Complete genome sequence of a novel fusarivirus from the phytopathogenic fungus Fusarium sp.

Fusarium diseases include wilts, blights, rots, and cankers of many horticultural, field, ornamental, and forest crops in both agricultural and natural ecosystems, and they significantly hinder food plant production. Here, we describe a novel mycovirus, tentatively designated as "Fusarium fusarivirus 1" (FuFV1), which was discovered in an isolate of the phytopathogenic fungus Fusarium sp. FuFV1 has a positive-sense single-stranded RNA (+ssRNA) genome of 6,391 nucleotides (nt) containing three open reading frames (ORFs). ORF1 encodes a large polypeptide of 1,501 amino acids (aa) with conserved RNA-dependent RNA polymerase (RdRp) and helicase (Hel) domains. ORF2, overlapping ORF1 by 122 nucleotides, encodes a polypeptide with a conserved Smc domain. The third and smaller ORF (ORF3) encodes a polypeptide with an unknown function. BLASTp analysis of the ORF1-encoded polypeptide revealed that FuFV1 shares the highest aa sequence similarity (68.5% identity, E-value 0.0) with Fusarium poae fusarivirus 1 (FpFV1, genus Alphafusarivirus). Phylogenetic analysis of the RdRp and helicase (Hel) sequences indicated that FuFV1 clustered closely with FpFV1 in a separate branch within the clade containing members of the genus Alphafusarivirus. Based on these results, we propose that FuFV1 should be considered a novel mycovirus belonging to the genus Alphafusarivirus of the family Fusariviridae.

Effects of ADIPOQ polymorphisms on PCOS risk: a meta-analysis.

BACKGROUND: Whether adiponectin (ADIPOQ) polymorphisms are associated with the risk of polycystic ovary syndrome (PCOS) remain controversial. Therefore, we performed this study to better explore correlations between ADIPOQ polymorphisms and PCOS risk. METHODS: Literature retrieve was conducted in PubMed, Medline and Embase. Odds ratios (ORs) and 95% confidence intervals (CIs) were calculated. RESULTS: Eighteen studies were enrolled for analyses. Pooled overall analyses showed that rs1501299 polymorphism was significantly associated with PCOS risk (recessive model: p = 0.02, OR = 0.77, 95%CI 0.62-0.95; allele model: p = 0.001, OR = 1.15, 95%CI 1.06-1.26). Further subgroup analyses according to ethnicity of participants revealed that rs1501299 and rs2241766 polymorphisms were both significantly correlated with PCOS risk in Caucasians. In addition, rs1501299 polymorphism was also significantly correlated with PCOS risk in East Asians. CONCLUSIONS: Our findings indicated that rs1501299 and rs2241766 polymorphisms might serve as genetic biomarkers of PCOS in certain ethnicities.

Molecular characterization of a new human echovirus 11 isolate associated with severe hand, foot and mouth disease in Yunnan, China, in 2010.

Human echovirus 11 (E-11), a member of the species Enterovirus B, frequently causes aseptic meningitis and hand, foot and mouth disease (HFMD). We determined the complete genome sequence of strain 520K/YN/CHN/2010, isolated from a subject with HFMD and aseptic meningitis in Yunnan Province, China, in 2010. The strain shared 78.8% and 81.1% nucleotide sequence similarity with prototype strain Gregory in the complete VP1 gene and the complete genome, respectively. Only the VP2-VP3-VP1 genome region of 520K/YN/CHN/2010 was similar to that of the E-11 strain; the other genome regions were most similar to those of other members of the species Enterovirus B. Using phylogenetic analysis and sequence comparisons of the complete VP1 gene, E-11 strains could be divided into five genogroups, and the 520K/YN/CHN/2010 strain was found to belong to genogroup A. Recombination analysis showed evidence of recombination with other member of the species Enterovirus B, especially the E-9 strain MSH/KM812/2010. Persistent surveillance of HFMD pathogens might help predict potential emerging viruses and related disease outbreaks.

Complete genome sequence analysis of two human coxsackievirus A9 strains isolated in Yunnan, China, in 2009.

Human coxsackievirus A9 (CVA9) is a member of Enterovirus B species and may cause aseptic meningitis. The complete genome analyses of two strains CVA9 A242/YN/CHN/2009 and A108/YN/CHN/2009 isolated from aseptic meningitis cases in Yunnan Province, China, in 2009 were performed. These two strains shared 81.3 and 80.7, 81.0 and 81.1 % nucleotide similarity with prototype strain Griggs in the VP1-encoding sequence and the complete genome sequence, respectively. Through phylogenetic analysis and homogeneity analysis for twenty-eight VP1-encoding sequences, CVA9 strains could be divided into four genotypes and the Chinese strains might belong to genotype D. Similarity plot and bootscanning analyses showed evidence of recombination with other EVB viruses. In conclusion, persistent surveillance of circulating enterovirus might help understand the enterovirus evolution.

Upregulation of SPI1 during myocardial infarction aggravates cardiac tissue injury and disease progression through activation of the TLR4/NFκB axis.

OBJECTIVE: Spleen focus forming virus proviral integration oncogene (SPI1) belongs to the ETS family of transcription factors participating in an array of cellular processes such as inflammation and cell apoptosis. This research focused on the role of SPI1 in the myocardial infarction (MI). METHODS: A murine model of MI was established. HL-1 cells were exposed to hypoxic treatment to simulate an MI-like condition. Tissue injury, inflammatory infiltration, and fibrosis in the cardiac tissues, and the apoptosis and the production of inflammation-related factors in cells were examined. Expression of SPI1 was determined. The downstream targets of SPI1 were identified by bioinformatics tools and luciferase assays. Artificial up- or downregulation of SPI1 and toll like receptor 4 (TLR4) were induced to examine their involvements in MI progression. RESULTS: SPI1 was expressed at high levels in the cardiac tissues of MI mice and in hypoxia-induced HL-1 cells. SPI1 downregulation reduced apoptosis and the production of inflammatory cytokines in the hypoxia-induced HL-1 cells. SPI1 bound to TLR4 promoter to induce transcriptional activation. TLR4 induced NFκB phosphorylation and blocked the protective role of SPI1 silencing in cells. In vivo, SPI1 inhibition restored the cardiac function and ameliorated MI-induced inflammation and fibrosis in mice. The protective role of SPI1 inhibition in mice was blocked by TLR4 activation. Aberrant upregulation of SPI1 was caused by the reduced DNA methylation during MI. CONCLUSION: This study demonstrated that upregulation of SPI1, caused by reduced DNA methylation, augmented development of myocardial infarction by activating the TLR4/NFκB axis.

ZNF277 regulates ovarian cancer cell proliferation and invasion through inhibition of PTEN.

BACKGROUND: ZNF277 is a transcription factor that is overexpressed in several cancers. However, its clinical role in ovarian cancer (OC) has not been reported yet. The present study aims to investigate the expression of ZNF277 in patients with OC, and to reveal the effects of ZNF277 on the proliferation, migration, and invasion of OC cells. METHODS: Using The Cancer Genome Atlas database, we found that higher expression of ZNF277 was correlated with poorer survival times of OC patients. This study used functional experiments, such as Cell Counting Kit-8 assay, colony formation assay, wound healing assay, and transwell invasion assay. Mechanistically, using quantitative chromatin immunoprecipitation assay, luciferase reporter assay, quantitative reverse-transcription PCR, and Western blot we identified the potential mechanism. RESULTS: We confirmed for the first time that the expression of ZNF277 is significantly increased in OC tissues and cell lines and that it is closely associated with the adverse clinical features of OC patients. We demonstrated that overexpression of ZNF277 potentiated the proliferation, migration, and invasion of SKOV3 and OVCAR3 loss-of-function experiments showed that the silencing of ZNF277 reduced the proliferation, migration, and invasion of OC cells. Mechanistically, using quantitative chromatin immunoprecipitation assay, luciferase reporter assay, quantitative reverse-transcription PCR, and Western blot we identified that PTEN was a direct downstream target for ZNF277. PTEN expression antagonized the tumor-promoting function of ZNF277. CONCLUSION: Taken together, the results of the current study demonstrated that ZNF277 exerted a promoting role in the progression of OC and might act as a promising biomarker and therapeutic target for OC patients.

Up-regulation of miRNA-148a inhibits proliferation, invasion, and migration while promoting apoptosis of cervical cancer cells by down-regulating RRS1.

The purpose of the present study is to figure out the role of miRNA-148a (miR-148a) in growth, apoptosis, invasion, and migration of cervical cancer cells by binding to regulator of ribosome synthesis 1 (RRS1). Cervical cancer and adjacent normal tissues, as well as cervical cancer cell line Caski, HeLa, C-33A, and normal cervical epithelial cell line H8 were obtained to detect the expression of miR-148a and RRS1. Relationship between miR-148a and RRS1 expression with clinicopathological characteristics was assessed. The selected Caski and HeLa cells were then transfected with miR-148a mimics, miR-148a inhibitors or RRS1 siRNA to investigate the role of miR-148a and RRS1 on proliferation, apoptosis, colony formation, invasion, and migration abilities of cervical cancer cells. Bioinformatics information and dual luciferase reporter gene assay was for used to detect the targetting relationship between miR-148a and RRS1. Down-regulated miR-148a and up-regulated RRS1 were found in cervical cancer tissues and cells. Down-regulated miR-148a and up-regulated RRS1 are closely related with prognostic factors of cervical cancer. RRS1 was determined as a target gene of miR-148a and miR-148a inhibited RRS1 expression in cervical cancer cells. Up-regulation of miR-148a inhibited cell proliferation, migration, and invasion while promoting apoptosis in Caski and HeLa cells. Our study suggests that miR-148a down-regulates RRS1 expression, thereby inhibiting the proliferation, migration, and invasion while promoting cell apoptosis of cervical cancer cells.