Infectious Spleen and Kidney Necrosis Virus (ISKNV) is the causative agent of a fatal disease in many fish species, resulting in mass mortalities and significant economic losses. Since its introduction to Ghana in late 2018, in the absence of effective vaccines, the crude practice of heat-shock treatment (HST) on deliberately exposed cultured tilapia fingerlings was widely adopted by farmers to control the disease in Ghana with some apparent success. This study investigated the interplay between the expression of heat shock protein (HSPs) and viral replication during ISKNV infection.
An in vitro experimental challenge study which involved deliberate infection and subsequent exposure of primary Oreochromis niloticus (Tilapia) brain (TiB) cell lines at 48 hours post-infection to HST was carried out. The test groups and control groups were screened at various time points for viral proliferation and HSP markers expression using quantitative real-time PCR (qPCR).
Exposure to heat-shock significantly increased HSP 90 and 47 expressions by 4 and 6-folds respectively, with a concomitant 10-fold decrease in viral load as compared to the non-heat shock group. Viral apoptosis gene ORL005L was significantly down regulated following increase in HSPs expression.
This initial finding implies that heat-shock treatment may play an important role in suppressing viral replication through the apoptosis regulatory gene ORF005L. This information will contribute to the understanding of the beneficial effect of heat-shock therapy used in control of the viral pathogen in aquaculture. Further studies in controlled in-vivo experiments will give more clarity to the general effect of this treatment on tilapia growth and ISKNV persistence in infected fish populations.