These results suggest that HBV genomic mutations, serum viral loads and titers of anti-HBc-IgM might be predictive of the efficacy of IFN therapy. These clinical findings should be further investigated by in vivo and in vitro experiments.
Soybean mosaic virus (SMV) is one of the most widespread and devastating viral diseases worldwide. The genetic architecture of qualitative resistance to SMV in soybean remains unclear. Here, the Rsvg2 locus was identified as underlying soybean resistance to SMV by genome-wide association and linkage analyses. Fine mapping results showed that soybean resistance to SMV strains G2 and G3 was controlled by a single dominant gene, GmST1, on chromosome 13, encoding a sulfotransferase (SOT). A key variation at position 506 in the coding region of GmST1 associated with the structure of the encoded SOT and changed SOT activity levels between RSVG2-S and RSVG2-R alleles. In RSVG2-S allele carrier "Hefeng25", the overexpression of GmST1 carrying the RSVG2-R allele from the SMV-resistant line "Dongnong93-046" conferred resistance to SMV strains G2 and G3. Compared to Hefeng25, the accumulation of SMV was decreased in transgenic plants carrying the RSVG2-R allele. SMV infection differentiated both the accumulation of jasmonates and expression patterns of genes involved in jasmonic acid (JA) signalling, biosynthesis and catabolism in RSVG2-R and RSVG2-S allele carriers. This characterization of GmST1 suggests a new scenario explaining soybean resistance to SMV.
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