Genetic characterization of Sus scrofa papillomavirus type 1 from domestic pigs in Guangxi Province, China.

Sus scrofa papillomatosis (SsP) is a tumour caused by Sus scrofa papillomaviruses (SsPVs). To investigate the presence of SsPVs in China, 354 domestic pig skin samples collected from Guangxi Province were examined for SsPV DNA by PCR. Three SsPV1s (GX12, GX14, and GX18) were identified with a prevalence of 0.847% (3/354). Sequence analysis showed that L1 of SsPV1/GX12 and SsPV1/GX14 had 99.7% and 99.6% nucleotide identify with the reference SsPV1a, respectively. Phylogenetic and evolutionary analyses showed that SsPV1/GX12 and SsPV1/14 clustered into SsPV1a and that SsPV1/GX18 clustered into SsPV1b. Compared with other SsPV L1 and L2 proteins, we found that the SsPV1/GX18 and SsPV1b strains shared the same unique substitutions, and SsPV1/GX12, SsPV1/GX14, and SsPV1a shared almost identical amino acid sequences. This study reports the first detection of SsPV DNA in China based on whole genome information and provides a scientific basis for the development of SsPV pathogenic biology, epidemiology, and prevention, as well as control technology research.

Cross-species transmission potential of chicken anemia virus and avian gyrovirus 2.

The Gyrovirus genus consists of nonenveloped, icosahedral viruses with small circular single-stranded DNA genomes. Gyroviruses have been detected in diverse hosts, including humans, chickens, rodents, and cats. Two Gyroviruses were detected in canine serum samples using PCR in this study. The results indicated that four serum samples were positive for CAV (0.28%, 2/700) or AGV2 (0.28%, 2/700). Additionally, recombination analysis showed that AGV2 and CAV might have originated from the recombination of viruses similar to those detected in chickens and humans. We detected a total of 14 mutations in CAV VP1 amino acid sequences and identified new mutations at positions 31, 388, 390, 399, and 421 for the first time. The identification of T390C, C912T, T1230C, and T1297C mutations in AGV2 VP1, R93C mutations in AGV2 VP2, and R58C mutations AGV2 VP3 indicated that the differences might be related to a transboundary movement among hosts, which requires further elucidation. To the best of our knowledge, this study is the first report of an AGV2-infected dog in China, suggesting that the cross-species transmission of viruses with circular single-stranded DNA genomes is a public health concern.

FGF10 ameliorates lipopolysaccharide-induced acute lung injury in mice via the BMP4-autophagy pathway.

Introduction: Damage to alveolar epithelial cells caused by uncontrolled inflammation is considered to be the main pathophysiological change in acute lung injury. FGF10 plays an important role as a fibroblast growth factor in lung development and lung diseases, but its protective effect against acute lung injury is unclear. Therefore, this study aimed to investigate protective effect and mechanism of FGF10 on acute lung injury in mice. Methods: ALI was induced by intratracheal injection of LPS into 57BL/6J mice. Six hours later, lung bronchoalveolar lavage fluid (BALF) was acquired to analyse cells, protein and the determination of pro-inflammatory factor levels, and lung issues were collected for histologic examination and wet/dry (W/D) weight ratio analysis and blot analysis of protein expression. Results: We found that FGF10 can prevent the release of IL-6, TNF-α, and IL-1ß, increase the expression of BMP4 and autophagy pathway, promote the regeneration of alveolar epithelial type Ⅱ cells, and improve acute lung injury. BMP4 gene knockdown decreased the protective effect of FGF10 on the lung tissue of mice. However, the activation of autophagy was reduced after BMP4 inhibition by Noggin. Additionally, the inhibition of autophagy by 3-MA also lowered the protective effect of FGF10 on alveolar epithelial cells induced by LPS. Conclusions: These data suggest that the protective effect of FGF10 is related to the activation of autophagy and regeneration of alveolar epithelial cells in an LPS-induced ALI model, and that the activation of autophagy may depend on the increase in BMP4 expression.

Construction and characterization of the full-length cDNA of an infectious clone of emerging porcine teschovirus-2.

Porcine teschovirus (PTV) is a causative agent of polioencephalomyelitis, encephalomyelitis, reproductive disorders and gastrointestinal and respiratory diseases in swine. In the present study, the PTV2 GX/2020 strain was isolated from pig intestinal tissue through the use of ST cells. Phylogenetic analysis of VP1 nucleotide sequences indicated that the GX/2020 isolate is closely related to PTV2. Furthermore, the full-length cDNA of an infectious GX/2020 clone was constructed using seamless ligation technology. The genome sequence of the rescued virus is largely consistent with the sequence of the parental virus, and it exhibits viral growth properties. The PTV2 virus was successfully isolated in the present study, and the reverse-genetic platform provides a foundation for studies of the pathogenic mechanisms of porcine teschovirus.

AadA36, a novel chromosomal aminoglycoside nucleotidyltransferase from a clinical isolate of Providencia stuartii.

In this study, we characterized a novel chromosome-encoded aminoglycoside nucleotidyltransferase (ANT), AadA36, from the Providencia stuartii strain P14 isolated from the sputum specimen of a burn patient at a hospital in Wenzhou, China. Among the functionally characterized ANTs, AadA36 shared the highest amino acid sequence identity of 51.91% with AadA14. The whole genome of P. stuartii P14 consisted of one chromosome and two plasmids (designated pP14-166 and pP14-114). A total of 19 genes with ≥80% similarity with functionally characterized antimicrobial resistance genes (ARGs) were identified in the whole genome, including aminoglycosides [aac(2')-Ia, aph(6)-Id, aph(3″)-Ib, aac(6')-Ib, ant(3″)-IIa, aph(3')-Ia], ß-lactams (bla CMY-2 and bla OXA-10) and so on. Antimicrobial susceptibility testing showed that the aadA36 gene conferred specific resistance to spectinomycin and streptomycin, and the minimum inhibitory concentration (MIC) of these antimicrobials increased 128- and 64-fold compared with the control strain. The kinetic parameters of AadA36 were consistent with the MIC data of spectinomycin and streptomycin, with kcat /Km ratios of (1.07 ± 2.23) × 104 M-1 s-1 and (8.96 ± 1.01) × 103 M-1 s-1, respectively. The identification of a novel aminoglycoside resistance gene will help us further understand the complexity of the resistance mechanisms and provide deep insights into the dissemination of resistance genes in the microbial population.