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A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Microbiology".

Deadline for manuscript submissions: closed (30 June 2023) | Viewed by 9151

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Special Issue Editor

Dr. Monica Miranda-Saksena

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Guest Editor

The Westmead Institute for Medical Research and The University of Sydney, Sydney, Australia
Interests: herpes simplex virus; axonal transport; growth cone; capsid; neurons

Special Issue Information

Dear Colleagues,

Alphaherpesviruses are widespread human and animal pathogens characterized by their ability to establish lifelong latent infection in the peripheral nervous system of their host. Alphaherpesviruses are a subfamily of the family Herpesviridae, and there are 45 known species in this subfamily. Some of the most studied viruses of this subfamily include the human alphaherpesvirus 1 and 2 (HHV-1/2 or herpes simplex virus 1 and 2, HSV-1/2), human alphaherpesvirus 3 (HHV-3 or varicella-zoster virus, VZV), the Swine Suid herpesvirus 1 (SuHV-1) (pseudorabies virus), the equine Equid alphaherpesvirus 1 (also known as equine herpes virus, EHV-1), and chicken Gallid alphaherpesvirus 2 (also known as Marek’s disease virus, MDV). Infections by alphaherpesviruses can range from mild lesions or benign tumors in the skin, eye, or mucosa to a life-threatening central nervous system infection. Given their characteristic directional spread to the nervous system from peripheral sites and their ability to persist in their hosts, these viruses have evolved mechanisms to utilize the host cytoskeleton for long-distance transport and subvert the host’s immune response to evade detection. This Special Issue will focus on providing up-to-date research to the readers on the mechanisms of alphaherpesviruses replication and spread in their respective host, virus–host interactions, innate and adaptive immune responses, viral immune evasion strategies, latency and reactivation, and future directions for novel antiviral strategies and vaccine development.

Dr. Monica Miranda-Saksena
Guest Editor

Manuscript Submission Information

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Keywords

Alphaherpesvirues
Peripheral nervous system
Axonal transport
Immune evasion
Innate and adaptive immune response
Latency and reactivation
Antivirals
Vaccine development
Virus–host interactions

Published Papers (4 papers)

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Research

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21 pages, 1372 KiB

Open AccessArticle

Herpes Simplex Virus 1 (HSV-1) Infected Cell Protein 0 (ICP0) Targets of Ubiquitination during Productive Infection of Primary Adult Sensory Neurons

by Telvin L. Harrell, David J. Davido and Andrea S. Bertke

Int. J. Mol. Sci. 2023, 24(3), 2931; https://doi.org/10.3390/ijms24032931 - 2 Feb 2023

Cited by 2 | Viewed by 2412

Abstract

Herpes simplex virus 1 (HSV-1) enters sensory neurons with the potential for productive or latent infection. For either outcome, HSV-1 must curtail the intrinsic immune response, regulate viral gene expression, and remove host proteins that could restrict viral processes. Infected cell protein 0 (ICP0), a virus-encoded E3 ubiquitin ligase, supports these processes by mediating the transfer of ubiquitin to target proteins to change their location, alter their function, or induce their degradation. To identify ubiquitination targets of ICP0 during productive infection in sensory neurons, we immunoprecipitated ubiquitinated proteins from primary adult sensory neurons infected with HSV-1 KOS (wild-type), HSV-1 n212 (expressing truncated, defective ICP0), and uninfected controls using anti-ubiquitin antibody FK2 (recognizing K29, K48, K63 and monoubiquitinated proteins), followed by LC-MS/MS and comparative analyses. We identified 40 unique proteins ubiquitinated by ICP0 and 17 ubiquitinated by both ICP0 and host mechanisms, of which High Mobility Group Protein I/Y (HMG I/Y) and TAR DNA Binding Protein 43 (TDP43) were selected for further analysis. We show that ICP0 ubiquitinates HMG I/Y and TDP43, altering protein expression at specific time points during productive HSV-1 infection, demonstrating that ICP0 manipulates the sensory neuronal environment in a time-dependent manner to regulate infection outcome in neurons. Full article

(This article belongs to the Special Issue Alphaherpesviruses)

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15 pages, 3160 KiB

Open AccessArticle

Nicotinamide n-Oxide Attenuates HSV-1-Induced Microglial Inflammation through Sirtuin-1/NF-κB Signaling

by Xiaowei Song, Wenyan Cao, Zexu Wang, Feng Li, Ji Xiao, Qiongzhen Zeng, Yuan Wang, Shan Li, Cuifang Ye, Yifei Wang and Kai Zheng

Int. J. Mol. Sci. 2022, 23(24), 16085; https://doi.org/10.3390/ijms232416085 - 16 Dec 2022

Cited by 8 | Viewed by 1785

Abstract

HSV-1 is a typical neurotropic virus that infects the brain and causes keratitis, cold sores, and occasionally, acute herpes simplex encephalitis (HSE). The large amount of proinflammatory cytokines induced by HSV-1 infection is an important cause of neurotoxicity in the central nervous system (CNS). Microglia, as resident macrophages in CNS, are the first line of defense against neurotropic virus infection. Inhibiting the excessive production of inflammatory cytokines in overactivated microglia is a crucial strategy for the treatment of HSE. In the present study, we investigated the effect of nicotinamide n-oxide (NAMO), a metabolite mainly produced by gut microbe, on HSV-1-induced microglial inflammation and HSE. We found that NAMO significantly inhibits the production of cytokines induced by HSV-1 infection of microglia, such as IL-1β, IL-6, and TNF-α. In addition, NAMO promotes the transition of microglia from the pro-inflammatory M1 type to the anti-inflammatory M2 type. More detailed studies revealed that NAMO enhances the expression of Sirtuin-1 and its deacetylase enzymatic activity, which in turn deacetylates the p65 subunit to inhibit NF-κB signaling, resulting in reduced inflammatory response and ameliorated HSE pathology. Therefore, Sirtuin-1/NF-κB axis may be promising therapeutic targets against HSV-1 infection-related diseases including HSE. Full article

(This article belongs to the Special Issue Alphaherpesviruses)

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9 pages, 1525 KiB

Open AccessArticle

Mutation and Interaction Analysis of the Glycoprotein D and L and Thymidine Kinase of Pseudorabies Virus

by Xue Li, Si Chen, Liying Zhang, Jiawei Zheng, Guyu Niu, Lin Yang, Xinwei Zhang and Linzhu Ren

Int. J. Mol. Sci. 2022, 23(19), 11597; https://doi.org/10.3390/ijms231911597 - 30 Sep 2022

Cited by 2 | Viewed by 1501

Abstract

Pseudorabies (also called Aujeszky’s disease) is a highly infectious viral disease caused by the pseudorabies virus (PRV, or Suid herpesvirus 1). Although the disease has been controlled by immunization with the PRV-attenuated vaccine, the emerging PRV variants can escape the immune surveillance in the vaccinated pig, resulting in recent outbreaks. Furthermore, the virus has been detected in other animals and humans, indicating cross-transmission of PRV. However, the mechanism of PRV cross-species transmission needs further study. In this study, we compared the amino acid sequences of glycoproteins (gD), gL, and thymidine kinase (TK) of PRV strains, human PRV hSD-1 2019 strain, and the attenuated strain Bartha-K61, followed by predication of their spatial conformation. In addition, the interactions between the viral gD protein and host nectin-1, nectin-2, and HS were also evaluated via molecular docking. The results showed that the amino acid sequence homology of the gD, gL, and TK proteins of hSD-1 2019 and JL-CC was 97.5%, 94.4%, and 99.1%, respectively. Moreover, there were mutations in the amino acid sequences of gD, gL, and TK proteins of hSD-1 2019 and JL-CC compared with the corresponding reference sequences of the Bartha strain. The mutations of gD, gL, and TK might not affect the spatial conformation of the protein domain but may affect the recognition of antibodies and antigen epitopes. Moreover, the gD protein of JL-CC, isolated previously, can bind to human nectin-1, nectin-2, and HS, suggesting the virus may be highly infectious and pathogenic to human beings. Full article

(This article belongs to the Special Issue Alphaherpesviruses)

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Review

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19 pages, 1937 KiB

Open AccessReview

Interplay between Autophagy and Herpes Simplex Virus Type 1: ICP34.5, One of the Main Actors

by Inés Ripa, Sabina Andreu, José Antonio López-Guerrero and Raquel Bello-Morales

Int. J. Mol. Sci. 2022, 23(21), 13643; https://doi.org/10.3390/ijms232113643 - 7 Nov 2022

Cited by 1 | Viewed by 2938

Abstract

Herpes simplex virus type 1 (HSV-1) is a neurotropic virus that occasionally may spread to the central nervous system (CNS), being the most common cause of sporadic encephalitis. One of the main neurovirulence factors of HSV-1 is the protein ICP34.5, which although it initially seems to be relevant only in neuronal infections, it can also promote viral replication in non-neuronal cells. New ICP34.5 functions have been discovered during recent years, and some of them have been questioned. This review describes the mechanisms of ICP34.5 to control cellular antiviral responses and debates its most controversial functions. One of the most discussed roles of ICP34.5 is autophagy inhibition. Although autophagy is considered a defense mechanism against viral infections, current evidence suggests that this antiviral function is only one side of the coin. Different types of autophagic pathways interact with HSV-1 impairing or enhancing the infection, and both the virus and the host cell modulate these pathways to tip the scales in its favor. In this review, we summarize the recent progress on the interplay between autophagy and HSV-1, focusing on the intricate role of ICP34.5 in the modulation of this pathway to fight the battle against cellular defenses. Full article

(This article belongs to the Special Issue Alphaherpesviruses)

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