Wang Wei, Pan Changkun, Huang Zongliang, Yuan Huifang, Chen Jianming
Institute of Oceanography, Minjiang University, Fuzhou, Fujian, 350108, China.
Technology and Data Department of Technology Center, PoolingMed Co., Ltd., Hangzhou, Zhejiang, 310053, China.
Dev Comp Immunol. 2019 Mar;92:20-28. doi: 10.1016/j.dci.2018.11.003. Epub 2018 Nov 7.
The Janus kinase/signal transducers and activators of transcription (JAK/STAT) pathway plays a critical role in host defense against viral infections. Here, we report the use of the Drosophila model system to investigate the modulation of the JAK/STAT pathway by the white spot syndrome virus (WSSV) protein WSV181. WSV181 overexpression in transgenic flies resulted in the downregulation of STAT92E and STAT92E-targeted genes. This result indicates that WSV181 can suppress JAK/STAT signaling by controlling STAT92E expression. An infection experiment was carried out on transgenic Drosophila infected with Drosophila C virus and on Litopenaeus vannamei injected with recombinant WSV181 and WSSV. The increased viral load and suppressed transcript levels of JAK/STAT pathway components indicate that WSV181 can promote viral proliferation by inhibiting the JAK/STAT pathway. This study provided evidence for the role of WSV181 in viral replication and revealed a new mechanism through which WSSV evades host immunity to maintain persistent infection.
Janus激酶/信号转导子和转录激活子（JAK/STAT）通路在宿主抵御病毒感染中起关键作用。在此，我们报道利用果蝇模型系统研究白斑综合征病毒（WSSV）蛋白WSV181对JAK/STAT通路的调控。转基因果蝇中WSV181的过表达导致STAT92E及其靶向基因的下调。这一结果表明WSV181可通过控制STAT92E的表达来抑制JAK/STAT信号传导。对感染果蝇C病毒的转基因果蝇以及注射重组WSV181和WSSV的凡纳滨对虾进行了感染实验。病毒载量增加以及JAK/STAT通路组分的转录水平受到抑制，表明WSV181可通过抑制JAK/STAT通路促进病毒增殖。本研究为WSV181在病毒复制中的作用提供了证据，并揭示了WSSV逃避宿主免疫以维持持续感染的新机制。
