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Viruses
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Viral Infections and Immune Dysregulation 2024–2025
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Viral Infections and Immune Dysregulation 2024–2025

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

Deadline for manuscript submissions: 31 December 2025 | Viewed by 13885

Special Issue Editors

Dr. Ester Ballana Guix

E-Mail Website
Guest Editor
1. IrsiCaixa Immunopathology Research Institute, 08916 Badalona, Spain
2. Health Research Institute Germans Trias i Pujol (IGTP), 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 (6 papers)

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Research

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22 pages, 1605 KiB  
Article
Latent Human Cytomegalovirus Infection Activates the STING Pathway but p-IRF3 Translocation Is Limited
by Wang Ka Lee, Zuodong Ye and Allen Ka Loon Cheung
Viruses 2025, 17(8), 1109; https://doi.org/10.3390/v17081109 - 12 Aug 2025
Abstract
Human cytomegalovirus (HCMV) is a ubiquitous betaherpesvirus that establishes lifelong latent infection in CD34+ haematopoietic stem and progenitor cells. A unique subset of viral genes is expressed during latency, which functions to modulate cellular mechanisms without supporting viral replication. One potential function [...] Read more.
Human cytomegalovirus (HCMV) is a ubiquitous betaherpesvirus that establishes lifelong latent infection in CD34+ haematopoietic stem and progenitor cells. A unique subset of viral genes is expressed during latency, which functions to modulate cellular mechanisms without supporting viral replication. One potential function of these genes is to regulate the differentiation state of latently infected CD34+ cells, thereby preventing their progression into antigen-presenting cells, e.g., dendritic cells. In this study, we first compared CD34+ cells that supported productive and latent infections using the RV-TB40-BACKL7-SE-EGFP virus. Over a seven-day time course, the proportion of latently infected CD34+ cell subsets within the myeloid progenitor population remained similar to that in the mock-infected control. However, starting from day 3 post-infection, there was an increase in the proportion of the early progenitor subsets, including haematopoietic stem cells (HSCs) and multipotent progenitors (MPPs). In contrast, productively infected cells, which constituted less than 1% of the population, only accounted for a small portion of the myeloid progenitors. Importantly, our data revealed that the innate immune STING/p-TBK1/p-IRF3 pathway was activated in latently infected CD34+ cells, yet type I interferon (IFN) expression was decreased. This decrease was attributed to impaired p-IRF3 nuclear translocation, limiting the induction of an autocrine type I IFN response. However, treatment with IFN-β could induce myelopoiesis in latently infected cells. In summary, HCMV modulates a key component of the STING pathway to inhibit antiviral immune responses by decreasing the type I IFN-mediated cell differentiation of CD34+ progenitor cells. This study uncovered a new mechanism of latent HCMV-mediated regulation of the host cell differentiation response. Full article
(This article belongs to the Special Issue Viral Infections and Immune Dysregulation 2024–2025)
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15 pages, 1201 KiB  
Article
Immune Responses and Replication of Rescued Torque Teno Virus (TTSuV1) in Mice
by Md-Tariqul Islam, Brett Webb and Sheela Ramamoorthy
Viruses 2025, 17(8), 1105; https://doi.org/10.3390/v17081105 - 12 Aug 2025
Abstract
Although Torque Teno Viruses (TTVs) were initially considered to be ubiquitous members of the mammalian virome, the finding that swine TTVs (TTSuV) can act as primary pathogens elevates the possible status of swine TTVs (TTSuVs) to an emerging swine pathogen. Since their discovery, [...] Read more.
Although Torque Teno Viruses (TTVs) were initially considered to be ubiquitous members of the mammalian virome, the finding that swine TTVs (TTSuV) can act as primary pathogens elevates the possible status of swine TTVs (TTSuVs) to an emerging swine pathogen. Since their discovery, the molecular mechanisms of TTV–host interactions remain largely unknown as robust in vitro culture systems and in vivo animal models have not been available. This study was undertaken to address some of these long-standing gaps. Recombinant TTSuV1 rescued from an infectious clone was used to infect C57BL/J6 mice. Infected mice seroconverted within 15 days post-infection and mounted virus neutralizing antibody responses. Viral DNA was detected in blood and lung tissue for the duration of the study. TTSuV1 isolated from the lung tissue of infected mice productively and serially infected PK-15 cells in vitro, indicating that the treatment produced viable, replicative viral particles in the host. TTSuV1 antigen was also detected by flow cytometry in lymphocytes, including the T and B lymphocyte subsets. Infected mice exhibited mild splenic hyperplasia and lymphopenia. The ability to respond to mitogenic stimuli was highly diminished in infected mice and a striking lack of virus-specific recall responses was observed for the 30-day duration of the study. Therefore, this study is the first to provide experimental evidence that recombinant TTSuV1 rescued from an infectious clone is infective and induces immune responses in laboratory mice. This model provides a critical tool for advancing research on TTV immunopathogenesis. Full article
(This article belongs to the Special Issue Viral Infections and Immune Dysregulation 2024–2025)
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18 pages, 2198 KiB  
Article
COVID-19 and HIV: Clinical Outcomes and Inflammatory Markers in a Cohort from a Reference Hospital in Rio de Janeiro, Brazil
by Nathalia Beatriz Ramos de Sá, Karine Venegas Macieira, Mariana Rosa Inacio Coelho, Milena Neira Goulart, Marcelo Ribeiro-Alves, Leonardo Azevedo da Silva Rosadas, Kim Mattos Geraldo, Maria Pia Diniz Ribeiro, Sandra Wagner Cardoso, Beatriz Grinsztejn, Valdiléa G. Veloso, Andressa da Silva Cazote, Dalziza Victalina de Almeida, Carmem Beatriz Wagner Giacoia-Gripp, Fernanda Heloise Côrtes and Mariza Gonçalves Morgado
Viruses 2025, 17(1), 91; https://doi.org/10.3390/v17010091 - 13 Jan 2025
Viewed by 1234
Abstract
Background: Severe COVID-19 presents a variety of clinical manifestations associated with inflammatory profiles. People living with HIV (PLWH) could face a higher risk of hospitalization and mortality from COVID-19, depending on their immunosuppression levels. This study describes inflammatory markers in COVID-19 clinical outcomes [...] Read more.
Background: Severe COVID-19 presents a variety of clinical manifestations associated with inflammatory profiles. People living with HIV (PLWH) could face a higher risk of hospitalization and mortality from COVID-19, depending on their immunosuppression levels. This study describes inflammatory markers in COVID-19 clinical outcomes with and without HIV infection. Methods: We analyzed 112 inpatients of the Hospital Center for COVID-19 (INI/FIOCRUZ), including 22 cases of COVID-19 in PLWH (COVID/PLWH group). Plasma samples were tested for a panel of 15 cytokines by Luminex. Sociodemographic, clinical, and laboratory data were collected from patients’ clinical records. Results: COVID-19 individuals were stratified according to the WHO clinical severity profiles at hospitalization. Significant differences in clinical scores, symptoms (coughs), and the occurrence of HIV infection were found among the groups. Clinical blood parameters and plasma cytokines were analyzed among COVID-19 groups with distinct severity profiles. Critical COVID-19 cases showed higher levels of inflammatory markers (Bilirubin, D-dimer, PCR, and urea, as well as IL-8, IL-10, TNF-α, INF-α, IL-1β, IL-17A, IL-23, IL-6) than moderate and severe groups. The COVID/PLWH group had lower CD4 counts (64 cells/mm3) and cytokine levels than other COVID-19 patients. Conclusions: Overall, critically ill COVID-19 patients exhibited heightened inflammatory responses, while COVID/PLWH demonstrated unique immunological characteristics without increased mortality risk. Full article
(This article belongs to the Special Issue Viral Infections and Immune Dysregulation 2024–2025)
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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
Cited by 1 | Viewed by 1985
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 2024–2025)
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Review

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22 pages, 1569 KiB  
Review
HIV, Inflammation, and Immunometabolism: A Model of the Inflammatory Theory of Disease
by Eman Teer, Nyasha C. Mukonowenzou and M. Faadiel Essop
Viruses 2025, 17(6), 839; https://doi.org/10.3390/v17060839 - 11 Jun 2025
Cited by 1 | Viewed by 1842
Abstract
Inflammation is a crucial component of the immune response essential for host defense and tissue repair. However, when the immune response becomes dysregulated, it can contribute to the pathogenesis of chronic diseases. While acute inflammation is a short-lived, protective response, chronic inflammation is [...] Read more.
Inflammation is a crucial component of the immune response essential for host defense and tissue repair. However, when the immune response becomes dysregulated, it can contribute to the pathogenesis of chronic diseases. While acute inflammation is a short-lived, protective response, chronic inflammation is sustained over time and can lead to immune dysfunction, tissue damage, and disease progression. The chronic inflammation theory of disease suggests that persistent immune activation/inflammation underlies both infectious and non-infectious conditions and serves as a unifying mechanism across distinct pathological states. In this review article, we argue that human immunodeficiency virus (HIV) infection represents a prime model for studying chronic inflammation, and that despite effective viral suppression with antiretroviral therapy (ART), people living with HIV (PLWH) exhibit persistent immune activation, systemic inflammation, and an increased risk of cardiovascular, metabolic, and neurodegenerative diseases. Here, the interplay between microbial translocation, immune dysregulation, and metabolic reprogramming fuels a state of chronic inflammation that accelerates disease progression beyond HIV itself. Key factors such as T-cell exhaustion, persistent monocyte/macrophage activation, and immunometabolic dysfunction contribute to such a sustained inflammatory state. This review explores the molecular and cellular mechanisms driving chronic inflammation in HIV infection with a focus on immunometabolism and its implications for broader inflammatory diseases. By understanding such pathways, we can identify novel therapeutic targets to mitigate inflammation-driven disease progression not only in HIV but across a spectrum of chronic inflammatory conditions. Full article
(This article belongs to the Special Issue Viral Infections and Immune Dysregulation 2024–2025)
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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
Cited by 4 | Viewed by 7399
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 2024–2025)
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