Abstract
The scallop Chlamys farreri is one of the most important aquaculture species in northern coastal provinces. However, the sustainable development of scallop industry is currently threatened by a notorious pathogen named as acute viral necrobiotic virus (AVNV), which often causes mass mortality of the animals. Despite that great attention has been focused on this novel pathogen, little knowledge about the host–virus interactions is available. In this study, suppression subtractive hybridization (SSH) was employed to identify the up-regulated differentially expressed genes in the hemocytes of C. farreri challenged by AVNV. A forward subtracted cDNA library was finally constructed and 288 positive colonies representing differentially genes were screened to perform sequencing. A total of 275 ESTs were used for further analysis using bioinformatics tools after vector screening, among which 167 ESTs could be finally identified, with significant match (E values <1 × 10−3) to the deposited genes (proteins) in the corresponding databases. These genes could be classified into ten categories according to their Gene Ontology annotations of biological processes and molecular functions, i.e. cell defense and homeostasis (13.82%), cellular protein metabolic process (14.90), cellular metabolism (13.09%), cytoskeletal or cellular component (5.82%), transcription regulation or RNA processing (2.18%), cell division (meiosis)/apoptosis (2.18%), DNA metabolic process and repair (1.45%), cell adhesion/signaling (1.09%), microsatellite (0.73%), and ungrouped or unknown functions (6.88). The possible biological significance of some novel genes (mainly immune and homeostasis related genes) in the host response to AVNV were discussed. This study is the first global analysis of differentially expressed genes in hemocytes from AVNV-infected C. farreri, and in addition to increasing our understanding of the molecular pathogenesis of this virus-associated scallop disease, the results presented here should provide new insights into the molecular basis of host–pathogen interactions in C. farreri.
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