{"title":"Effect of thymidine kinase-deficiency (∆ORF38) on neuropathogenicity of equine herpesvirus-1 in the mouse model and expression of neighboring genes.","authors":"Samy Kasem, Ahmed S Abdel-Moneim, Hideto Fukushi","doi":"10.1007/s11262-024-02128-w","DOIUrl":null,"url":null,"abstract":"<p><p>Previous studies showed that deletion of the viral thymidine kinase (TK) gene in several alphaherpesviruses including EHV-1 reduced their virulence. Previously, we found that deletion of ORF37, which is located head-to-head with TK, decreased EHV-1 virulence in mice but did not affect the expression of TK mRNA. Therefore, deletion of ORF38 might also affect virulence by partially deleting the ORF37 promoter. To investigate the role of the TK gene-encoding region in the pathogenesis of EHV-1 as well as the expression of ORF37, we generated a TK deletion mutant by using a bacterial artificial chromosome carrying the neuropathogenic strain Ab4p. Deletion of TK increased the transcription of ORF37, did not cause any neurological disorders in CBA/N1 mice, and its growth in cultured neural cells was impaired. These results suggest deletion of ORF38 does not affect the ORF37 promoter and confirm that TK plays an important role in the neuropathogenicity of EHV-1.</p>","PeriodicalId":51212,"journal":{"name":"Virus Genes","volume":" ","pages":""},"PeriodicalIF":1.9000,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Virus Genes","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s11262-024-02128-w","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"GENETICS & HEREDITY","Score":null,"Total":0}
Effect of thymidine kinase-deficiency (∆ORF38) on neuropathogenicity of equine herpesvirus-1 in the mouse model and expression of neighboring genes.
Previous studies showed that deletion of the viral thymidine kinase (TK) gene in several alphaherpesviruses including EHV-1 reduced their virulence. Previously, we found that deletion of ORF37, which is located head-to-head with TK, decreased EHV-1 virulence in mice but did not affect the expression of TK mRNA. Therefore, deletion of ORF38 might also affect virulence by partially deleting the ORF37 promoter. To investigate the role of the TK gene-encoding region in the pathogenesis of EHV-1 as well as the expression of ORF37, we generated a TK deletion mutant by using a bacterial artificial chromosome carrying the neuropathogenic strain Ab4p. Deletion of TK increased the transcription of ORF37, did not cause any neurological disorders in CBA/N1 mice, and its growth in cultured neural cells was impaired. These results suggest deletion of ORF38 does not affect the ORF37 promoter and confirm that TK plays an important role in the neuropathogenicity of EHV-1.
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Viruses are convenient models for the elucidation of life processes. The study of viruses is again on the cutting edge of biological sciences: systems biology, genomics, proteomics, metagenomics, using the newest most powerful tools.
Huge amounts of new details on virus interactions with the cell, other pathogens and the hosts – animal (including human), insect, fungal, plant, bacterial, and archaeal - and their role in infection and disease are forthcoming in perplexing details requiring analysis and comments.
Virus Genes is dedicated to the publication of studies on the structure and function of viruses and their genes, the molecular and systems interactions with the host and all applications derived thereof, providing a forum for the analysis of data and discussion of its implications, and the development of new hypotheses.
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