畜牧兽医学报 ›› 2022, Vol. 53 ›› Issue (6): 1895-1904.doi: 10.11843/j.issn.0366-6964.2022.06.023

• 基础兽医 • 上一篇    下一篇

两株不同J亚群禽白血病毒株诱发组织增生病变和细胞因子表达的比较

刘俊宏, 赵月, 李宏梅, 王莹, 王沫宇, 成子强, 邱建华, 侯秋玲*, 郭慧君*   

  1. 山东省动物生物工程与疾病防治重点实验室 山东省畜禽疫病防治工程技术研究中心 山东农业大学动物科技学院,泰安 271018
  • 收稿日期:2021-06-03 出版日期:2022-06-23 发布日期:2022-06-25
  • 通讯作者: 郭慧君,主要从事动物感染免疫研究,E-mail: hjguo@sdau.edu.cn;侯秋玲,主要从事动物发育及其调控研究,E-mail: houql@sdau.edu.cn
  • 作者简介:刘俊宏(1995-),男,重庆垫江人,硕士生,主要从事家禽免疫调控研究,1299315108@qq.com;赵月(1997-),女,内蒙古赤峰人,硕士生,主要从事家禽免疫调控研究,1316548557@qq.com
  • 基金资助:
    山东省自然科学基金(ZR2019MC044);山东省重大技术集成重点研发项目(2019JZZY010735);国家重点研发专项(2016YFD0500800);山东省“双一流”奖补资金

Comparison of Tissue Hyperplasia Lesions and Cytokines' Expressions Induced by Two Different Avian Leukosis Virus Subgroup J Strains

LIU Junhong, ZHAO Yue, LI Hongmei, WANG Ying, WANG Moyu, CHENG Ziqiang, QIU Jianhua, HOU Qiuling*, GUO Huijun*   

  1. College of Animal Science and Veterinary Medicine, Shandong Agricultural University, Shandong Key Laboratory of Animal Biotechnology and Disease Control and Prevention, Shandong Research Center of Animal Disease Control and Prevention, Tai 'an 271018, China
  • Received:2021-06-03 Online:2022-06-23 Published:2022-06-25

摘要: 旨在比较ALV-J-SD1005毒株和ALV-J-NX0101毒株感染鸡只致病性、诱发先天性免疫因子和致肿瘤因子表达的差异,用感染剂量为103TCID50的两株病毒分别颈部皮下接种75只1日龄海兰褐鸡,感染后7、14、21 d检测体重、肿瘤病变、死亡率、血液和皮下纤维组织中病毒含量以及肝中鸡TRIM25、MDA5、IRF7、IFN-α/β、14-3-3σP53、STAT1等免疫因子或肿瘤因子的mRNA表达量。结果显示,雏鸡感染ALV-J-SD1005毒株后最早于第10天出现纤维组织增生,14 d致纤维组织增生率为100%(18/18),死亡率为5.2%(1/19);随着感染日龄的增加,增生组织指数和死亡率不断升高,21 d时分别达34.4%(74.5/209.5)和58.3%(7/12)。血液和皮下纤维组织的病毒载量显著升高;同时,显著上调鸡肝中MDA5、IRF7、P53等基因的表达量,下调IFN-α/β和14-3-3σ基因的表达量;而鸡TRIM25基因呈现感染早期(7 d)表达显著下调,后期(14~21 d)表达显著上调。ALV-J-NX0101毒株感染后21 d未检测到肿瘤发生,也没有鸡只死亡,但见鸡血液等组织中病毒载量显著增多,鸡TRIM25、MDA5、IRF7、IFN-βIFN-α基因表达显著下降,STAT1基因表达显著上调。上述结果可以看出,ALV-J-SD1005毒株与ALV-J-NX0101毒株在感染鸡体内诱发不同的抗病毒反应和抗肿瘤反应,导致产生明显不同的病毒增殖和致病特点。本研究为深入理解两株ALV-J病毒致肿瘤机制、探索新诊断标识提供重要科学依据。

关键词: ALV-J, 鸡, 纤维组织增生, 细胞增殖相关因子, TRIM25

Abstract: The aim of this study was to compare the differences of pathogenicity, innate immune factors and oncogenic factors expressions of chickens induced by two different avian leukosis virus subgroup J (ALV-J) strains. Seventy-five 1-day-old chickens were inoculated with 103 TCID50 acute fibrosarcoma ALV-J strain (ALV-J-SD1005), 103 TCID50 myeloma ALV-J strain (ALV-J-NX0101), and same dose sterile PBS saline. The body weight, tissue hyperplasia lesions, mortality, viral loads in blood and subcutaneous fibrous tissues, innate immune factors (MDA5, IRF7, IFN-α/β) and cell proliferation-related factors (TRIM25, P53, 14-3-3σ, STAT1) of the infected chickens were detected at 7 days post inoculation (dpi), 14 dpi, 21 dpi. The results showed that the fibrosarcoma in ALV-J-SD1005 group was firstly observed at 10 dpi, the fibrosarcoma incidence was 100% (18/18) and mortality was 5.2% (1/19) at 14 dpi, and the sarcoma index and the mortality increased continuously from 14 dpi to 21 dpi, and respectively reached 34.4%(74.5/209.5) and 58.3% (7/12) at 21 dpi. Viral loads in blood and subcutaneous fibrous tissues were also significantly increased. Meanwhile, the mRNA expressions of MDA5, IRF7, P53 in the livers were significantly up-regulated, and the mRNA expressions of IFN-α/β and 14-3-3σ genes were significantly down-regulated, while chicken TRIM25 was significantly down-regulated at the early stage of virus infection (at 7 dpi), and significantly up-regulated at the late stage (14~21 dpi). In ALV-J-NX0101 group, the tissue hyperplasia lesions and death were not observed within 21 days after infection, but the viral loads increased significantly, the mRNA expressions of TRIM25, MDA5, IRF7 and IFN-α/β genes were decreased significantly, and the expression of STAT1 gene was up-regulated significantly. It can be concluded that ALV-J-SD1005 strain and ALV-J-NX0101 strain can cause significantly different antiviral immune responses and antitumor responses during their infections, which result into dramatically different virus proliferation and pathogenicity. This study provides scientific basis for further undestanding the tumorigenic mechanism of two ALV-J viruses and exploring new diagnostic markers.

Key words: ALV-J, chicken, fibrous tissue hyperplasia, cell proliferation-related factors, TRIM25

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