Abstract

Genotype II of grass carp reovirus (GCRV) is an epidemic strain that is devastating to the grass carp industry in China. Infections of grass carp caused with virulent GCRV-HuNan1307 and avirulent GCRV-GD1108 isolates were carried out to determine the underlying pathogenic mechanisms. The differential host protein response was examined after infection with both virus isolates using an iTRAQ-based comparative quantitative proteomics. Differentially expressed proteins for GD1108 (34) and HuNan1307 (222) infections were identified and determined canonical pathways and functional networks involved in both GCRV infections. Infection with HuNan1307 activated the RIG-I pathway leading to antiviral response as well as the Jak-STAT pathway that governs general metabolic functions. These pathways were not activated by infection with the avirulent isolate. Infection with HuNan1307 also induced an abbreviated an intense immune response and lead to major disorders of the metabolism. In contrast, the GD1108 infection induced a mild and moderate immune response leaving basic metabolism unchanged. This study provides a comprehensive view at the protein level of the underlying pathogenic mechanisms used by a virulent GCRV type II isolate. SignificanceGenotype II of grass carp reovirus (GCRV) is an epidemic strain that is devastating to the grass carp industry in China. The unclear etiological characters, genetic variation and pathogenesis of GCRV genotype II blocked the development of techniques as well as products on prevention and control of grass carp haemorrhagic disease (GCHD). Here, iTRAQ strategy was firstly used to compare the proteomes of grass carp infected with virulent and avirulent isolates of GCRV genotype II. The obtained data showed that abbreviated and intense immune response and disorders of the metabolism were reasons for the mortality of fish infected with virulent GCRV isolate. The results would provide a train of thought to promote the development of techniques as well as products on prevention and control of GCHD.

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