Mass mortality in bivalves and the intricate case of the Pacific oyster, Crassostrea gigas.

Massive mortality outbreaks in cultured bivalves have been reported worldwide and they have been associated with infection by a range of viral and bacterial pathogens. Due to their economic and social impact, these episodes constitute a particularly sensitive issue in Pacific oyster (Crassostrea gigas) production. Since 2008, mortality outbreaks affecting C.

Dual transcriptomics of virus-host interactions: comparing two Pacific oyster families presenting contrasted susceptibility to ostreid herpesvirus 1.

Background: Massive mortality outbreaks affecting Pacific oyster (Crassostrea gigas) spat in various countries have been associated with the detection of a herpesvirus called ostreid herpesvirus type 1 (OsHV-1). However, few studies have been performed to understand and follow viral gene expression, as it has been done in vertebrate herpesviruses. In this work, experimental infection trials of C.

Genotyping of a microsatellite locus to differentiate clinical Ostreid herpesvirus 1 specimens.

Ostreid herpesvirus 1 (OsHV-1) is a DNA virus belonging to the Malacoherpesviridae family from the Herpesvirales order. OsHV-1 has been associated with mortality outbreaks in different bivalve species including the Pacific cupped oyster, Crassostrea gigas. Since 2008, massive mortality events have been reported among C.

Dengue virus type 2 infections of Aedes aegypti are modulated by the mosquito's RNA interference pathway.

A number of studies have shown that both innate and adaptive immune defense mechanisms greatly influence the course of human dengue virus (DENV) infections, but little is known about the innate immune response of the mosquito vector Aedes aegypti to arbovirus infection. We present evidence here that a major component of the mosquito innate immune response, RNA interference (RNAi), is an important modulator of mosquito infections. The RNAi response is triggered by double-stranded RNA (dsRNA), which occurs in the cytoplasm as a result of positive-sense RNA virus infection, leading to production of small interfering RNAs (siRNAs).