Synergistic Immunosuppression of Avian Leukosis Virus Subgroup J and Infectious Bursal Disease Virus Is Responsible for Enhanced Pathogenicity

文献类型： 外文期刊

第一作者： Chen, Weiguo

作者： Chen, Weiguo;Chen, Sheng;Nie, Yu;Li, Wenxue;Li, Hongxin;Zhang, Xinheng;Xie, Qingmei;Chen, Weiguo;Chen, Sheng;Nie, Yu;Li, Wenxue;Li, Hongxin;Zhang, Xinheng;Xie, Qingmei;Chen, Weiguo;Chen, Sheng;Nie, Yu;Li, Wenxue;Li, Hongxin;Zhang, Xinheng;Xie, Qingmei;Chen, Weiguo;Chen, Sheng;Nie, Yu;Li, Wenxue;Li, Hongxin;Zhang, Xinheng;Chen, Feng;Xie, Qingmei;Chen, Weiguo;Chen, Sheng;Chen, Feng;Xie, Qingmei

作者机构：

关键词： Avian Leukosis Virus Subgroup J (ALV-J); Infectious Bursal Disease Virus (IBDV); superinfection; pathogenicity; immunosuppression; lymphocyte subsets

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 10 期

页码：

收录情况： SCI

摘要： In recent years, superinfections of avian leukosis virus subgroup J (ALV-J) and infectious bursal disease virus (IBDV) have been frequently observed in nature, which has led to the increasing virulence in infected chickens. However, the reason for the enhanced pathogenicity has remained unclear. In this study, we demonstrated an effective candidate model for studying the outcome of superinfections with ALV-J and IBDV in cells and specific-pathogen-free (SPF) chicks. Through in vitro experiments, we found that ALV-J and IBDV can establish the superinfection models and synergistically promote the expression of IL-6, IL-10, IFN-alpha, and IFN-gamma in DF-1 and CEF cells. In vivo, the weight loss, survival rate, and histopathological observations showed that more severe pathogenicity was present in the superinfected chickens. In addition, we found that superinfections of ALV-J and IBDV synergistically increased the viral replication of the two viruses and inflammatory mediator secretions in vitro and in vivo. Moreover, by measuring the immune organ indexes and blood proportions of CD3(+), CD4(+), and CD8 alpha(+) cells, our results showed that the more severe instances of immunosuppression were observed in the superinfected chickens. In the present study, we concluded that the more severe immunosuppression induced by the synergistic viral replication of ALV-J and IBDV is responsible for the enhanced pathogenicity.

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