Viral nervous necrosis virus persistently replicates in the central nervous system of asymptomatic gilthead seabream and promotes a transient inflammatory response followed by the infiltration of IgM+ B lymphocytes

The viral nervous necrosis virus (VNNV) is the causal agent of viral encephalopathy and retinopathy (VER), a worldwide fish disease that is responsible for high mortality in both marine and freshwater species. Infected fish suffer from encephalitis, which leads to abnormal swimming behavior and extensive cellular vacuolation and neuronal degeneration in the central nervous system (CNS) and retina. The marine fish gilthead seabream (Sparus aurata) does not develop VER but it is an asymptomatic carrier of VNNV. In this study, we report that VNNV was able to replicate and persist for up to 3 months in the CNS of the gilthead seabream without causing any neural damage. In addition, we found an early inflammatory response in the CNS that was characterized by the induction of genes encoding pro-inflammatory cytokines, a delayed but persistent induction of anti-inflammatory cytokines, and the infiltration of IgM+ B lymphocytes, suggesting that local adaptive immunity played a major role in the control of VNNV in the CNS of this species.

► VNNV is able to replicate and persist for up to 3 months in the seabream CNS.
► VNNV does not cause any neural damage.
► VNNV infection results in an early inflammatory response in the CNS.
► The early inflammatory response is followed by an anti-inflammatory phase.
► VNNV infection promotes the infiltration of IgM+ B lymphocytes in the CNS.