdoviridae family, since it has evolved to be fully adapted to warm-blooded hosts and spread directly between them. There are differences [...] Read more.
In contrast to most other rhabdoviruses, which spread by insect vectors, the rabies virus (RABV) is a very unusual member of the Rhabdoviridae family, since it has evolved to be fully adapted to warm-blooded hosts and spread directly between them. There are differences in the immune responses to laboratory-attenuated RABV and wild-type rabies virus infections. Various investigations showed that whilst laboratory-attenuated RABV elicits an innate immune response, wild-type RABV evades detection. Pathogenic RABV infection bypasses immune response by antagonizing interferon induction, which prevents downstream signal activation and impairs antiviral proteins and inflammatory cytokines production that could eliminate the virus. On the contrary, non-pathogenic RABV infection leads to immune activation and suppresses the disease. Apart from that, through recruiting leukocytes into the central nervous system (CNS) and enhancing the blood–brain barrier (BBB) permeability, which are vital factors for viral clearance and protection, cytokines/chemokines released during RABV infection play a critical role in suppressing the disease. Furthermore, early apoptosis of neural cells limit replication and spread of avirulent RABV infection, but street RABV strains infection cause delayed apoptosis that help them spread further to healthy cells and circumvent early immune exposure. Similarly, a cellular regulation mechanism called autophagy eliminates unused or damaged cytoplasmic materials and destroy microbes by delivering them to the lysosomes as part of a nonspecific immune defense mechanism. Infection with laboratory fixed RABV strains lead to complete autophagy and the viruses are eliminated. But incomplete autophagy during pathogenic RABV infection failed to destroy the viruses and might aid the virus in dodging detection by antigen-presenting cells, which could otherwise elicit adaptive immune activation. Pathogenic RABV P and M proteins, as well as high concentration of nitric oxide, which is produced during rabies virus infection, inhibits activities of mitochondrial proteins, which triggers the generation of reactive oxygen species, resulting in oxidative stress, contributing to mitochondrial malfunction and, finally, neuron process degeneration. Full article
(This article belongs to the Special Issue Viral Infections and Immune Dysregulation 2024)
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