文献类型： 外文期刊

作者： Sato, Jumpei ¹ ; Murata, Shiro ¹ ; Yang, Zhiyuan ¹ ; Kaufer, Benedikt B. ⁴ ; Fujisawa, Sotaro ¹ ; Seo, Hikari ¹ ; Maekawa, Naoya ² ; Okagawa, Tomohiro ² ; Konnai, Satoru ¹ ; Osterrieder, Nikolaus ⁴ ; Parcells, Mark S. ⁶ ; Ohashi, Kazuhiko ¹ ;

作者机构： 1.Hokkaido Univ, Fac Vet Med, Dept Dis Control, Sapporo, Hokkaido 0600818, Japan

2.Hokkaido Univ, Fac Vet Med, Dept Adv Pharmaceut, Sapporo, Hokkaido 0600818, Japan

3.Beijing Acad Agr & Forestry Sci, Inst Anim Husb & Vet Med, Beijing 100097, Peoples R China

4.Free Univ Berlin, Inst Virol, D-14163 Berlin, Germany

5.City Univ Hong Kong, Dept Infect Dis & Publ Hlth, Kowloon, Hong Kong, Peoples R China

6.Univ Delaware, Dept Anim & Food Sci, Newark, DE 19716 USA

关键词： Marek's disease virus; Marek's disease; Meq; CVI988; tumorigenesis; pathogenicity; transactivation activity

期刊名称：VIRUSES-BASEL （ 影响因子：5.818； 五年影响因子：5.811 ）

ISSN：

年卷期： 2022 年 14 卷 2 期

页码：

收录情况： SCI

摘要： Marek's disease virus (MDV) causes malignant lymphoma in chickens (Marek's disease, MD). Although MD is currently controlled by vaccination, MDV strains have continuously increased in virulence over the recent decades. Polymorphisms in Meq, an MDV-encoded oncoprotein that serves as a transcription factor, have been associated with the enhanced virulence of the virus. In addition, insertions and deletions in Meq have been observed in MDV strains of higher virulence, but their contribution to said virulence remains elusive. In this study, we investigated the contribution of an insertion (L-Meq) and a deletion in the Meq gene (S-Meq) to its functions and MDV pathogenicity. Reporter assays revealed that both insertion and deletion enhanced the transactivation potential of Meq. Additionally, we generated RB-1B-based recombinant MDVs (rMDVs) encoding each Meq isoform and analyzed their pathogenic potential. rMDV encoding L-Meq indueced the highest mortality and tumor incidence in infected animals, whereas the rMDV encoding S-Meq exhibited the lowest pathogenicity. Thus, insertion enhanced the transactivation activity of Meq and MDV pathogenicity, whereas deletion reduced pathogenicity despite having increased transactivation activity. These data suggest that other functions of Meq affect MDV virulence. These data improve our understanding of the mechanisms underlying the evolution of MDV virulence.