Regulatory effects of potassium channel blockers on potassium channel genes upon nervous necrosis virus infection in sevenband grouper Hyporthodus septumfasciatus.

Ion channels in fishes regulate the flow of important ions that play an active role in the excitation and transmission of impulses through neuronal cells. Specific housekeeping genes translates into proteins and selectively permeabilize and facilitate ion crossover transmissions. Potassium (K) channels play a crucial role in a wide range of functions such as cell volume regulation, hormone secretion, synaptic transmission and muscle contraction. The dysfunction of ion channels result in channelopathies, which hinder critical cellular activities. Recent studies have indicated that viral pathogens tend to regulate cellular ion channels for entry into host cells. Hence, the present study aimed to elucidate the role of K channels during nervous necrosis virus (NNV) infections in the sevenband grouper (Hyporthodus septumfasciatus). Real-time PCR with the standardized potassium genes revealed the downregulation of potassium two pore domain channel subfamily member - KCNK10, KCNK9, KCNK2, and KCNK1 genes post infection at both 17 °C and 25 °C whereas an upregulation was noted in the case of gill tissues. SMART analysis revealed a transmembrane region in all genes. Multiple sequence alignment using MultAlin and phylogenetic analysis revealed true homology of potassium genes with other higher vertebrates. In vitro and in vivo challenge study of NNV using Tetra ethyl ammonium (TEA) as potential drug showed inverse relation to that of viral replication and a corresponding downregulation of K channel gene expression was observed which was further confirmed by an immunofluorescence assay. These findings indicate that K channels play a crucial role during viral infection. Moreover, the observed downregulation can be related to rapid endocytosis resulting from recycling endosomes during a viral infection. Hence, further studies are warranted to better understand the role of K channel genes during NNV infection.