Arthrobacter pascens ZZ21 is a plant-beneficial, fluoranthene-degrading bacterial strain found in the rhizosphere. The production of the phytohormone indole-3-aectic acid (IAA) by ZZ21 is thought to contribute to its ability to promote plant growth and remediate fluoranthene-contaminated soil. Using genome-wide analysis combined with metabolomic and high-performance liquid chromatography-mass spectrometry (HPLC-MS) analyses, we characterized the potential IAA biosynthesis pathways in A. pascens ZZ21. IAA production increased 4.5-fold in the presence of 200 mg·L−1 tryptophan in the culture medium. The transcript levels of prr and aldH, genes which were predicted to encode aldehyde dehydrogenases, were significantly upregulated in response to exogenous tryptophan. Additionally, metabolomic analysis identified the intermediates indole-3-acetamide (IAM), indole-3-pyruvic acid (IPyA), and the enzymatic reduction product of the latter, indole-3-lactic acid (ILA), among the metabolites of ZZ21, and subsequently also IAM, ILA, and indole-3-ethanol (TOL), which is the enzymatic reduction product of indole-3-acetaldehyde, by HPLC-MS. These results suggest that the tryptophan-dependent IAM and IPyA pathways function in ZZ21.

Grass carp reovirus (GCRV), the representative strain of the species Aquareovirus C, serves as a model for studying the pathogenesis of aquareoviruses. Previously, epigallocatechin gallate (EGCG) was shown to inhibit orthoreovirus infection. The aim of this study was to test its potential in blocking infection by GCRV. We show that adhesion to the CIK (Ctenopharyngodon idellus kidney) cell surface by GCRV particles is inhibited in a dose-dependent manner by EGCG, as well as by a crude extract of green tea. We also evaluated the safety of EGCG and green tea extract using CIK cells, and the results suggest that EGCG is a promising compound that may be developed as a plant-derived small molecular therapeutic agent against grass carp hemorrhagic disease caused by GCRV infection. As the ligand for the 37/67-kDa laminin receptor (LamR), EGCG's blocking effect on GCRV attachment was associated with the binding potential of GCRV particles to LamR, which was inferred from a VOPBA assay.

Infectious bursal disease virus (IBDV) is a birnavirus that causes immunosuppressive disease in chickens. The emergence of very virulent IBDV (vvIBDV) has brought new challenges for this disease. The molecular determinants for the high pathogenicity of vvIBDV are not fully understood. Previous studies focused mostly on the VP2 protein on segment A, but recent evidence suggests that segment B also plays an important role. Previously we identified eight amino acid changes in the VP1 protein of vvIBDV. In this study, we investigated effect of amino acids substitutions in VP1 on viral replication and pathogenicity. We identified a Valine to Isoleucine substitution at amino acid position 4 (V4I) of VP1 that attenuates viral pathogenicity and reduces viral replication in SPF chickens but increases viral replication in CEF cells. This study confirms that VP1 of segment B play an important role in viral replication and pathogenicity of vvIBDV.

BackgroundGrass carp reovirus (GCRV) is responsible for viral hemorrhagic disease in cultured grass carp (Ctenopharyngon idellus). GCRV is a non-enveloped, double-stranded RNA virus in the genus Aquareovirus, of the family Reoviridae, which encodes seven structural proteins (VP1-VP7) and five nonstructural proteins (NS80, NS38, NS31, NS26, and NS16). To date, the mechanism of GCRV entry into CIK Ctenopharyngon idellus kidney (CIK) cells remains poorly understood.ResultsHere, we present a study of the GCRV internalization mechanism in CIK cells. Our results indicated that GCRV infection was inhibited by chlorpromazine, the specific inhibitor for clathrin-mediated endocytosis. Colocalization of GCRV virions with endogenous clathrin was observed during early infection by confocal microscopy. Moreover, GCRV infection of CIK cells depended on acidification of the endosome. This was indicated by significant inhibition of viral infection following prophylactic treatment with the lysosomotropic drugs chloroquine or ammonium chloride. In addition, the disturbance of dynamin activity blocked GCRV entry, which confirmed the dynamin-dependent nature of clathrin-mediated endocytosis.ConclusionOur findings suggest that GCRV might enter CIK cells via clathrin-mediated endocytosis in a pH-dependent manner. Additionally, dynamin is critical for efficient viral entry.Electronic supplementary materialThe online version of this article (doi:10.1186/s12985-016-0485-7) contains supplementary material, which is available to authorized users.