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 Snail2α and Snail2β, containing 5 C2H2 at C-terminus, were identified in Procambarus clarkii. Snail2α was highly expressed in heart, gills and intestine, and Snail2β in gills, stomach and intestine. Decreased expression of Snail2α and Snail2β in gills and intestine at 6 h after White spot syndrome virus (WSSV) infection. Early WSSV replication levels are inhibited in dsSnail2α or dsSnail2β-injected crayfish compared to dsGFP-injected crayfish. The early WSSV replication levels are increased in rSnail2α or rSnail2β-injection crayfish. Further studies revealed that both Snail2α and Snail2β 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 Snail2α and Snail2β 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 Snail2α and Snail2β at early stage of WSSV infection. This study provides new insights in immune response of crayfish to WSSV escape.