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Viruses
Special Issues
Viral Mechanisms of Immune Evasion
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Viral Mechanisms of Immune Evasion

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

Deadline for manuscript submissions: 31 August 2025 | Viewed by 1975

Special Issue Editor

Dr. Xiaoyong Bao

E-Mail Website
Guest Editor
Department of Pediatrics, University of Texas Medical Branch, Galveston, TX, USA
Interests: molecular mechanisms underlying the pathogenesis and host immune responses associated with RSV and hMPV infections; respiratory tract infections; antiviral pathways; viral evasion mechanisms; sncRNAs
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues, 

We will launch a Special Issue in Viruses, entitled "Viral Mechanisms of Immune Evasion". The intricate interplay between viruses and host immune systems is a key determinant of viral pathogenesis and persistence. This Special Issue highlights the latest advancements in understanding how viruses subvert host defenses, providing insights into viral evolution, immune system manipulation, and potential therapeutic interventions. We welcome original research, reviews, and perspectives on mechanisms contributing to immune evasion at molecular, cellular, and systemic levels and innovative approaches to counteract these strategies. Your expertise and contributions will be instrumental in advancing our knowledge and shaping future research in this critical field.

Dr. Xiaoyong Bao
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. 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 evasion
  • virulent factor
  • antiviral signaling
  • pathogenesis
  • antiviral strategy

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Published Papers (2 papers)

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Research

15 pages, 2726 KiB  
Article
The Impact of EPAC2-Associated Junction Plakoglobin on Respiratory Syncytial Virus Infection
by Chaitra A. Takle, Eun-Jin Choi, Eun Seok Choi, Devang Deepak, Kashish Khatkar, Jong Min Choi, Ke Zhang, Sung Yun Jung, Tian Wang, Wenzhe Wu and Xiaoyong Bao
Viruses 2025, 17(5), 627; https://doi.org/10.3390/v17050627 - 26 Apr 2025
Viewed by 306
Abstract
Respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infections in infants, young children, and immunocompromised individuals. Currently, FDA-approved monoclonal antibody therapies are limited to infants and young children with severe RSV disease. As a result, there is an urgent [...] Read more.
Respiratory syncytial virus (RSV) is a leading cause of lower respiratory tract infections in infants, young children, and immunocompromised individuals. Currently, FDA-approved monoclonal antibody therapies are limited to infants and young children with severe RSV disease. As a result, there is an urgent need for comprehensive studies of RSV pathogenesis to support the development of new therapeutic strategies. Exchange proteins directly activated by cAMP (EPAC) have recently emerged as key regulators in various viral infections. Our previous work identified EPAC isoform 2 (EPAC2) as a critical factor in RSV replication and host innate immune responses. However, the molecular mechanisms underlying EPAC2’s role in RSV infection remain unclear. In this study, we investigated EPAC2-mediated RSV infection by identifying EPAC2-interacting proteins. Proteomics and immunoprecipitation analyses revealed that junction plakoglobin (JUP) interacts with EPAC2 in both mock- and RSV-infected cells, with this interaction notably enhanced during RSV infection. To determine JUP’s role in RSV infection, we compared viral replication in JUP-deficient and control cells. JUP downregulation significantly reduced the production of infectious RSV particles, likely by impairing viral budding and viral gene transcription. Moreover, our findings indicate that JUP is essential for an effective cellular immune response to RSV infection. Together, these results suggest that EPAC2 and JUP may cooperatively regulate RSV replication and dissemination. Full article
(This article belongs to the Special Issue Viral Mechanisms of Immune Evasion)
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13 pages, 1219 KiB  
Article
eEF-2K Deficiency Boosts the Virus-Specific Effector CD8+ T Cell Responses During Viral Infection
by Liqing Wang, Benny Shone Song, Rayansh Poojary, Xiaofang Xiong, Xingcong Ren, Jin-Ming Yang and Jianxun Song
Viruses 2025, 17(1), 26; https://doi.org/10.3390/v17010026 - 28 Dec 2024
Viewed by 921
Abstract
In this study, we revealed a critical role of eukaryotic elongation factor-2 kinase (eEF-2K), a negative regulator of protein synthesis, in regulating T cells during vaccinia virus (VACV) infection. We found that eEF-2K-deficient (eEF-2K⁻/⁻) mice exhibited a significantly higher proportion of VACV-specific effector [...] Read more.
In this study, we revealed a critical role of eukaryotic elongation factor-2 kinase (eEF-2K), a negative regulator of protein synthesis, in regulating T cells during vaccinia virus (VACV) infection. We found that eEF-2K-deficient (eEF-2K⁻/⁻) mice exhibited a significantly higher proportion of VACV-specific effector CD8+ T cells without compromising the development of VACV-specific memory CD8+ T cells. RNA sequencing demonstrated that eEF-2K⁻/⁻ VACV-specific effector CD8+ T cells had enhanced functionality, which improves their capacity to combat viral infection during the effector phase. Moreover, we identified tumor necrosis factor receptor-associated factor 3 (TRAF3) as a critical mediator of the stronger antiviral response observed in eEF-2K⁻/⁻ effector CD8+ T cells. These findings suggest that targeting eEF-2K may provide a novel strategy to augmenting effector CD8+ T cell responses against viral infections. Full article
(This article belongs to the Special Issue Viral Mechanisms of Immune Evasion)
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