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Lorf9 deletion significantly eliminated lymphoid organ atrophy induced by meq-deleted very virulent Marek's disease virus

文献类型： 外文期刊

作者： Sun, Aijun 1 ; Luo, Jun 2 ; Wan, Bo 1 ; Du, Yongkun 1 ; Wang, Xiangru 1 ; Weng, Haoyu 1 ; Cao, Xinru 1 ; Zhang, Tianlu 1 ; C 1 ;

作者机构： 1.Henan Agr Univ, Coll Anim Sci & Vet Med, Zhengzhou 450002, Henan, Peoples R China

2.Henan Acad Agr Sci, Henan Prov Key Lab Anim Immunol, Minist Agr, Key Lab Anim Immunol, Zhengzhou 450002, Henan, Peoples R China

关键词： Marek's disease virus; Meq; LORF9; Lymphoid organ atrophy

期刊名称：VETERINARY MICROBIOLOGY （ 影响因子：3.293； 五年影响因子：3.599 ）

ISSN： 0378-1135

年卷期： 2019 年 235 卷

页码：

收录情况： SCI

摘要： Marek's disease virus (MDV) is a highly contagious alphaherpesvirus that causes rapid onset of T cell lymphomas in chickens. MDV continues to break through vaccinal immunity due to the emergence of highly virulent field strains. Earlier studies revealed that deletion of the meq gene from MDV results in attenuated vaccines that protect against disease when chickens are infected with highly virulent strains. However, meq-deleted viruses still retain the ability to induce lymphoid organ atrophy, which raises safety concerns. In an earlier study, we found that deletion of lorf9 counteracts this lymphoid organ atrophy. Here, we describe the generation of a double deletion mutant virus lacking virus-encoded meq and lorf9. In vitro studies revealed that during replication, the mutant virus had kinetic characteristics similar to the parental virus; however, in vivo the replication capability was significantly reduced. Results of animal studies revealed no obvious MDV-specific symptoms and lesions. Importantly, the double deletion mutant virus lost the capacity to induce lymphoid organ atrophy, which has been the main obstacle during development of a good vaccine candidate.

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