Peng Duo, Hu Xiaoyang, Huang Jingjing, Li Qiong, Song Yinuo, Zhang Dabing
National Key Laboratory of Veterinary Public Health and Safety, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, People's Republic of China.
Key Laboratory of Animal Epidemiology of the Ministry of Agriculture and Rural Affairs, College of Veterinary Medicine, China Agricultural University, Beijing, 100193, People's Republic of China.
Arch Virol. 2025 Sep 24;170(10):211. doi: 10.1007/s00705-025-06384-5.
The roles of RIG-I, MDA5, and TLR7 in duck hepatitis A virus genotype 3 (DHAV-3) infection were investigated using duck embryo fibroblasts (DEFs). DHAV-3 infection induced significant upregulation of RIG-I, MDA5, and TLR7 and high IFN-β, IL-6, and OASL responses. Overexpression and knockdown of RIG-I, MDA5, and TLR7 exerted significant effects on DHAV-3-induced IFN-β, IL-6, and OASL expression and DHAV-3 replication. Overexpression and inhibition of TLR7 altered DHAV-3-induced RIG-I and MDA5 expression. Together, these findings suggest that TLR7 and RIG-I/MDA5 play a coordinated role in detection and initiation of innate immunity against DHAV-3 infection.
利用鸭胚成纤维细胞（DEFs）研究了视黄酸诱导基因I（RIG-I）、黑色素瘤分化相关基因5（MDA5）和Toll样受体7（TLR7）在鸭甲型肝炎病毒3型（DHAV-3）感染中的作用。DHAV-3感染可显著上调RIG-I、MDA5和TLR7的表达，并引发较高的干扰素-β（IFN-β）、白细胞介素-6（IL-6）和2'-5'-寡腺苷酸合成酶样蛋白（OASL）应答。RIG-I、MDA5和TLR7的过表达和敲低对DHAV-3诱导的IFN-β、IL-6和OASL表达以及DHAV-3复制产生显著影响。TLR7的过表达和抑制改变了DHAV-3诱导的RIG-I和MDA5表达。这些研究结果共同表明，TLR7与RIG-I/MDA5在针对DHAV-3感染的天然免疫检测和启动过程中发挥协同作用。
