Recombination analysis based on the complete genome of bocavirus

Bocavirus include bovine parvovirus, minute virus of canine, porcine bocavirus, gorilla bocavirus, and Human bocaviruses 1-4 (HBoVs). Although recent reports showed that recombination happened in bocavirus, no systematical study investigated the recombination of bocavirus. The present study performed the phylogenetic and recombination analysis of bocavirus over the complete genomes available in GenBank. Results confirmed that recombination existed among bocavirus, including the likely inter-genotype recombination between HBoV1 and HBoV4, and intra-genotype recombination among HBoV2 variants. Moreover, it is the first report revealing the recombination that occurred between minute viruses of canine

The Functional Variant in the 3'UTR of IGF1 with the Risk of Gastric Cancer in a Chinese Population

Background/Aims: IGF-1 can act as an endocrine hormone and its signaling server as essential roles in regulating tumorigenesis. Polymorphisms in IGF-1 have been reported associated bad prognosis of with human cancer, but their association with the risk of human gastric cancer (GC) has not been found so far. In this study rs6218 located in the 3'UTR of IGF-1 was selected to evaluate its relationship with the risk of GC among Chinese population. Methods: Questionnaire, SNaPshot genotype assay, real time PCR assay, cell transfection and the dual luciferase reporter assay were used in our study. Results: SNP rs6218 in IGF-1 3'-UTR was involved in the occurrence of GC by acting as a tumor promotion factor while rs6128 acting as a risk factor. SNP rs6128 was also could be regulated by miR-603 which caused an up-regulation of IGF-1 in patients with UC and CC genotype. Furthermore, the carriers of UC and CC genotype presented a big tumor size as well as the high probability of metastasis. Conclusion: In conclusion, our findings have shown that the SNP rs6218 in IGF-1 3'-UTR, through disrupting the regulatory role of miR-603 in IGF-1 expression, rs16128 in IGF-1 might act as a promotion factor in the pathogenesis of GC

LincRNA-Cox2 regulates IL6/JAK3/STAT3 and NF-κB P65 pathway activation in Listeria monocytogenes-infected RAW264.7 cells

Listeria monocytogenes (Lm) can lead to high mortality rates relative to other foodborne pathogens. Lm-induced inflammation is partly characterized by macrophage activation. Long non-coding RNAs (lncRNAs) have important roles in various biological processes. However, it is unknown how lncRNAs regulate the host response to Lm infection. To identify the role of lncRNA in Lm infection, we used in vitro and in vivo models. We found that lincRNA-Cox2 was highly expressed in Lm-infected RAW264.7 cells. LincRNA-Cox2 knockdown resulted in reduced proinflammatory cytokines, apoptosis, migration ability and enhanced phagocytosis of Lm. LincRNA-Cox2 knockdown also reduced the phosphorylation of Janus kinase 3 (JAK3) and signal transducer and activator of transcription (STAT3) and the nuclear translocation of nuclear factor (NF)-κB P65, which are known to be involved in inflammatory responses. Experimentally inhibiting the protein and phosphorylation levels of STAT3 resulted in reduced proinflammatory cytokines and enhanced phagocytosis of Lm by the RAW264.7 cells. Our research suggests that lincRNA-Cox2 plays important roles in inflammation, the phagocytic function and cell migration ability of RAW264.7 cells by activating interleukin (IL)-6/JAK3/STAT3 signaling, and lincRNA-Cox2 also regulates NF-κB P65 nuclear translocation. Our research provides new insights into the regulatory role of lincRNA-Cox2 in Lm infection

Recombination analysis based on the complete genome of bocavirus

Abstract Bocavirus include bovine parvovirus, minute virus of canine, porcine bocavirus, gorilla bocavirus, and Human bocaviruses 1-4 (HBoVs). Although recent reports showed that recombination happened in bocavirus, no systematical study investigated the recombination of bocavirus. The present study performed the phylogenetic and recombination analysis of bocavirus over the complete genomes available in GenBank. Results confirmed that recombination existed among bocavirus, including the likely inter-genotype recombination between HBoV1 and HBoV4, and intra-genotype recombination among HBoV2 variants. Moreover, it is the first report revealing the recombination that occurred between minute viruses of canine.</p

The presence of baseline HBsAb-Specific B cells can predict HBsAg or HBeAg seroconversion of chronic hepatitis B on treatment

ABSTRACTIndices for predicting HBsAg or HBeAg seroconversion in patients with chronic hepatitis B virus (HBV) infection during antiviral therapy remain elusive. We aimed to investigate if the presence of HBsAb-specific B cells at baseline can predict HBsAg or HBeAg seroconversion. In this study, 134 treatment-naive patients with chronic HBV were enrolled. A baseline HBsAb-specific B cell ELISpot assay was performed for all the patients that enrolled. Serum samples were collected at 12, 24, and 48 weeks for patients treated with Peg-IFN-α, or at 1 year, 3 years, and 5 years for patients treated with NAs. Laboratory testing of HBsAg, HBsAb, HBeAg, HBeAb, HBcAb, HBV DNA, ALT, and AST was done. We observed a significantly lower frequency of HBsAb-specific B cells in patients with chronic HBV than in healthy individuals . In the Peg-IFN-α-treated group, 41.2% of patients with baseline HBsAb-specific B cells achieved HBsAg seroconversion, while only 13.6% of patients without baseline HBsAb-specific B cells achieved HBsAg seroconversion (p = 0.006). By logistic regression analysis, patients with baseline HBsAb-specific B cells and HBsAg ≤ 1500 had higher HBsAg clearance at the end of treatment (p < 0.05). In the NA-treated group, 58.3% of patients with baseline HBsAb-specific B cells achieved HBeAg seroconversion, whereas only 30.0% of patients without baseline HBsAb-specific B cells achieved HBeAg seroconversion (p = 0.114). Our result revealed that baseline HBsAb-specific B cells by ELISpot assay might be a valuable predictive biomarker of HBsAg or HBeAg seroconversion in patients with chronic HBV on treatment