A novel L-type lectin was required for the multiplication of WSSV in red swamp crayfish (Procambarus clakii)

• PcL-lectin was widely expressed in the several tissues.
• PcL-lectin was downregulated expression after challenge with white spot syndrome virus (WSSV).
• PcL-lectin knockdown inhibit the replication of WSSV, and it could be rescued by injected with recombinant PcL-lectin.
• PcL-lectin may interact with VP24, an envelope protein of WSSV.

L-type lectins are involved in glycoproteins secretory pathways and are associated with many immune responses. There is growing evidence that L-type lectins are also involved in viral replication. In this study, a novel L-type lectin (named as PcL-lectin) was identified from red swamp crayfish (Procambarus clakii). Gene sequencing and phylogenetic tree analysis results showed that the PcL-lectin was a kind of endoplasmic reticulum Golgi intermediate compartment-53 (ERGIC-53). The expression level of PcL-lectin was significantly down regulated in crayfish after challenged with white spot syndrome virus (WSSV). Recombinant PcL-lectin protein facilitated the replication of WSSV in crayfish. In addition, WSSV replication was decreased when endogenous PcL-lectin was knocked down by RNA interference in crayfish. Furthermore, PcL-lectin may interact with VP24, an envelope protein of WSSV. Our results suggest that PcL-lectin may be required for the multiplication of WSSV, and will pave a new way for the developing of strategies against WSSV infection.