Siripong ThitamadeeJiraporn SrisalaSuparat TaengchaiyaphumKallaya SritunyalucksanaMahidol UniversityThailand National Center for Genetic Engineering and Biotechnology2018-11-092018-11-092014-01-01Fish and Shellfish Immunology. Vol.40, No.2 (2014), 478-48410959947105046482-s2.0-84908343871https://repository.li.mahidol.ac.th/handle/123456789/33145In our research efforts to reduce the impact of white spot syndrome virus (WSSV) disease outbreaks in shrimp aquaculture, we studied the effect of β-glucan administration to activate the prophenoloxidase (proPO) enzymatic cascade prior to WSSV challenge. Injection of a single dose of β-glucan (5μg/g) prior to WSSV challenge resulted in activation of the proPO system and reduced shrimp mortality (25-50%) when compared to controls (100%). By contrast, no significant reduction was observed using yellow head virus (YHV) in a similar protocol. We subsequently hypothesized that administration of a second dose of β-glucan after WSSV challenge might reduce shrimp mortality further. Surprisingly, the opposite occurred, and mortality of the WSSV-infected shrimp increased to 100% after the second β-glucan dose. Both immunofluorescence and RT-PCR assays revealed low WSSV levels in hemocytes of shrimp collected after the second dose of β-glucan administration, suggesting that the cause of increased mortality was unlikely to be increased WSSV replication. We found from measured phenoloxidase acitivity (PO) and H<inf>2</inf>O<inf>2</inf> production that the higher mortality may have resulted from a combination of WSSV infection plus over-production of reactive oxygen species (ROS) stimulated by two doses of β-glucan. Thus, caution may be prudent in continuous or prolonged activation of the shrimp immune system by β-glucan administration lest it exacerbate shrimp mortality in the event of WSSV infection. © 2014 Elsevier Ltd.Mahidol UniversityAgricultural and Biological SciencesEnvironmental ScienceMedicineDouble-dose β-glucan treatment in WSSV-challenged shrimp reduces viral replication but causes mortality possibly due to excessive ROS productionArticleSCOPUS10.1016/j.fsi.2014.07.033