A novel clip domain-containing C-type lectin from Macrobrachium rosenbergii promotes DIV1 replication.
TL;DR
Mr-clip-CTL, a clip domain-containing CTL from M. rosenbergii, is identified as a novel host factor that promotes DIV1 replication, with its pro-viral function correlated with altered AMP expression and PO activity.
Abstract
C-type lectins (CTLs) are key pattern recognition receptors in invertebrate innate immunity, but the functions of clip domain-containing CTLs in crustaceans during infection by decapod iridescent virus 1 (DIV1) remain largely unknown. Here, we identified a novel clip domain-containing CTL, Mr-clip-CTL, from Macrobrachium rosenbergii. The gene encodes a protein containing an N-terminal clip domain and two C-terminal CRDs. Mr-clip-CTL shares 77.78% amino acid identity with M. nipponense CLIP-LEC and is predominantly expressed in the stomach. Following DIV1 infection, its expression was significantly upregulated in the stomach. Using RNAi-mediated knockdown, we found that Mr-clip-CTL knockdown significantly decreased DIV1 major capsid protein (MCP) expression, indicating a positive role. Conversely, knockdown of Mr-clip-CTL significantly increased antimicrobial peptides (AMPs) expression and phenoloxidase (PO) activity, implicating a possible negative regulatory role of this protein in these immune responses, although direct regulation remains to be established. In summary, this study identifies Mr-clip-CTL, a clip domain-containing CTL from M. rosenbergii, as a novel host factor that promotes DIV1 replication, with its pro-viral function correlated with altered AMP expression and PO activity. These findings provide a potential target for antiviral research in crustaceans and open avenues for mechanistic investigation.