Members of the UL24 herpesvirus gene family are determinants of pathogenesis. The gene is widely conserved across the Orthoherpesviridae family, also commonly referred to as Herpesviridae. In this review, the impact of UL24 homologs on pathogenesis as studied with different model systems is presented, as well as mechanistic aspects related to the different roles of UL24 proteins in virus-host cell interactions. The targeting of UL24 for the development of therapeutic applications is also discussed.
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UL24 herpesvirus determinants of pathogenesis: Roles in virus-host interactions.
Virology
December 2024
Institut National de La Recherche Scientifique, Laval, Québec, Canada.
Members of the UL24 herpesvirus gene family are determinants of pathogenesis. The gene is widely conserved across the Orthoherpesviridae family, also commonly referred to as Herpesviridae. In this review, the impact of UL24 homologs on pathogenesis as studied with different model systems is presented, as well as mechanistic aspects related to the different roles of UL24 proteins in virus-host cell interactions.
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October 2024
State Key Laboratory of Virology, Wuhan Institute of Virology, Center for Biosafety Mega-Science, Chinese Academy of Sciences, Wuhan 430071, China.
Herpes simplex virus type 2 (HSV-2) is a sexually transmitted virus, the cause of genital herpes, and its infection can increase the risk of HIV-1 infection. After initial infection, HSV-2 can establish lifelong latency within the nervous system, which is likely associated with the virus-mediated immune evasion. In this study, we found that HSV-2 UL24 significantly inhibited the activation of the IFN-β promoter and the production of IFN-β at both mRNA and protein levels.
View Article and Find Full Text PDFComparative Review of the Conserved UL24 Protein Family in Herpesviruses.
Int J Mol Sci
October 2024
The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan 5290002, Israel.
The UL24 protein family, conserved across all subfamilies of Orthoherpesviridae, plays diverse and significant roles in viral replication, host-virus interactions and pathogenesis. Understanding the molecular mechanisms and interactions of UL24 proteins is key to unraveling the complex interplay between herpesviruses and their hosts. This review provides a comparative and comprehensive overview of current knowledge on UL24 family members, including their conservation, expression patterns, cellular localization, and functional roles upon their expression and during viral infection, highlighting their significance in herpesvirus biology and their potential functions.
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Key Laboratory of Animal Disease and Human Health of Sichuan Province, Chengdu 611130, China; International Joint Research Center for Animal Disease Prevention and Control of Sichuan Province, Chengdu 611130, China; College of Veterinary Medicine, Institute of Veterinary Medicine and Immunology, Sichuan Agricultural University, Chengdu 611130, China; Research Center of Avian Disease, College of Veterinary Medicine, Sichuan Agricultural University, Chengdu 611130, China; Engineering Research Center of Southwest Animal Disease Prevention and Control Technology, Ministry of Education of the People's Republic of China, Chengdu 611130, China.
Duck plague virus (DPV), which is the causative agent of duck viral enteritis, is highly infectious and can cause severe disease and death in ducks, geese and other waterfowl. Several tegument proteins of DPV have been shown to affect the cyclic GMP-AMP synthase (cGAS)-STING signaling pathway to modulate host innate immune responses. DPV UL24, an important DPV tegument protein, can inhibit the activity of the IFN-β promoter.
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Viruses
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The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat Gan 5290002, Israel.
Article Synopsis
- - KSHV is a cancer-causing virus linked to Kaposi's sarcoma and other rare blood cancers, and this study investigates the role of a specific protein, ORF20, in its lifecycle.
- - Researchers created a virus that lacks the ORF20 gene (ORF20-Null KSHV) and found that this mutant virus resulted in faster viral gene expression but ultimately led to cell death and decreased viral production upon reactivation.
- - The study highlights that reinstating the short form of ORF20 could restore viral production and reduce cell death, suggesting ORF20's role in enhancing viral reactivation and potential infectious particle production through its endonuclease function.
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