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Viruses
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Advances in HSV Research
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Advances in HSV Research

A special issue of Viruses (ISSN 1999-4915). This special issue belongs to the section "Human Virology and Viral Diseases".

Deadline for manuscript submissions: 31 May 2024 | Viewed by 6975

Special Issue Editors

Prof. Dr. Anthony V. Nicola

E-Mail Website
Guest Editor
Department of Veterinary Microbiology and Pathology, College of Veterinary Medicine, Washington State University, Pullman, WA, USA
Interests: virology; virus-host interactions; viral entry; antivirals; herpesviruses; endocytosis; membrane fusion; viral glycoproteins
Special Issues, Collections and Topics in MDPI journals
Dr. Maria Kalamvoki

E-Mail Website
Guest Editor
Department of Microbiology, Molecular Genetics and Immunology, University of Kansas Medical Center, 3901 Rainbow Blvd, Kansas City, KS 66160, USA
Interests: herpesviruses; virus–host interactions; pathogenesis; innate immunity; intercellular communications; autophagy; transcription; protein trafficking; viral envelopment; antiviral targets
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Herpes simplex virus (HSV) is a large, double-stranded linear DNA virus that belongs to the family Herpesviridae. HSV-1 and HSV-2 remain major pathogens. HSV-1 is a prototype of the alphaherpesvirus subfamily. The majority of humans worldwide are seropositive for HSV. Asymptomatic infection is most common, but HSV disease is painful and distressing for many. HSV infection can manifest as orofacial lesions. HSV is also an important sexually transmitted infection, the most common cause of genital ulcer disease worldwide. Genital herpes increases the risk of HIV-1 acquisition and transmission. For some, HSV can result in severe, often life-threatening outcomes. HSV is the leading viral cause of blindness and encephalitis. Untreated neonatal infections develop central nervous system disease. HSV latent infection is life-long. There is no cure and no vaccine. HSV has more than 70 genes and can infect most cell types in culture; it also causes disease in several experimental animal models. This Special Issue will explore all aspects of HSV, including virus entry, gene expression, replication, assembly, egress, latency, HSV–cell interactions, pathogenesis, interventions, immunity and vaccines. We welcome updated reviews and research papers from our colleagues. We look forward to your contribution and to publishing your important work.

Prof. Dr. Anthony V. Nicola
Dr. Maria Kalamvoki
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.

Published Papers (4 papers)

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Research

12 pages, 1397 KiB  
Article
Herpes Simplex Virus 1 Glycoprotein B from a Hyperfusogenic Virus Mediates Enhanced Cell–Cell Fusion
by Katrina A. Gianopulos, Albina O. Makio, Suzanne M. Pritchard, Cristina W. Cunha, McKenna A. Hull and Anthony V. Nicola
Viruses 2024, 16(2), 251; https://doi.org/10.3390/v16020251 - 04 Feb 2024
Viewed by 947
Abstract
Herpes simplex virus 1 (HSV-1) causes significant morbidity and death in humans worldwide. Herpes simplex virus 1 has a complex fusion mechanism that is incompletely understood. The HSV-1 strain ANG has notable fusion and entry activities that distinguish it from wild type. HSV-1 [...] Read more.
Herpes simplex virus 1 (HSV-1) causes significant morbidity and death in humans worldwide. Herpes simplex virus 1 has a complex fusion mechanism that is incompletely understood. The HSV-1 strain ANG has notable fusion and entry activities that distinguish it from wild type. HSV-1 ANG virions fused with the Vero cell surface at 4 °C and also entered cells more efficiently at 15 °C, relative to wild type HSV-1 strain KOS virions, consistent with a hyperfusogenic phenotype. Understanding the molecular basis for the unique entry and fusion activities of HSV-1 strain ANG will help decipher the HSV fusion reaction and entry process. Sequencing of HSV-1 ANG genes revealed multiple changes in gB, gC, gD, gH, and gL proteins relative to wild type HSV-1 strains. The ANG UL45 gene sequence, which codes for a non-essential envelope protein, was identical to wild type KOS. HSV-1 ANG gB, gD, and gH/gL were necessary and sufficient to mediate cell–cell fusion in a virus-free reporter assay. ANG gB, when expressed with wild type KOS gD and gH/gL, increased membrane fusion, suggesting that ANG gB has hyperfusogenic cell–cell fusion activity. Replacing the KOS gD, gH, or gL with the corresponding ANG alleles did not enhance cell–cell fusion. The novel mutations in the ANG fusion and entry glycoproteins provide a platform for dissecting the cascade of interactions that culminate in HSV fusion and entry. Full article
(This article belongs to the Special Issue Advances in HSV Research)
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13 pages, 4487 KiB  
Article
Discovery of a Novel Intron in US10/US11/US12 of HSV-1 Strain 17
by Weizhong Chang, Ming Hao, Ju Qiu, Brad T. Sherman and Tomozumi Imamichi
Viruses 2023, 15(11), 2144; https://doi.org/10.3390/v15112144 - 25 Oct 2023
Viewed by 1118
Abstract
Herpes Simplex Virus type 1 (HSV-1) infects humans and causes a variety of clinical manifestations. Many HSV-1 genomes have been sequenced with high-throughput sequencing technologies and the annotation of these genome sequences heavily relies on the known genes in reference strains. Consequently, the [...] Read more.
Herpes Simplex Virus type 1 (HSV-1) infects humans and causes a variety of clinical manifestations. Many HSV-1 genomes have been sequenced with high-throughput sequencing technologies and the annotation of these genome sequences heavily relies on the known genes in reference strains. Consequently, the accuracy of reference strain annotation is critical for future research and treatment of HSV-1 infection. In this study, we analyzed RNA-Seq data of HSV-1 from NCBI databases and discovered a novel intron in the overlapping coding sequence (CDS) of US10 and US11, and the 3′ UTR of US12 in strain 17, a commonly used HSV-1 reference strain. To comprehensively understand the shared US10/US11/US12 intron structure, we used US11 as a representative and surveyed all US11 gene sequences from the NCBI nt/nr database. A total of 193 high-quality US11 sequences were obtained, of which 186 sequences have a domain of uninterrupted tandemly repeated RXP (Arg-X-Pro) in the C-terminus half of the protein. In total, 97 of the 186 sequences encode US11 protein with the same length of the mature US11 in strain 17:26 of them have the same structure of US11 and can be spliced as in strain 17; 71 of them have transcripts that are the same as mature US11 mRNA in strain 17. In total, 76 US11 gene sequences have either canonical or known noncanonical intron border sequences and may be spliced like strain 17 and obtain mature US11 CDS with the same length. If not spliced, they will have extra RXP repeats. A tandemly repeated RXP domain was proposed to be essential for US11 to bind with RNA and other host factors. US10 protein sequences from the same strains have also been studied. The results of this study show that even a frequently used reference organism may have errors in widely used databases. This study provides accurate annotation of the US10, US11, and US12 gene structure, which will build a more solid foundation to study expression regulation of the function of these genes. Full article
(This article belongs to the Special Issue Advances in HSV Research)
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20 pages, 9927 KiB  
Article
The Disruption of a Nuclear Export Signal in the C-Terminus of the Herpes Simplex Virus 1 Determinant of Pathogenicity UL24 Protein Leads to a Syncytial Plaque Phenotype
by Carmen Elena Gonzalez, Nawel Ben Abdeljelil and Angela Pearson
Viruses 2023, 15(9), 1971; https://doi.org/10.3390/v15091971 - 21 Sep 2023
Viewed by 1061
Abstract
UL24 of herpes simplex virus 1 (HSV-1) has been shown to be a determinant of pathogenesis in mouse models of infection. The N-terminus of UL24 localizes to the nucleus and drives the redistribution of nucleolin and B23. In contrast, when expressed alone, the [...] Read more.
UL24 of herpes simplex virus 1 (HSV-1) has been shown to be a determinant of pathogenesis in mouse models of infection. The N-terminus of UL24 localizes to the nucleus and drives the redistribution of nucleolin and B23. In contrast, when expressed alone, the C-terminal domain of UL24 accumulates in the Golgi apparatus; its importance during infection is unknown. We generated a series of mammalian expression vectors encoding UL24 with nested deletions in the C-terminal domain. Interestingly, enhanced nuclear staining was observed for several UL24-deleted forms in transient transfection assays. The substitution of a threonine phosphorylation site had no effect on UL24 localization or viral titers in cell culture. In contrast, mutations targeting a predicted nuclear export signal (NES) significantly enhanced nuclear localization, indicating that UL24 is able to shuttle between the nucleus and the cytoplasm. Recombinant viruses that encode UL24-harboring substitutions in the NES led to the accumulation of UL24 in the nucleus. Treatment with the CRM-1-specific inhibitor leptomycin B blocked the nuclear export of UL24 in transfected cells but not in the context of infection. Viruses encoding UL24 with NES mutations resulted in a syncytial phenotype, but viral yield was unaffected. These results are consistent with a role for HSV-1 UL24 in late cytoplasmic events in HSV-1 replication. Full article
(This article belongs to the Special Issue Advances in HSV Research)
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14 pages, 2616 KiB  
Article
A Trivalent HSV-2 gC2, gD2, gE2 Nucleoside-Modified mRNA-LNP Vaccine Provides Outstanding Protection in Mice against Genital and Non-Genital HSV-1 Infection, Comparable to the Same Antigens Derived from HSV-1
by Kevin P. Egan, Sita Awasthi, Giulia Tebaldi, Lauren M. Hook, Alexis M. Naughton, Bernard T. Fowler, Mitchell Beattie, Mohamad-Gabriel Alameh, Drew Weissman, Gary H. Cohen and Harvey M. Friedman
Viruses 2023, 15(7), 1483; https://doi.org/10.3390/v15071483 - 30 Jun 2023
Cited by 2 | Viewed by 2780
Abstract
HSV-1 disease is a significant public health burden causing orofacial, genital, cornea, and brain infection. We previously reported that a trivalent HSV-2 gC2, gD2, gE2 nucleoside-modified mRNA-lipid nanoparticle (LNP) vaccine provides excellent protection against vaginal HSV-1 infection in mice. Here, we evaluated whether [...] Read more.
HSV-1 disease is a significant public health burden causing orofacial, genital, cornea, and brain infection. We previously reported that a trivalent HSV-2 gC2, gD2, gE2 nucleoside-modified mRNA-lipid nanoparticle (LNP) vaccine provides excellent protection against vaginal HSV-1 infection in mice. Here, we evaluated whether this HSV-2 gC2, gD2, gE2 vaccine is as effective as a similar HSV-1 mRNA LNP vaccine containing gC1, gD1, and gE1 in the murine lip and genital infection models. Mice were immunized twice with a total mRNA dose of 1 or 10 µg. The two vaccines produced comparable HSV-1 neutralizing antibody titers, and surprisingly, the HSV-2 vaccine stimulated more potent CD8+ T-cell responses to gE1 peptides than the HSV-1 vaccine. Both vaccines provided complete protection from clinical disease in the lip model, while in the genital model, both vaccines prevented death and genital disease, but the HSV-1 vaccine reduced day two vaginal titers slightly better at the 1 µg dose. Both vaccines prevented HSV-1 DNA from reaching the trigeminal or dorsal root ganglia to a similar extent. We conclude that the trivalent HSV-2 mRNA vaccine provides outstanding protection against HSV-1 challenge at two sites and may serve as a universal prophylactic vaccine for HSV-1 and HSV-2. Full article
(This article belongs to the Special Issue Advances in HSV Research)
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