Spring viraemia of carp virus (SVCV) can cause a high mortality in common carp (Cyprinus carpio), and its main
pathological processes include the inflammatory response. However, the detailed mechanism is still unclear.
Reactive oxygen species (ROS) have been shown to play critical roles in the immune response, including
inflammation, in different models. Our previous studies have demonstrated that SVCV
infection results in the accumulation of ROS, including H2O2, in
epithelioma papulosum cyprini (
EPC) cells. In this study, we aimed to explore the relationship between H2O2 accumulation and
inflammation during SVCV
infection. After
EPC cells were infected with SVCV, the expression levels of the inflammatory factors
tumor necrosis factor (TNF)-α,
cyclooxygenase (COX)-2, and
interleukin (IL)-8 were up-regulated, while the expression of the anti-inflammatory factor
interleukin (IL)-10 was down-regulated, compared with that in mock-infected
EPC cells. The
antioxidant N-acetyl-l-cysteine (NAC) could dampen the increased TNF-ɑ and COX-2 expression induced by SVCV and H2O2, suggesting a relationship between ROS accumulation and
inflammation during SVCV
infection. Dual
luciferase reporter assays demonstrated that SVCV could not activate the NF-κB pathway. In addition, inhibition of NF-κB by
pyrrolidine dithiocarbamate (
PDTC) treatment had no effect on the expression of inflammatory factors. Furthermore, inhibition of the ERK, JNK, and p38MAPK signaling pathways by
U0126,
SP600125, and
SB203580, respectively, reduced the expression of TNF-ɑ, COX-2, and
IL-8, indicating that these three signaling pathways were all involved in the inflammatory response after SVCV
infection. In addition, the PI3K signaling pathway was involved in the expression of the
chemokine IL-8 in the SVCV-induced inflammatory response. We also showed that inhibition of the MAPK or PI3K signaling pathway facilitated the expression of SVCV-G as well as increased the SVCV viral titer. Altogether these results reveal the mechanism of the SVCV-mediated inflammatory response. Thus, targeting these signaling pathways may provide novel treatment strategies for SVCV-mediated diseases.