Infection of equine monocyte-derived macrophages with an attenuated equine infectious anemia virus (EIAV) strain induces a strong resistance to the infection by a virulent EIAV strain

文献类型： 外文期刊

第一作者： Ma, Jian

作者： Ma, Jian;Wang, Shan-Shan;Lin, Yue-Zhi;Liu, Hai-Fang;Liu, Qiang;Wei, Hua-Mian;Wang, Xue-Feng;Du, Cheng;Kong, Xian-Gang;Zhou, Jian-Hua;Wang, Xiaojun;Wang, Yu-Hong

作者机构：

期刊名称：VETERINARY RESEARCH （ 影响因子：3.683； 五年影响因子：4.106 ）

ISSN： 0928-4249

年卷期： 2014 年 45 卷

页码：

收录情况： SCI

摘要： The Chinese attenuated equine infectious anemia virus (EIAV) vaccine has successfully protected millions of equine animals from EIA disease in China. Given that the induction of immune protection results from the interactions between viruses and hosts, a better understanding of the characteristics of vaccine strain infection and host responses would be useful for elucidating the mechanism of the induction of immune protection by the Chinese attenuated EIAV strain. In this study, we demonstrate in equine monocyte-derived macrophages (eMDM) that EIAV(FDDV13), a Chinese attenuated EIAV strain, induced a strong resistance to subsequent infection by a pathogenic strain, EIAV(UK3). Further experiments indicate that the expression of the soluble EIAV receptor sELR1, Toll-like receptor 3 (TLR3) and interferon beta (IFN beta) was up-regulated in eMDM infected with EIAV(FDDV13) compared with eMDM infected with EIAV(UK3). Stimulating eMDM with poly I:C resulted in similar resistance to EIAV infection as induced by EIAV(FDDV13) and was correlated with enhanced TLR3, sELR1 and IFN beta expression. The knock down of TLR3 mRNA significantly impaired poly I:C-stimulated resistance to EIAV, greatly reducing the expression of sELR1 and IFN beta and lowered the level of infection resistance induced by EIAV(FDDV13). These results indicate that the induction of restraining infection by EIAV(FDDV13) in macrophages is partially mediated through the up-regulated expression of the soluble viral receptor and IFN beta, and that the TLR3 pathway activation plays an important role in the development of an EIAV-resistant intracellular environment.

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