Mechanisms of Herpesvirus Resistance

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 September 2025 | Viewed by 1679

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Special Issue Information

Dear Colleagues,

Herpesviruses are common human pathogens, generally causing mild to asymptomatic infections in immunocompetent hosts. However, human herpesvirus infections are more serious when the host has a weak immune system, causing significant morbidity and mortality among different populations of immunocompromised hosts. An important feature of all herpesviruses is their ability to establish lifelong latent infections after a primary infection, remaining dormant. Reactivation of herpesviruses often occurs when the immune system is impaired, causing life-threatening persistent infections that require prolonged treatment. Such prolonged treatment coupled with an impaired immune system provides the perfect selective landscape for the emergence and selection of drug-resistant mutants. Herpesviruses bearing mutations in genes associated with drug resistance can cause severe infections and extreme discomfort and eventually death among immunocompromised patients. Drug resistance is also increasingly being recognized in immunocompetent individuals suffering from herpetic keratitis.

This Special Issue of Viruses will focus on the latest advances in understanding the mechanism of herpesvirus drug resistance for the different classes of anti-herpesvirus drugs, encompassing in vitro, in vivo, and clinical research. We will also delve into the diagnosis of herpesvirus drug resistance as well as the development of new drugs and strategies to manage drug-resistant herpesvirus infections in the clinic. We invite you to share your most insightful primary research work, reviews, and hypotheses on these important topics.

Prof. Dr. Graciela Andrei
Guest Editor

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Keywords

  • human herpesviruses
  • cytomegalovirus
  • drug resistance
  • antiviral agents
  • immunocompromised host
  • novel anti-herpesvirus therapies
  • DNA polymerase
  • terminase

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Published Papers (1 paper)

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Research

11 pages, 1311 KiB  
Article
A Mutation in the Herpes Simplex Virus Type 1 (HSV-1) UL29 Gene is Associated with Anti-Herpesvirus Drugs’ Susceptibility
by Souichi Yamada, Shizuko Harada, Hikaru Fujii, Hitomi Kinoshita, Phu Hoang Anh Nguyen, Miho Shibamura, Tomoki Yoshikawa, Madoka Kawahara, Hideki Ebihara, Masayuki Saijo and Shuetsu Fukushi
Viruses 2024, 16(12), 1813; https://doi.org/10.3390/v16121813 - 21 Nov 2024
Viewed by 1095
Abstract
Herpes simplex virus type 1 (HSV-1) acyclovir (ACV) resistance is acquired by mutations in the viral thymidine kinase (TK) or DNA polymerase (DNApol) genes. We previously obtained an ACV-resistant clone (HSV-1_VZV_TK_clone α) by sequential passages of HSV-1_VZV-TK, a recombinant virus which lacked its [...] Read more.
Herpes simplex virus type 1 (HSV-1) acyclovir (ACV) resistance is acquired by mutations in the viral thymidine kinase (TK) or DNA polymerase (DNApol) genes. We previously obtained an ACV-resistant clone (HSV-1_VZV_TK_clone α) by sequential passages of HSV-1_VZV-TK, a recombinant virus which lacked its endogenous TK activity and instead expressed the varicella-zoster virus (VZV) TK ectopically. HSV-1_VZV_TK_clone α had been generated using an HSV-1_BAC in the presence of increasing concentrations of ACV. The ACV-resistant clone bore normal TK and DNApol genes. Here, we deployed next-generation full-genome sequencing of HSV-1_VZV_TK_clone α and identified a single nucleotide substitution, resulting in a P597L missense mutation in the UL29 gene product, the ICP8 protein. Recombinant HSV-1 encoding a P597L ICP8 protein was generated, and its properties and ability to confer drug resistance were analyzed. No difference in virus growth and UL29 expression was observed between the mutant recombinant, the wild type, and a revertant mutant viral strain, and susceptibility tests of these strains to ACV and other drugs using Vero, HEL, and ARPE19 cells identified that the recombinant UL29 mutant virus was resistant only to ACV. These results indicate that ICP8 may be involved in the anti-herpesvirus drugs’ mechanism of action on HSV-1. Full article
(This article belongs to the Special Issue Mechanisms of Herpesvirus Resistance)
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