Effects on viral suppression and the early-immune expression of ribavirin against spring viremia of carp virus in vitro

Spring viremia of carp virus (SVCV) is a globally distributed virus that causes severe clinical symptoms and high mortality in fish belonging to the families Cyprinidae and Siluridae. To protect the host against viral infection, understanding the relatedness between viral susceptibility and antiviral mechanisms must be crucial. Thus, we evaluated the viral suppression efficacy of ribavirin by measuring the transcription levels of viral and immune genes in vitro. The results showed that following ribavirin treatment after SVCV infection (MOI 0.1), ribavirin inhibited SVCV replication in epithelioma papulosum cyprini (EPC) cells and completely inhibited viral gene (G and N) expression at concentrations above 10 mu g/mL at 48 h post-infection. Ribavirin does not directly damage SVCV particles but inhibits early viral replication. In the absence of SVCV infection, the immunological dynamics triggered by ribavirin resulted in upregulated pattern recognition receptors and proinflammatory cytokinerelated genes (i.e., PI3K, MYD88, IRAK1, RIG-CYRILLIC CAPITAL LETTER BYELORUSSIAN-UKRAINIAN I, MAVS, Mx1, TNF-alpha, and NF-kappa B). Furthermore, EPC cells treated with ribavirin following SVCV infection showed upregulation of PI3K, MYD88, IRAK1, RIG-CYRILLIC CAPITAL LETTER BYELORUSSIAN-UKRAINIAN I, TNF-alpha, and NF-kappa B genes within 24 h post-SVCV infection, suggesting that ribavirin positively inhibits the SVCV infection in vitro.