<p>Spring viremia of carp virus (SVCV) is highly lethal in common carp (<i>Cyprinus carpio</i>) and other cyprinid fish species. In this study, we evaluated the effect of the SVCV phosphoprotein (P protein) on the virulence of snakehead rhabdovirus (SHRV) by generating a recombinant SHRV expressing the SVCV P protein. The SVCV P gene was inserted between the N and P genes of the SHRV genome, resulting in the generation of rSHRV-A-Psvcv, which contains not only its own P gene but also the P gene of SVCV. In preliminary experiments, we determined the minimum titer of SHRV that was lethal in zebrafish (<i>Danio rerio</i>). We then conducted experiments using titers below this threshold to assess the <i>in vivo</i> virulence of rSHRV-A-Psvcv in zebrafish. Under these conditions, no mortality was observed in fish infected with rSHRV-A-eGFP, a modified SHRV containing the enhanced green fluorescent protein (eGFP) gene between the N and P genes, which was used as a control. However, fish infected with rSHRV-A-Psvcv exhibited mortality accompanied by hemorrhage and ophthalmia. In a minigenome assay, the SVCV P protein failed to induce reporter protein expression when co-expressed with the SHRV N and L proteins, suggesting that the SVCV P protein is unable to form a ribonucleoprotein complex with SHRV N and L proteins. Therefore, the enhanced virulence of rSHRV-A-Psvcv resulting from the addition of the SVCV P gene can probably be attributed to the intrinsic properties of the SVCV P protein itself. Epithelioma papulosum cyprini (EPC) cells infected with rSHRV-A-Psvcv exhibited significantly lower type I interferon (IFN) responses compared to those infected with rSHRV-A-eGFP, suggesting that the SVCV P protein expressed by the recombinant SHRV inhibits type I IFN responses. Thus, the immune-suppressive activity of the SVCV P protein might be one of the causes of the enhanced virulence of rSHRV-A-Psvcv.</p>