Abstract: The hemolymph coagulation was inhibited after white spot syndrome virus (WSSV) and decapod iridescent virus 1 (DIV1) infection in Litopenaeus vannamei. In this study, the role of clotting reaction genes in antiviral immunity was investigated. The expression of LvTGI, LvTGII and LvCP was assessed by qPCR after virus-stimulated to explore the interaction between clotting reaction genes and virus infection. RNAi was performed to further explore the function of LvTGI and LvTGII in antiviral immunity. It showed that the expression of LvTGI, LvTGII and LvCP could respond to WSSV and DIV1 infection, which were induced or inhibited in gills and hepatopancreas. Besides, knockdown of LvTGI and LvTGII by RNAi suppressed shrimp hemolymph coagulation, indicating that LvTGI and LvTGII play an important role in the clotting system. Silencing of LvTGI and LvTGII resulted in a higher cumulative mortality observed in virus infected shrimp, thus rendering shrimp more susceptibility to WSSV and DIV1. These results provided some insights into the interplay between the coagulation system and viral infection in shrimp.

Key words: Litopenaeus vannamei, hemolymph coagulation, WSSV, DIV1, antiviral immunity