White spot syndrome virus achieves early infection through Snail2 suppression of Relish nuclear translocation

In vertebrates, Snails are evolutionarily conserved and consist of 4-6 Cys2-His2 (C2H2)-Zinc finger domains. The key role of the Snails is well illustrated in cancer, but its role in immunity is limited. Two Snail2 genes, named Snail2 alpha and Snail2 beta, containing 5 C2H2 at C-terminus, were identified in Procambarus clarkii. Snail2 alpha was highly expressed in heart, gills and intestine, and Snail2 beta in gills, stomach and intestine. Decreased expression of Snail2 alpha and Snail2 beta in gills and intestine at 6 h after White spot syndrome virus (WSSV) infection. Early WSSV replication levels are inhibited in dsSnail2 alpha or dsSnail2 beta-injected crayfish compared to dsGFP-injected crayfish. The early WSSV replication levels are increased in rSnail2 alpha or rSnail2 beta-injection crayfish. Further studies revealed that both Snail2 alpha and Snail2 beta regulate the nuclear translocation of Relish. Relish entry into the nucleus promotes the expression of the WSSV immediate-early genes ie1 and ie15. WSSV abducts the host Snail2 alpha and Snail2 beta in an unknown manner, facilitating the nuclear translocation of Relish and inducing ie1 and ie15 transcription. Crayfish responds to this escape mechanism of WSSV by reducing the expression of Snail2 alpha and Snail2 beta at early stage of WSSV infection. This study provides new insights in immune response of crayfish to WSSV escape.

Automated summary

This study reveals the crucial role of Snail2 alpha and Snail2 beta in the immune response of crayfish against White spot syndrome virus (WSSV). The research shows that WSSV induces the transcription of immediate-early genes ie1 and ie15 through the nuclear translocation of Snail2 alpha and Snail2 beta. However, crayfish responds to WSSV escape by reducing the expression of these two proteins.