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Viruses
Special Issues
Unraveling the Pathogenesis of Persistent Virus Infection
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Unraveling the Pathogenesis of Persistent Virus Infection

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

Deadline for manuscript submissions: 30 November 2024 | Viewed by 7594

Special Issue Editors

Prof. Dr. Yasuko Tsunetsugu-Yokota

E-Mail Website1 Website2
Guest Editor
1. Department of Medical Technology, School of Health Sciences, Tokyo University of Technology, Tokyo 144-8535, Japan
2. Research Institute, The World New Prosperity (WNP), Tokyo 169-0075, Japan
Interests: virus infection; immune responses; virus-host interaction; HIV latency; influenza; SARS; coronaviruses
Dr. Mie Kobayashi-Ishihara

E-Mail Website
Guest Editor
Department of Molecular Biology, Keio University School of Medicine, Tokyo 160-8582, Japan
Interests: retroviruses; latency; reactivation; virus-host interactions; HIV; innate immunity

Special Issue Information

Dear Colleague,

Viruses can cause chronic diseases by introducing and maintaining their genetic materials in host cells. Examples include herpesviruses and retroviruses, which employ several tactics to escape from the immune system, allowing them to establish latent/persistent infections. However, the mechanisms underlying the maintenance of these viruses and disease onsets remain largely unclear.

This Special Issue entitled “Unraveling the Pathogenesis of Persistent Virus Infection" aims to present recent research on any aspect of persistent virus infections. Some of its focal points include, but are not limited to, the following:

  1. Understanding the pathophysiology of persistent virus infections;
  2. Advancements in methodologies for studying persistent virus infections in tissues/organs;
  3. Development of novel therapeutics against persistent virus infections;
  4. Perspectives on the pathophysiology of virus-induced chronic diseases.

Reviews, original research, and communications are welcome for submission.

Prof. Dr. Yasuko Tsunetsugu-Yokota
Dr. Mie Kobayashi-Ishihara
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

  • pathophysiology
  • persistent virus infections
  • chronic diseases
  • latency
  • reactivation

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Published Papers (6 papers)

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Research

Jump to: Review, Other

21 pages, 3291 KiB  
Article
NSC95397 Is a Novel HIV-1 Latency-Reversing Agent
by Randilea Nichols Doyle, Vivian Yang, Yetunde I. Kayode, Robert Damoiseaux, Harry E. Taylor and Oliver I. Fregoso
Viruses 2024, 16(11), 1783; https://doi.org/10.3390/v16111783 - 16 Nov 2024
Viewed by 389
Abstract
The latent viral reservoir represents one of the major barriers to curing HIV-1. Focus on the “kick and kill” (also called “shock and kill”) approach, in which virus expression is reactivated, and then cells producing virus are selectively depleted, has led to the [...] Read more.
The latent viral reservoir represents one of the major barriers to curing HIV-1. Focus on the “kick and kill” (also called “shock and kill”) approach, in which virus expression is reactivated, and then cells producing virus are selectively depleted, has led to the discovery of many latency-reversing agents (LRAs) that have furthered our understanding of the mechanisms driving HIV-1 latency and latency reversal. Thus far, individual compounds have yet to be robust enough to work as a therapy, highlighting the importance of identifying new compounds that target novel pathways and synergize with known LRAs. In this study, we identified a promising LRA, NSC95397, from a screen of ~4250 compounds. We validated that NSC95397 reactivates latent viral transcription and protein expression from cells with unique integration events and across different latency models. Co-treating cells with NSC95397 and known LRAs demonstrated that NSC95397 synergizes with different drugs under both standard normoxic and physiological hypoxic conditions. NSC95397 does not globally increase open chromatin, and bulk RNA sequencing revealed that NSC95397 does not greatly increase cellular transcription. Instead, NSC95397 downregulates pathways key to metabolism, cell growth, and DNA repair—highlighting the potential of these pathways in regulating HIV-1 latency. Overall, we identified NSC95397 as a novel LRA that does not largely alter global transcription, shows potential for synergy with known LRAs, and may act through novel pathways not previously recognized for their ability to modulate HIV-1 latency. Full article
(This article belongs to the Special Issue Unraveling the Pathogenesis of Persistent Virus Infection)
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19 pages, 6714 KiB  
Article
Conserved Antagonization of Type I Interferon Signaling by Arterivirus GP5 Proteins
by Rissar Siringo Ringo, Amonrat Choonnasard, Tamaki Okabayashi and Akatsuki Saito
Viruses 2024, 16(8), 1240; https://doi.org/10.3390/v16081240 - 1 Aug 2024
Viewed by 874
Abstract
Arteriviruses can establish persistent infections in animals such as equids, pigs, nonhuman primates, rodents, and possums. Some Arteriviruses can even cause overt and severe diseases such as Equine Arteritis in horses and Porcine Reproductive and Respiratory Syndrome in pigs, leading to huge economic [...] Read more.
Arteriviruses can establish persistent infections in animals such as equids, pigs, nonhuman primates, rodents, and possums. Some Arteriviruses can even cause overt and severe diseases such as Equine Arteritis in horses and Porcine Reproductive and Respiratory Syndrome in pigs, leading to huge economic losses. Arteriviruses have evolved viral proteins to antagonize the host cell’s innate immune responses by inhibiting type I interferon (IFN) signaling, assisting viral evasion and persistent infection. So far, the role of the Arterivirus glycoprotein 5 (GP5) protein in IFN signaling inhibition remains unclear. Here, we investigated the inhibitory activity of 47 Arterivirus GP5 proteins derived from various hosts. We demonstrated that all GP5 proteins showed conserved activity for antagonizing TIR-domain-containing adapter proteins inducing interferon-β (TRIF)-mediated IFN-β signaling through TRIF degradation. In addition, Arterivirus GP5 proteins showed a conserved inhibitory activity against IFN-β signaling, induced by either pig or human TRIF. Furthermore, certain Arterivirus GP5 proteins could inhibit the induction of IFN-stimulated genes. These findings highlight the role of Arterivirus GP5 proteins in supporting persistent infection. Full article
(This article belongs to the Special Issue Unraveling the Pathogenesis of Persistent Virus Infection)
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18 pages, 3831 KiB  
Article
Chronic and Latent Viral Infections and Leukocyte Telomere Length across the Lifespan of Female and Male Individuals Living with or without HIV
by Nancy Yi Yang, Anthony Y. Y. Hsieh, Zhuo Chen, Amber R. Campbell, Izabella Gadawska, Fatima Kakkar, Laura Sauve, Ari Bitnun, Jason Brophy, Melanie C. M. Murray, Neora Pick, Mel Krajden, Hélène C. F. Côté and CIHR Team on Cellular Aging and HIV Comorbidities in Women and Children (CARMA)
Viruses 2024, 16(5), 755; https://doi.org/10.3390/v16050755 - 10 May 2024
Viewed by 1400
Abstract
Background: Chronic/latent viral infections may accelerate immunological aging, particularly among people living with HIV (PLWH). We characterized chronic/latent virus infections across their lifespan and investigated their associations with leukocyte telomere length (LTL). Methods: Participants enrolled in the CARMA cohort study were randomly selected [...] Read more.
Background: Chronic/latent viral infections may accelerate immunological aging, particularly among people living with HIV (PLWH). We characterized chronic/latent virus infections across their lifespan and investigated their associations with leukocyte telomere length (LTL). Methods: Participants enrolled in the CARMA cohort study were randomly selected to include n = 15 for each decade of age between 0 and >60 y, for each sex, and each HIV status. Cytomegalovirus (CMV), Epstein–Barr virus (EBV), human herpesvirus 8 (HHV-8), herpes simplex virus 1 (HSV-1), and HSV-2 infection were determined serologically; HIV, hepatitis C (HCV), and hepatitis B (HBV) were self-reported. LTLs were measured using monochrome multiplex qPCR. Associations between the number of viruses, LTL, and sociodemographic factors were assessed using ordinal logistic and linear regression modeling. Results: The study included 187 PLWH (105 female/82 male) and 190 HIV-negative participants (105 female/84 male), ranging in age from 0.7 to 76.1 years. Living with HIV, being older, and being female were associated with harbouring a greater number of chronic/latent non-HIV viruses. Having more infections was in turn bivariately associated with a shorter LTL. In multivariable analyses, older age, living with HIV, and the female sex remained independently associated with having more infections, while having 3–4 viruses (vs. 0–2) was associated with a shorter LTL. Conclusions: Our results suggest that persistent viral infections are more prevalent in PLWH and females, and that these may contribute to immunological aging. Whether this is associated with comorbidities later in life remains an important question. Full article
(This article belongs to the Special Issue Unraveling the Pathogenesis of Persistent Virus Infection)
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Review

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12 pages, 1890 KiB  
Review
Roles Played by DOCK11, a Guanine Nucleotide Exchange Factor, in HBV Entry and Persistence in Hepatocytes
by Ying-Yi Li, Kazuhisa Murai, Junyan Lyu and Masao Honda
Viruses 2024, 16(5), 745; https://doi.org/10.3390/v16050745 - 8 May 2024
Cited by 1 | Viewed by 1535
Abstract
HBV infection is challenging to cure due to the persistence of viral covalently closed circular viral DNA (cccDNA). The dedicator of cytokinesis 11 (DOCK11) is recognized as a guanine nucleotide exchange factor (GEF) for CDC42 that has been reported to be required for [...] Read more.
HBV infection is challenging to cure due to the persistence of viral covalently closed circular viral DNA (cccDNA). The dedicator of cytokinesis 11 (DOCK11) is recognized as a guanine nucleotide exchange factor (GEF) for CDC42 that has been reported to be required for HBV persistence. DOCK11 is expressed in both the cytoplasm and nucleus of human hepatocytes and is functionally associated with retrograde trafficking proteins Arf-GAP with GTPase domain, ankyrin repeat, and pleckstrin homology domain-containing protein 2 (AGAP2), and ADP-ribosylation factor 1 (ARF1), together with the HBV capsid, in the trans-Golgi network (TGN). This opens an alternative retrograde trafficking route for HBV from early endosomes (EEs) to the TGN and then to the endoplasmic reticulum (ER), thereby avoiding lysosomal degradation. DOCK11 also facilitates the association of cccDNA with H3K4me3 and RNA Pol II for activating cccDNA transcription. In addition, DOCK11 plays a crucial role in the host DNA repair system, being essential for cccDNA synthesis. This function can be inhibited by 10M-D42AN, a novel DOCK11-binding peptide, leading to the suppression of HBV replication both in vitro and in vivo. Treatment with a combination of 10M-D42AN and entecavir may represent a promising therapeutic strategy for patients with chronic hepatitis B (CHB). Consequently, DOCK11 may be seen as a potential candidate molecule in the development of molecularly targeted drugs against CHB. Full article
(This article belongs to the Special Issue Unraveling the Pathogenesis of Persistent Virus Infection)
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15 pages, 1269 KiB  
Review
Post-Transcriptional HIV-1 Latency: A Promising Target for Therapy?
by Mie Kobayashi-Ishihara and Yasuko Tsunetsugu-Yokota
Viruses 2024, 16(5), 666; https://doi.org/10.3390/v16050666 - 24 Apr 2024
Cited by 1 | Viewed by 1322
Abstract
Human Immunodeficiency Virus type 1 (HIV-1) latency represents a significant hurdle in finding a cure for HIV-1 infections, despite tireless research efforts. This challenge is partly attributed to the intricate nature of HIV-1 latency, wherein various host and viral factors participate in multiple [...] Read more.
Human Immunodeficiency Virus type 1 (HIV-1) latency represents a significant hurdle in finding a cure for HIV-1 infections, despite tireless research efforts. This challenge is partly attributed to the intricate nature of HIV-1 latency, wherein various host and viral factors participate in multiple physiological processes. While substantial progress has been made in discovering therapeutic targets for HIV-1 transcription, targets for the post-transcriptional regulation of HIV-1 infections have received less attention. However, cumulative evidence now suggests the pivotal contribution of post-transcriptional regulation to the viral latency in both in vitro models and infected individuals. In this review, we explore recent insights on post-transcriptional latency in HIV-1 and discuss the potential of its therapeutic targets, illustrating some host factors that restrict HIV-1 at the post-transcriptional level. Full article
(This article belongs to the Special Issue Unraveling the Pathogenesis of Persistent Virus Infection)
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Other

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9 pages, 3172 KiB  
Brief Report
Anti-PD-L1 Immunotherapy of Chronic Virus Infection Improves Virus Control without Augmenting Tissue Damage by Fibrosis
by Valentina Casella, Paula Cebollada Rica, Jordi Argilaguet, Enric Vidal, María González-Cao, Roberto Güerri-Fernandez, Gennady Bocharov and Andreas Meyerhans
Viruses 2024, 16(5), 799; https://doi.org/10.3390/v16050799 - 17 May 2024
Viewed by 1354
Abstract
Immunotherapy with checkpoint inhibitors, albeit commonly used against tumors, is still at its infancy against chronic virus infections. It relies on the reinvigoration of exhausted T lymphocytes to eliminate virus-infected cells. Since T cell exhaustion is a physiological process to reduce immunopathology, the [...] Read more.
Immunotherapy with checkpoint inhibitors, albeit commonly used against tumors, is still at its infancy against chronic virus infections. It relies on the reinvigoration of exhausted T lymphocytes to eliminate virus-infected cells. Since T cell exhaustion is a physiological process to reduce immunopathology, the reinvigoration of these cells might be associated with an augmentation of pathological changes. To test this possibility, we here analyzed in the model system of chronic lymphocytic choriomeningitis virus (LCMV)-infected mice whether treatment with the checkpoint inhibitor anti-PD-L1 antibody would increase CD8 T cell-dependent fibrosis. We show that pre-existing spleen fibrosis did not worsen under conditions that increase CD8 T cell functionality and reduce virus loads suggesting that the CD8 T cell functionality increase remained below its pathogenicity threshold. These promising findings should further encourage immunotherapeutic trials against chronic virus infections. Full article
(This article belongs to the Special Issue Unraveling the Pathogenesis of Persistent Virus Infection)
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