The influence of temperature on viral replication and antiviral-related genes response in hirame rhabdovirus-infected flounder (Paralichthys olivaceus)

Hirame rhabdovirus (HIRRV) is a rhabdovirus that causes severe disease in fish. The mortality due to HIRRV infection occurs at temperatures below 15 degrees C, but no mortality is observed over 20 degrees C. In this study, Japanese flounder (Paralichthys olivaceus) was artificially infected with the HIRRV CNPo2015 strain at 10 degrees C or 20 degrees C. Absolute quantitative real-time PCR was employed to examine the viral replication in spleens after HIRRV infection. Expression profiles of four interferon-related genes (type I IFN, Mx, ISG15, MDA5) and two proinflammatory genes (TNF-alpha and IL-1 beta) were also investigated by quantitative real-time PCR. Results showed that viral Copies in spleens increased gradually over time and peaked at 72 h post infection (hpi) in the 10 degrees C group, while viral Copies in the 20 degrees C group increased within 24 hpi, but afterwards decreased to very low levels. Moreover, the expressions of IFNs in the 10 degrees C group reached the highest levels at 72 hpi, whereas their peak levels appeared much earlier in the 20 degrees C group, at 12 hpi. The expression levels of TNF-alpha and IL-1 beta in the 10 degrees C group peaked at 12 hpi and then quickly declined. However, the two genes were highly expressed during 6-24 hpi in the 20 degrees C group. Based on these findings, we concluded that HIRRV infection induced an efficient antiviral immune response at 20 degrees C, which might inhibit the viral transcription at early stages and finally prevent HIRRV infection. (C) 2017 Elsevier Ltd. All rights reserved.