The role of Litopenaeus vannamei p38 in white spot syndrome virus infection

• Three closely related p38 MAPK homologues were cloned from Litopenaeus vannamei.
• Three isoforms differ only in an internal 25-amino acid sequence.
• lvp38a, lvp38b and lvp38c have different tissue expression patterns.
• The activation of lvp38 took place in WSSV infection.
• Silencing lvp38 promoted WSSV replication at the early stage.

p38 as a member of MAPK family, has been conversed from yeast to mammals. It has been implicated in numerous biological processes, including the responses to stress and inflammation. In this study, three closely related p38 MAPK homologs, lvp38a, lvp38b and lvp38c, which differ only in an internal 25-amino acid sequence, have been cloned from Litopenaeus vannamei. Three isoforms shared p38 conserved TGY motif and catalytic center, as well as had maximum identities to human p38α and Drosophila p38b. Tissue distribution revealed that lvp38a and lvp38b were ubiquitously expressed in most tissues, while lvp38c showed at relatively low levels and in a tissue-specific manner. Western blotting analysis showed that lvp38 was activated by phosphorylation during WSSV infection. Furthermore, silencing lvp38 mediated by specific dsRNA in shrimps promoted white spot syndrome virus (WSSV) replication and viral gene transcription at the early stage. These results demonstrated that lvp38 was involved in WSSV infection and might participate in host defense at the early stage.