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Viruses
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15-Year Anniversary of Viruses
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15-Year Anniversary of Viruses

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

Deadline for manuscript submissions: 1 October 2025 | Viewed by 9392

Special Issue Editors

Dr. Eric O. Freed

E-Mail Website
Guest Editor
HIV Dynamics and Replication Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201, USA
Interests: HIV dynamics and replication
Special Issues, Collections and Topics in MDPI journals
Dr. Abdul A. Waheed

E-Mail Website
Guest Editor
HIV Dynamics and Replication Program, Center for Cancer Research, National Cancer Institute, Frederick, MD 21702-1201, USA
Interests: virology; retroviruses; virus assembly; cell biology; host factors; small-molecule inhibitors
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The journal Viruses has come a long way since its launch by MDPI in 2009. At that time, open-access publishing was a relatively new concept. Over the years, however, open access has become a cornerstone of scientific publishing, with global funding agencies increasingly requiring the research they support to be published as open access [1]. Since its inception, Viruses has experienced remarkable growth. In 2009, the journal published 70 articles; by 2017, this number rose to 391, and in 2024, the journal published 1887 papers. The growth of the journal reflects the dedication of our editorial team, the expertise of our Associate Editors and Editorial Board members, and the invaluable contributions of authors and reviewers worldwide.

Beyond publishing high-quality research, Viruses has actively supported the virology community through a variety of initiatives, including annual travel awards for students and postdoctoral researchers, the biennial Viruses Young Investigator Award [2], and the organization of international virology conferences. This includes conferences held in Basel, Switzerland (2016); Barcelona, Spain (2018, 2020, and 2024); and the virtual Viruses 2022 conference [3–7]. Additionally, the journal has established affiliations with leading virology societies, such as the American Society for Virology (ASV), the Spanish Society for Virology (SEV), the Canadian Society for Virology (CSV), the Italian Society for Virology (SIV-ISV), the Australasian Virology Society (AVS), the Brazilian Society for Virology (BSV), and Global Virus Network (GVN), furthering its mission to promote virology research globally.

In recent years, virology has undergone transformative advancements, highlighting its critical role in science and public health. The global response to SARS-CoV-2 has accelerated the development of mRNA vaccine platforms and antiviral drugs, while significantly strengthening the scientific community's capacity for genomic surveillance of emerging variants. At the same time, research into underexplored pathogens, such as Nipah and monkeypox, has highlighted the urgent need for integrated 'one-health' strategies to prevent zoonotic disease spillovers. Innovations such as AI-driven drug discovery, single-virus sequencing technologies, and the application of synthetic biology to engineer viral vectors for gene therapy are opening exciting new frontiers not only in understanding and combatting viruses as pathogens but also harnessing them for useful applications.

To celebrate the journal’s ongoing success and the remarkable advancements in virology, Viruses is proud to announce its Fifteenth Year Anniversary Special Issue. This special issue will highlight cutting-edge research and reflect the breadth of virology across all domains.

I am delighted to announce that Dr. Abdul Waheed, from the HIV Dynamics and Replication Program (HIV-DRP) of the U.S. National Cancer Institute, will join me as Co-Guest Editor for this Special Issue. Together, we are committed to assembling a compelling collection of articles that highlights the diversity, innovation, and impact of modern virology research.

References

  1. https://blog.mdpi.com/2024/12/24/open-access-policies/
  2. https://www.mdpi.com/journal/viruses/awards
  3. Viruses 2016: https://sciforum.net/event/viruses-2016
  4. Viruses 2018: https://sciforum.net/event/Viruses-2018
  5. Viruses 2020: https://sciforum.net/event/viruses2020
  6. Viruses 2022: https://sciforum.net/event/viruses2022
  7. Viruses 2024: https://sciforum.net/event/viruses2024

Dr. Eric O. Freed
Dr. Abdul A. Waheed
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

  • diversity, innovation, and impact of modern virology research
  • virology across all domains
  • Viruses fifteenth year anniversary
 

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Published Papers (10 papers)

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Research

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23 pages, 2511 KiB  
Article
The Role of Prion Protein in Reelin/Dab1 Signaling: Implications for Neurodegeneration
by Irene Giulia Rolle, Anna Burato, Merve Begüm Bacınoğlu, Fabio Moda and Giuseppe Legname
Viruses 2025, 17(7), 928; https://doi.org/10.3390/v17070928 - 29 Jun 2025
Viewed by 305
Abstract
The cellular prion protein (PrPC) is studied in prion diseases, where its misfolded isoform (PrPSc) leads to neurodegeneration. PrPC has also been implicated in several physiological functions. The protein is abundant in the nervous system, and it is [...] Read more.
The cellular prion protein (PrPC) is studied in prion diseases, where its misfolded isoform (PrPSc) leads to neurodegeneration. PrPC has also been implicated in several physiological functions. The protein is abundant in the nervous system, and it is critical for cell signaling in cellular communication, where it acts as a scaffold for various signaling molecules. The Reelin signaling pathway, implicated both in Alzheimer’s and prion diseases, engages Dab1, an adaptor protein influencing APP processing and amyloid beta deposition. Here, we show, using Prnp knockout models (Prnp0/0), that PrPC modulates Reelin signaling, affecting Dab1 activation and downstream phosphorylation in both neuronal cultures and mouse brains. Notably, Prnp0/0 mice showed reduced responsiveness to Reelin, associated with altered Dab1 phosphorylation and Fyn kinase activity. Even though no direct interaction between PrPC and Reelin/ApoER2 was found, Prnp0/0 neurons showed lower NCAM levels, a well-established PrPC interactor. Prion infection further disrupted the Reelin signaling pathway, thus downregulating Dab1 and Reelin receptors and altering Reelin processing, like Alzheimer’s disease pathology. These findings emphasize PrPC indirect role in Dab1 signaling via the NCAM and Fyn pathways, which influence synaptic function and neurodegeneration in prion diseases. Full article
(This article belongs to the Special Issue 15-Year Anniversary of Viruses)
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16 pages, 6386 KiB  
Article
Noncanonical Poly(A) Polymerase TENT4 Drives Expression of Subgenomic Hepatitis A Virus RNAs in Infected Cells
by You Li, Ankit Gupta, Brian N. Papas, David Aponte-Diaz, Jayden M. Harris, Ichiro Misumi, Jason K. Whitmire, Craig E. Cameron, Marcos Morgan and Stanley M. Lemon
Viruses 2025, 17(5), 665; https://doi.org/10.3390/v17050665 - 2 May 2025
Viewed by 881
Abstract
Both hepatitis B virus (HBV), an hepadnavirus with a DNA genome, and hepatitis A virus (HAV), a picornavirus, require the TRAMP-like host ZCCHC14-TENT4 complex for efficient replication. However, whereas HBV requires the nucleotidyltransferase activity of TENT4 to extend and stabilize the 3′ poly(A) [...] Read more.
Both hepatitis B virus (HBV), an hepadnavirus with a DNA genome, and hepatitis A virus (HAV), a picornavirus, require the TRAMP-like host ZCCHC14-TENT4 complex for efficient replication. However, whereas HBV requires the nucleotidyltransferase activity of TENT4 to extend and stabilize the 3′ poly(A) tails of mRNA transcribed from its genome, the role played by TENT4 in HAV replication is uncertain. HAV proteins are synthesized directly from its genomic RNA, which possesses a 3′ poly(A) tail, with its length and composition presumably maintained by 3Dpol-catalyzed RNA transcription during its replicative cycle. Using nanopore long-read sequencing of RNA from infected cells, we confirm here that the length of the HAV 3′ poly(A) tail is not altered by treating infected cells with RG7834, a small molecule TENT4 inhibitor with potent anti-HAV activity. Despite this, TENT4 catalytic activity is essential for HAV replication. Surprisingly, nanopore sequencing revealed a low abundance of HAV subgenomic RNAs (hsRNAs) that extend from the 5′ end of the genome to a site within the 5′ untranslated RNA (5′UTR) immediately downstream of a stem-loop to which the ZCCHC14-TENT4 complex is recruited. These hsRNAs are polyadenylated, and their abundance is sharply reduced by RG7834 treatment, implying they are likely products of TENT4. Similar subgenomic RNAs were not identified in poliovirus-infected cells. hsRNAs are present not only in HAV-infected cell culture but also in the liver of HAV-infected mice, where they represent 1–3% of all HAV transcripts, suggesting their physiological relevance. However, transfecting exogenous hsRNA into TENT4-depleted cells failed to rescue HAV replication, leaving the functional role of hsRNA unresolved. These findings reveal a novel picornaviral subgenomic RNA species while highlighting mechanistic differences in the manner in which HAV and HBV exploit the host ZCCHC4-TENT4 complex for their replication. Full article
(This article belongs to the Special Issue 15-Year Anniversary of Viruses)
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Review

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26 pages, 24138 KiB  
Review
Insights into the Landscape of Alphavirus Receptor and Antibody Interactions
by Shishir Poudyal, Abhishek Bandyopadhyay and Richard J. Kuhn
Viruses 2025, 17(7), 1019; https://doi.org/10.3390/v17071019 - 21 Jul 2025
Abstract
Alphaviruses engage a diverse array of attachment factors and receptors during viral entry, resulting in a broad host range and disease spectrum, and thus presenting them as a major global public health concern. The development of effective antivirals against these arboviruses relies on [...] Read more.
Alphaviruses engage a diverse array of attachment factors and receptors during viral entry, resulting in a broad host range and disease spectrum, and thus presenting them as a major global public health concern. The development of effective antivirals against these arboviruses relies on a comprehensive understanding of the molecular interplay between these viruses and host cell factors, as well as the wide range of immune responses that ensue following viral infection. In this review, we present the current understanding of the complex landscape of alphavirus interaction with attachment factors and entry receptors, some of which are characterized structurally, while others are characterized biochemically. Additionally, we provide an overview of the molecular bases of epitope recognition by neutralizing and non-neutralizing antibodies against alphaviruses, and how icosahedral symmetry influences these interactions, such as occupancy and neutralization potency. We further discuss the structural bases of epitope recognition of a few pan-alphavirus antibodies, their potential therapeutic implications, and offer future perspectives on the development of effective therapeutics against clinically relevant alphaviruses. Full article
(This article belongs to the Special Issue 15-Year Anniversary of Viruses)
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17 pages, 1262 KiB  
Review
Regulation and Deregulation of Viral Gene Expression During High-Risk HPV Infection
by Konstanze Schichl and John Doorbar
Viruses 2025, 17(7), 937; https://doi.org/10.3390/v17070937 - 30 Jun 2025
Viewed by 418
Abstract
Cervical cancer remains a global health burden, with persistent infection by high-risk human papillomaviruses (HR-HPVs) being the primary etiological factor. HR-HPVs target stem-like cells of the cervical epithelium to establish chronic infections. Upon infection of the cervical transformation zone (TZ)—a region adjacent to [...] Read more.
Cervical cancer remains a global health burden, with persistent infection by high-risk human papillomaviruses (HR-HPVs) being the primary etiological factor. HR-HPVs target stem-like cells of the cervical epithelium to establish chronic infections. Upon infection of the cervical transformation zone (TZ)—a region adjacent to the squamocolumnar junction (SCJ)—these viruses drive neoplastic transformation, which is due in part to the unique cellular composition and hormonal responsiveness of the TZ. Reserve cells, which can accumulate at the cervical crypt entrances of the TZ, are thought to be highly susceptible to HR-HPV infection because of their location beneath a single layer of columnar cells. Infection of the stratified ectocervical epithelium, in contrast, requires a wound to allow basal cell infection, replication, and the expression of early genes to adjust epithelial homeostasis while facilitating immune evasion. Persistent infection by HR-HPV types, particularly HPV16 and HPV18, can result in the deregulated expression of viral genes E6 and E7, driving cell cycle disruption, genomic instability, and subsequent viral genome integration. Differences in the microenvironment and transcriptional environment of the ectocervix compared with the TZ could explain the frequent deregulation of E6 and E7 at the latter site, which can drive disease progression towards cancer. Full article
(This article belongs to the Special Issue 15-Year Anniversary of Viruses)
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9 pages, 520 KiB  
Review
Trichomonas vaginalis Virus: Current Insights and Emerging Perspectives
by Keonte J. Graves, Jan Novak and Christina A. Muzny
Viruses 2025, 17(7), 898; https://doi.org/10.3390/v17070898 - 26 Jun 2025
Viewed by 334
Abstract
Trichomonas vaginalis, a prevalent sexually transmitted protozoan parasite, is associated with adverse birth outcomes, increased risk of HIV and other sexually transmitted infections, infertility, and cervical cancer. Despite its widespread impact, trichomoniasis remains underdiagnosed and underreported globally. Trichomonas vaginalis virus (TVV), a [...] Read more.
Trichomonas vaginalis, a prevalent sexually transmitted protozoan parasite, is associated with adverse birth outcomes, increased risk of HIV and other sexually transmitted infections, infertility, and cervical cancer. Despite its widespread impact, trichomoniasis remains underdiagnosed and underreported globally. Trichomonas vaginalis virus (TVV), a double-stranded RNA (dsRNA) virus infecting T. vaginalis, could impact T. vaginalis pathogenicity. We provide an overview of TVV, including its genomic structure, transmission, impact on protein expression, role in 5-nitroimidazole drug susceptibility, and clinical significance. TVV is a ~5 kbp dsRNA virus enclosed within a viral capsid closely associated with the Golgi complex and plasma membrane of infected parasites. Hypothetical mechanisms of TVV transmission have been proposed. TVV affects protein expression in T. vaginalis, including cysteine proteases and surface antigens, thus impacting its virulence and ability to evade the immune system. Additionally, TVV may influence the sensitivity of T. vaginalis to treatment; clinical isolates of T. vaginalis not harboring TVV are more likely to be resistant to metronidazole. Clinically, TVV-positive T. vaginalis infections have been associated with a range in severity of genital signs and symptoms. Further research into interactions between T. vaginalis and TVV is essential in improving diagnosis, treatment, and the development of targeted interventions. Full article
(This article belongs to the Special Issue 15-Year Anniversary of Viruses)
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17 pages, 5218 KiB  
Review
Trafficking and Activation of Henipavirus, Parahenipavirus, and Henipa-like Virus Fusion Proteins
by Chanakha K. Navaratnarajah and Roberto Cattaneo
Viruses 2025, 17(6), 866; https://doi.org/10.3390/v17060866 - 19 Jun 2025
Viewed by 497
Abstract
Henipaviruses are emerging zoonotic viruses that have caused deadly outbreaks in humans and livestock across several regions of the world. The fusion (F) protein of henipaviruses plays a critical role in viral entry into host cells and represents a key determinant of viral [...] Read more.
Henipaviruses are emerging zoonotic viruses that have caused deadly outbreaks in humans and livestock across several regions of the world. The fusion (F) protein of henipaviruses plays a critical role in viral entry into host cells and represents a key determinant of viral pathogenicity. This review provides a comprehensive analysis of current knowledge regarding trafficking, activation, as well as the role in particle assembly, of henipavirus F proteins. We discuss the unique characteristics of henipavirus F proteins compared to other paramyxovirus fusion proteins, with particular emphasis on their distinctive trafficking and activation mechanisms. Attention is also given to novel henipaviruses that have been detected in hosts other than bats, namely rodents and shrews. These viruses are sufficiently different that the International Committee on Taxonomy of Viruses has proposed a new genus for them, the Parahenipaviruses. We discuss how variations in F protein characteristics between Henipaviruses, Parahenipaviruses, and yet-unclassified henipa-like viruses might influence their trafficking and activation. Understanding these molecular mechanisms is crucial for developing effective therapeutic strategies against henipavirus infections and for predicting the emergence of novel henipavirus strains with pandemic potential. Full article
(This article belongs to the Special Issue 15-Year Anniversary of Viruses)
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11 pages, 2084 KiB  
Review
How HIV-1 Uses the Metabolite Inositol Hexakisphosphate to Build Its Capsid
by Leo C. James
Viruses 2025, 17(5), 689; https://doi.org/10.3390/v17050689 - 9 May 2025
Viewed by 554
Abstract
The HIV-1 capsid is one of virology’s most iconic structures, yet how it assembles has long remained elusive. Remarkably, the capsid is made from just a single protein, CA, which forms a lattice of ~250 hexamers and exactly 12 pentamers. Conical capsids form [...] Read more.
The HIV-1 capsid is one of virology’s most iconic structures, yet how it assembles has long remained elusive. Remarkably, the capsid is made from just a single protein, CA, which forms a lattice of ~250 hexamers and exactly 12 pentamers. Conical capsids form inside budded virions during maturation, but early efforts to reproduce this in vitro resulted instead in open-ended tubes with a purely hexameric lattice. The missing component in capsid assembly was finally identified as the metabolite inositol hexakisphosphate (IP6). Simply mixing soluble CA protein with IP6 is sufficient to drive the spontaneous assembly of conical capsids with a similar size and shape to those inside of infectious virions. Equally important, IP6 stabilises capsids once formed, increasing their stability from minutes to hours. Indeed, such is the dependence of HIV-1 on IP6 that the virus actively packages it into virions during production. These discoveries have stimulated work from multiple labs into the role and importance of IP6 in HIV-1 replication, and is the subject of this review. Full article
(This article belongs to the Special Issue 15-Year Anniversary of Viruses)
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20 pages, 686 KiB  
Review
Self-Amplifying RNA: Advantages and Challenges of a Versatile Platform for Vaccine Development
by Thomas Vallet and Marco Vignuzzi
Viruses 2025, 17(4), 566; https://doi.org/10.3390/v17040566 - 14 Apr 2025
Cited by 2 | Viewed by 2676
Abstract
Self-amplifying RNA is synthetic nucleic acid engineered to replicate within cells without generating viral particles. Derived from alphavirus genomes, saRNA retains the non-structural elements essential for replication while replacing the structural elements with an antigen of interest. By enabling efficient intracellular amplification, saRNA [...] Read more.
Self-amplifying RNA is synthetic nucleic acid engineered to replicate within cells without generating viral particles. Derived from alphavirus genomes, saRNA retains the non-structural elements essential for replication while replacing the structural elements with an antigen of interest. By enabling efficient intracellular amplification, saRNA offers a promising alternative to conventional mRNA vaccines, enhancing antigen expression while requiring lower doses. However, this advantage comes with challenges. In this review, we highlight the key limitations of saRNA technology and explore potential strategies to overcome them. By identifying these challenges, we aim to provide insights that can guide the future design of saRNA-based therapeutics, extending their potential beyond vaccine applications. Full article
(This article belongs to the Special Issue 15-Year Anniversary of Viruses)
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16 pages, 2293 KiB  
Review
Towards a Universal Translator: Decoding the PTMs That Regulate Orthoflavivirus Infection
by Hannah M. Schmidt and Stacy M. Horner
Viruses 2025, 17(2), 287; https://doi.org/10.3390/v17020287 - 19 Feb 2025
Cited by 1 | Viewed by 1130
Abstract
Post-translational modifications (PTMs) serve as critical regulators of protein function across biological systems, including during viral infection. For orthoflaviviruses, including human pathogens like dengue, Zika, and West Nile viruses, PTMs on viral proteins regulate multiple aspects of the viral lifecycle and pathogenesis. Here, [...] Read more.
Post-translational modifications (PTMs) serve as critical regulators of protein function across biological systems, including during viral infection. For orthoflaviviruses, including human pathogens like dengue, Zika, and West Nile viruses, PTMs on viral proteins regulate multiple aspects of the viral lifecycle and pathogenesis. Here, we review the mechanisms by which PTMs regulate orthoflavivirus infection in both vertebrate and arthropod hosts. We examine how ubiquitination and glycosylation on the viral envelope proteins facilitate viral entry and how phosphorylation, SUMOylation, and acetylation on non-structural proteins modulate viral RNA replication. Additionally, we describe how PTMs on viral structural proteins dynamically regulate viral assembly and egress. We also describe how PTMs can influence tissue tropism and host-specific pathogenesis, with some modifications showing divergent functions between arthropod vectors and vertebrate hosts, and how the host antiviral response can trigger specific PTMs on viral proteins to restrict infection, highlighting PTMs as key mediators of host-pathogen interactions. While significant progress has been made in identifying PTMs on viral proteins, many questions remain about their temporal dynamics, mechanisms of action, and conservation across the orthoflavivirus genus. Understanding how PTMs regulate orthoflavivirus infection may reveal new therapeutic strategies, particularly given recent advances in targeting specific protein modifications for disease treatment. Full article
(This article belongs to the Special Issue 15-Year Anniversary of Viruses)
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33 pages, 1893 KiB  
Review
Unraveling the Kaposi Sarcoma-Associated Herpesvirus (KSHV) Lifecycle: An Overview of Latency, Lytic Replication, and KSHV-Associated Diseases
by Victor A. Losay and Blossom Damania
Viruses 2025, 17(2), 177; https://doi.org/10.3390/v17020177 - 26 Jan 2025
Cited by 2 | Viewed by 2090
Abstract
Kaposi sarcoma-associated herpesvirus (KSHV) is an oncogenic gammaherpesvirus and the etiological agent of several diseases. These include the malignancies Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman disease (MCD), as well as the inflammatory disorder KSHV inflammatory cytokine syndrome (KICS). The [...] Read more.
Kaposi sarcoma-associated herpesvirus (KSHV) is an oncogenic gammaherpesvirus and the etiological agent of several diseases. These include the malignancies Kaposi sarcoma (KS), primary effusion lymphoma (PEL), and multicentric Castleman disease (MCD), as well as the inflammatory disorder KSHV inflammatory cytokine syndrome (KICS). The KSHV lifecycle is characterized by two phases: a default latent phase and a lytic replication cycle. During latency, the virus persists as an episome within host cells, expressing a limited subset of viral genes to evade immune surveillance while promoting cellular transformation. The lytic phase, triggered by various stimuli, results in the expression of the full viral genome, production of infectious virions, and modulation of the tumor microenvironment. Both phases of the KSHV lifecycle play crucial roles in driving viral pathogenesis, influencing oncogenesis and immune evasion. This review dives into the intricate world of the KSHV lifecycle, focusing on the molecular mechanisms that drive its latent and lytic phases, their roles in disease progression, and current therapeutic strategies. Full article
(This article belongs to the Special Issue 15-Year Anniversary of Viruses)
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