Spring Viraemia of Carp Virus Infection Activates Carp IL-10 Expression Through JAK-STAT, NF-κB and p38 MAPK Mapk Pathways
SSRN, ISSN: 1556-5068
2023
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Article Description
Interleukin-10 (IL-10) is a pleiotropic cytokine with both immune enhancement and immunosuppression, but the main role is immunosuppression and anti-inflammatory ability. In order to use the immunosuppressive function of IL-10, many viruses can evade the host's immune surveillance and clearance by increasing the expression of host IL-10, such as SARS-CoV-2, Hepatitis B virus, EB virus. However, it has not been reported whether aquatic animal virus infection can up-regulate the expression of host IL-10 and the mechanisms behind these effects still unknown. Spring viraemia of carp (SVC) is a fatal viral disease for many fish species, which was caused by spring viraemia of carp virus (SVCV). This disease has caused significant economic losses in aquaculture industry worldwide. In this study, the expression kinetics of carp IL-10 in SVCV-infected Epithelioma papulosum cyprinid (EPC) cells, carp head kidney (cHK) primary cells and common carp tissues was analyzed by RT-PCR and ELISA. The results showed that SVCV infection induced carp IL-10 mRNA and protein expression both in vitro and in vivo. Treated with specific inhibitors demonstrated that JAK-STAT, NF-κB and p38MAPK (mitogen-activated protein kinase) were required for SVCV-induced carp IL-10 expression. Furthermore, inhibition of various molecules of the JAK-STAT signaling pathway demonstrated that JAK1, JAK2, JAK3, TYK2 and STAT5 play an important role in carp IL-10 expression during SVCV infection. Taken together, SVCV infection significantly induced carp IL-10 expression and this induction depends on JAK-STAT, NF-κB and p38MAPK pathways. To our knowledge, this is the first time reported that fish-infections virus up-regulated host IL-10 expression through JAK-STAT, NF-κB and p38MAPK pathways. Altogether, fish viruses may have a similar mechanism as human or other mammal viruses to escape host immune surveillance and clearance.
Bibliographic Details
Elsevier BV
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