| 论文题目: | Infection of goats with goatpox virus triggers host antiviral defense through activation of innate immune signaling |
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| 作者: | Zeng Xiancheng, Wang Song, Chi Xiaojuan, Chen Shi-Long, Huang Shile, Lin Qunqun, Xie Baogui*, and Chen Ji-Long*. |
| 联系作者: | |
| 刊物名称: | Res Vet Sci |
| 期: | |
| 卷: | 104 |
| 页: | 40-9 |
| 年份: | 2016 |
| 影响因子: | 1.517 |
| 论文下载: | 下载地址 |
| 摘要: | Goatpox, caused by goatpox virus (GTPV), is one of the most serious infectious diseases associated with high morbidity and mortality in goats. However, little is known about involvement of host innate immunity during the GTPV infection. For this, goats were experimentally infected with GTPV. The results showed that GTPV infection significantly induced mRNA expression of type I interferon (IFN)-alpha and IFN-beta in peripheral blood lymphocytes, spleen and lung. In addition, GTPV infection enhanced expression of several inflammatory cytokines, including interleukin (IL)-1beta, IL-6, IL-18; and tumor necrosis factor-alpha (TNF-alpha). Strikingly, infection with GTPV activated signal transducers and activators of transcription 3 (STAT3), a critical cytokine signaling molecule. Interestingly, the virus infection induced expression of suppressor of cytokine signaling (SOCS)-1. Importantly, the infection resulted in an increased expression of some critical interferon-stimulated genes, such as interferon-induced transmembrane protein (IFITM) 1, IFITM3, interferon stimulated gene (ISG) 15 and ISG20. Furthermore, we found that infection with GTPV up-regulated expression of Toll-like receptor (TLR) 2 and TLR9. These results revealed that GTPV infection activated host innate immune signaling and thereby triggered antiviral innate immunity. The findings provide novel insights into complex mechanisms underlying GTPV-host interaction and pathogenesis of GTPV. |
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