Sirikwan PonprateepKornsunee PhiwsaiyaAnchalee TassanakajonVichien RimphanitchayakitChulalongkorn UniversityMahidol UniversityThailand National Center for Genetic Engineering and Biotechnology2018-10-192018-10-192013-09-01Fish and Shellfish Immunology. Vol.35, No.3 (2013), 957-96410959947105046482-s2.0-84882897048https://repository.li.mahidol.ac.th/handle/20.500.14594/30983White spot syndrome (WSS) is a viral disease caused by white spot syndrome virus (WSSV) which leads to severe mortality in cultured penaeid shrimp. In response to WSSV infection in Penaeus monodon, a Kazal serine proteinase inhibitor SPI. Pm2, normally stored in the granules of granular and semi-granular hemocytes is up-regulated and found to deter the viral replication. By using yeast two-hybrid screening, we have identified a viral target protein, namely WSV477. Instead of being a proteinase, the WSV477 was reported to be a Cys2/Cys2-type zinc finger regulatory protein having ATP/GTP-binding activity. Invitro pull down assay confirmed the protein-protein interaction between rSPI. Pm2 and rWSV477. Confocal laser scanning microscopy demonstrated that the SPI. Pm2 and WSV477 were co-localized in the cytoplasm of shrimp hemocytes. Using RNA interference, the silencing of WSV477 resulted in down-regulated of viral late gene VP28, the same result obtained with SPI. Pm2. In this instance, the SPI. Pm2 does not function as proteinase inhibitor but inhibit the regulatory function of WSV477. © 2013 Elsevier Ltd.Mahidol UniversityAgricultural and Biological SciencesEnvironmental ScienceInteraction between Kazal serine proteinase inhibitor SPIPm2 and viral protein WSV477 reduces the replication of white spot syndrome virusArticleSCOPUS10.1016/j.fsi.2013.07.009