In total, 335 serum samples were collected from rabbits from two farms in Gansu province, China, and tested for anti-hepatitis E virus (HEV) antibody using EIA and for HEV RNA using nested RT- PCR with ORF2 primers. The overall prevalence of anti-HEV antibody and HEV RNA was 57.0% (191/335) and 7.5% (25/335), respectively. The positivity rate of HEV RNA in the anti-HEV antibody negative group (7.6% (11/144)) did not differ significantly from that in the positive group (7.3% (14/191)). The concordance between HEV RNA and anti-HEV antibody was 43.3% with no significant correlation (P < 0.05). All 25 amplicons from the ORF2 region were cloned and sequenced. On the basis of nucleotide sequence comparison, they had 84-99% identity to each other and 73-77%, 70-76%, 75-82%, 71-77%, and 53-65% with the corresponding regions of genotypes 1, 2, 3, 4, and avian HEV, respectively. Samples that were positive with the ORF2 primers were amplified using ORF1 region primers; 17 were positive and shared 71-78%, 73-76%, 74-82%, 72-78%, and 39-58% identity with the corresponding regions of genotypes 1, 2, 3, 4, and avian HEV, respectively, at the nucleotide level. Two representative full-length sequences were determined. These two sequences shared 85% identity with each other and had 74%, 73%, 78-79%, 74-75%, and 46-47% identity to full-length genotypes 1, 2, 3, 4, and avian HEV, respectively. Thus, the sequences isolated from the rabbits represent a novel genotype of HEV. This study provides novel information about HEV genotypes infecting rabbits as well as evidence of a new mammalian genotype of HEV.

Aberrant expression of neuropilin and tolloid-like 2 (NETO2) has been observed during the progression of some human carcinomas. However, the expression pattern and clinical relevance of NETO2 in gastric cancer (GC) remain to be elucidated. In this study, we found that NETO2 expression was higher in GC tissues compared with paired non-cancerous tissues. Moreover, the expression of NETO2 was positively correlated with clinical stage, invasion depth, lymph node metastasis, and tumor size, but inversely correlated with overall and disease-free survival rates. Cox regression analysis identified NETO2 as an independent prognostic indicator for GC patients. Overexpression of NETO2 facilitated migration and invasion of GC cells in vitro and metastasis in vivo in association with induction of epithelial-mesenchymal transition. Conversely, knockdown of NETO2 had the opposite effects. Mechanistically, silencing NETO2 reduced the phosphorylation of PI3K, AKT, and NF-κB p65 as well as the expression of Snail, whereas NETO2 overexpression achieved the opposite results. Furthermore, we identified TNFRSF12A as a mediator for NETO2 to activate PI3K/AKT/NF-κB/Snail axis. Collectively, our results demonstrate that NETO2 promotes invasion and metastasis of GC cells and represents a novel prognostic indicator as well as a potential therapeutic target in GC.

A Gram-stain-negative, rod-shaped bacterium, designated strain Y9 T , was isolated from a soil sample collected in Ningxia Province in China and was characterized to determine its taxonomic position. Strain Y9 T contained Q-8 as the predominant ubiquinone. Major fatty acid components were summed feature 3 (C 16 : 1 v7c and/or iso-C 15 : 0 2-OH) and C 16 : 0 . The major polar lipids were phosphatidylethanolamine, phosphatidylglycerol and diphosphatidylglycerol. The G+C content of the genomic DNA of strain Y9 T was 68.7 mol%. A phylogenetic tree based on 16S rRNA gene sequences showed that the strain fell within the evolutionary radiation encompassed by the genus Massilia. Levels of 16S rRNA gene sequence similarity between strain Y9 T and the type strains of recognized Massilia species ranged from 95.2 to 98.2 %, the highest values being with Massilia albidiflava 45 T (98.2 %) and Massilia lutea 101 T (98.0 %). However, levels of DNA-DNA relatedness between strain Y9 T and M. albidiflava KCTC 12343 T and M. lutea KCTC 12345 T were 37 and 26 %, respectively. Strain Y9 T was clearly differentiated from its nearest phylogenetic relatives in the genus Massilia based on phenotypic, chemotaxonomic and phylogenetic properties. Therefore, strain Y9 T is considered to represent a novel species of the genus Massilia, for which the name Massilia flava sp. nov. is proposed. The type strain is Y9 T

Background The aberrant expression of myotubularin-related protein 2 (MTMR2) has been found in some cancers, but little is known about the roles and clinical relevance. The present study aimed to investigate the roles and clinical relevance of MTMR2 as well as the underlying mechanisms in gastric cancer (GC). Methods MTMR2 expression was examined in 295 GC samples by using immunohistochemistry (IHC). The correlation between MTMR2 expression and clinicopathological features and outcomes of the patients was analyzed. The roles of MTMR2 in regulating the invasive and metastatic capabilities of GC cells were observed using gain-and loss-of-function assays both in vitro and in vivo. The pathways involved in MTMR2-regulating invasion and metastasis were selected and identified by using mRNA expression profiling. Functions and underlying mechanisms of MTMR2-mediated invasion and metastasis were further investigated in a series of in vitro studies. Results MTMR2 was highly expressed in human GC tissues compared to adjacent normal tissues and its expression levels were significantly correlated with depth of invasion, lymph node metastasis, and TNM stage. Patients with MTMR2 high had significantly shorter lifespan than those with MTMR2 low . Cox regression analysis showed that MTMR2 was an independent prognostic indicator for GC patients. Knockdown of MTMR2 significantly reduced migratory and invasive capabilities in vitro and metastases in vivo in GC cells, while overexpressing MTMR2 achieved the opposite results. MTMR2 knockdown and overexpression markedly inhibited and promoted the epithelial-mesenchymal transition (EMT), respectively. MTMR2 mediated EMT through the IFNγ/STAT1/IRF1 pathway to promote GC invasion and metastasis. Phosphorylation of STAT1 and IRF1 was increased by MTMR2 knockdown and decreased by MTMR2 overexpression accompanying with ZEB1 down-regulation and up-regulation, respectively. Silencing IRF1 upregulated ZEB1, which induced EMT and consequently enhanced invasion and metastasis in GC cells. Conclusions Our findings suggest that MTMR2 is an important promoter in GC invasion and metastasis by inactivating IFNγ/STAT1 signaling and may act as a new prognostic indicator and a potential therapeutic target for GC. Electronic supplementary material The online version of this article (10.1186/s13046-019-1186-z) contains supplementary material, which is available to authorized users.