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Porcine epidemic diarrhea virus (PEDV) has emerged in American countries, and it has reemerged in Asia and Europe, causing significant economic losses to the pig industry worldwide. In the present study, the 17GXCZ-1ORF3d strain, which has a naturally large deletion at the 172–554 bp position of the ORF3 gene, together with the 17GXCZ-1ORF3c strain, was serially propagated in Vero cells for up to 120 passages. The adaptability of the two strains gradually increased through serial passages in vitro. Genetic variation analysis of the variants of the two strains from different generations revealed that the naturally truncated ORF3 gene in the 17GXCZ-1ORF3d variants was stably inherited. Furthermore, the survival, viral shedding and histopathological lesions following inoculation of piglets demonstrated that the virulence of 17GXCZ-1ORF3d-P120 was significantly attenuated. These results indicate that the naturally truncated ORF3 gene may accelerate the attenuation of virulence and is involved in PEDV virulence together with mutations in other structural genes. Importantly, immunization of sows with G2b 17GXCZ-1ORF3d-P120 increased PEDV-specific IgG and IgA antibody levels in piglets and conferred partial passive protection against heterologous G2a PEDV strains. Our findings suggest that an attenuated strain with a truncated ORF3 gene may be a promising candidate for protection against PEDV.

Since 2010, porcine epidemic diarrhea virus (PEDV) has swept across China and spread throughout the country, causing huge economic losses. In this study, 673 diarrhea samples from 143 pig farms in Guangxi during 2017–2022 were collected and detected for PEDV. Ninety-eight strains were selected for S1 gene analyses and these strains were classified into four subgroups (G1b, G2a, G2b and G2c), accounting for 1.02 (1/98), 75.51 (74/98), 16.33 (16/98) and 7.14% (7/98) of the total, respectively. Importantly, an increased number of strains in the G2c subgroup was found from 2019 onwards. Bayesian analysis revealed that Guigang may have been the epicenter of PEDVs in Guangxi. In addition, Guigang was identified as the primary hub from which PEDVs spread via two routes, namely Guigang–Wuzhou and Guigang–Laibin. Moreover, several coinfections of novel PEDV variants bearing large deletions in the partial S1 protein and PEDVs possessing an intact partial S1 protein were found in pigs. Further recombination analyses indicated that two of the strains, 18-GXNN-6 and 19-GXBH-2, originated from intra-genogroup recombination. Together, our data revealed a new profile of PEDV in Guangxi, China, which enhances our understanding of the distribution, genetic characteristics and evolutionary profile of the circulating PEDV strains in China.

While nutrient enrichment and herbivory have been well recognized as the main driving factors of seagrass meadow fragmentation and degradation, there is limited understanding of how their relative importance shifts across large spatial scales where environmental factors such as turbidity can vary. In this study, a field control experiment was conducted in two Zostera japonica meadows distributed on the two banks of the Yellow River Estuary with different turbidity, to investigate the combined effects of nutrient enrichment and herbivory on seagrass and macroalgae. Our results showed that turbidity had the mediating force of shifting the relative importance of nutrient enrichment and herbivory to seagrass and macroalgae. While herbivory played a vital role in maintaining the balance between the two primary producers in a turbid environment, nutrient enrichment tended to offset herbivory-induced biomass loss by promoting seagrass growth in a less turbid system. Additionally, two potential mechanisms that might regulate the responses of seagrasses and macroalgae to nutrient enrichment and herbivory under different turbidity are proposed. On the one hand, turbidity might mediate the feeding preference of herbivores. On the other hand, nutrient enrichment favors the growth of opportunistic macroalgae over seagrass in turbid systems. Our study emphasizes the mediating force of turbidity on seagrass ecosystems, and provides references for the protection and restoration of seagrass meadows under multiple environmental stressors, and prompts further studies on the feedback between sediment dynamics and seagrass meadows in the context of ecogeomorphology.

The causal relationships between plasma metabolites and cholelithiasis/cholecystitis risks remain elusive. Using two-sample Mendelian randomization, we found that genetic proxied plasma campesterol level showed negative correlation with the risk of both cholelithiasis and cholecystitis. Furthermore, the increased risk of cholelithiasis is correlating with the increased level of plasma campesterol. Lastly, genetic colocalization study showed that the leading SNP, rs4299376, which residing at the ABCG5/ABCG8 gene loci, was shared by plasma campesterol level and cholelithiasis, indicating that the aberrant transportation of plant sterol/cholesterol from the blood stream to the bile duct/gut lumen might be the key in preventing cholesterol gallstone formation.

Whether pristine ecosystems with intact trophic structures are more resilient to anthropogenic pressures than ecosystems facing human exploitation is a pressing question to ecological theory and management. For coastal vegetated ecosystems such as kelp forests and seagrass meadows, a number of studies recently highlighted that under eutrophic conditions, trophic cascades are particularly important in buffering or reducing negative effects of nutrient enrichment. Yet, it currently remains unclear how nutrient enrichment and trophic downgrading interact in oligotrophic coastal ecosystems with an intact trophic structure. Here, we factorially manipulated nutrient loading and the interactions within a tri-trophic food chain within a pristine, oligotrophic seagrass ecosystem to investigate how trophic downgrading affects its ability to buffer against eutrophication. Results revealed that nutrient addition stimulates seagrass production, while reducing the growth of benthic microalgae, presumably because the thicker seagrass canopy reduced light availability. Trophic downgrading by excluding predators, however, almost completely negated these nutrient effects, as the release of herbivores from predation strongly enhanced grazing pressure on seagrass. Exclusion of grazers in turn restored seagrass biomass by allowing the nutrient addition treatment to regain its effect, confirming that a tri-trophic cascade mediated how enhanced nutrient loading affected our system. Our results highlight that a healthy trophic structure is vital for the ability of pristine coastal ecosystems to buffer eutrophication, as trophic downgrading may degrade their ability to absorb enhanced nutrient loading. Hence, our findings emphasize the potential for multiple anthropogenic impacts to interact synergistically in degrading natural ecosystems.

The principal target organ of duck hepatitis A virus type 1 (DHAV-1) is duckling liver, which is an energy-intensive organ and plays important roles in body's energy metabolism and conversion. As the \"power house\" of the hepatocytes, mitochondria provide more than 90% of the energy. However, mitochondria are much vulnerable to the oxidative stress for their rich in polyunsaturated fatty acids. Although previous researches have demonstrated that DHAV-1 could induce the oxidative stress in the serum of the infected ducklings, no related study on the mitochondria during the pathological process of DVH has been reported by far. To address this issue, we examined the HE stained tissue pathological slices, detected the hepatic SOD, CAT and GPX activities and MDA contents and analyzed the ATP content, mitochondrial ultrastructure and the mitochondrial SOD, GPX activities and MDA content in the liver tissues. The results showed that the hepatic redox status was significantly disturbed so that causing the mitochondrial dysfunction, ATP depletion and mitochondrial oxidative stress during the process of the DHAV-1 infection, and a prescription formulated with Hypericum japonicum flavone, Radix Rehmanniae Recens polysaccharide and Salvia plebeia flavone (HRS), which had been demonstrated with good anti-oxidative activity in serum, could effectively alleviate the hepatic injury and the oxidative stress in liver tissue induced by DHAV-1 thus alleviating the mitochondrial injury and oxidative stress. In a word, this research discovers the oxidative stress induced mitochondrial dysfunction and oxidative stress during the DVH pathological process and demonstrates HRS exerts good anti-oxidative activity in liver tissue to protect mitochondria against reactive oxygen species (ROS).

Background Duck viral hepatitis (DVH) is an acute disease of young ducklings with no effective veterinary drugs for treatment. Gynostemma pentaphyllum is a well-known traditional Chinese medicine that plays an important role in the treatment of various diseases. Gypenoside (GP), one of the main ingredients of Gynostemma pentaphyllum , was reported with good hepatoprotective effects. However, its low solubility limits its application in the clinics. To improve its solubility and bioactivity, a phosphorylated derivative of gypenoside (pGP) was prepared by the sodium trimetaphosphate-sodium tripolyphosphate (STMP-STPP) method. An infrared spectroscopy method was applied to analyse the structures of GP and pGP. Then, a methyl thiazolyl tetrazolium (MTT) colorimetric assay was applied to study the hepatocyte protective efficacy of these two drugs against duck hepatitis A virus type 1 (DHAV-1) infection, and qPCR, TUNEL labelling and flow cytometry methods were used to study the relevant hepatocyte protective in vitro. Results The infrared spectroscopy detection results showed that the phosphorylation modification of GP was successful. The MTT colorimetric assay results showed that both GP and pGP possessed good hepatocyte protective efficacy in vitro, and pGP performed better than GP when the drug was added before or after virus inoculation. Furthermore, the qPCR results revealed that both drugs could effectively inhibit the adsorption (when adding GP and pGP pre-virus inoculation), replication and release of DHAV-1, and the viral inhibition rate of pGP was greater than that of GP. The subsequent TUNEL labelling and flow cytometry assays showed that both GP and pGP could significantly inhibit duck embryo hepatocyte apoptosis induced by DHAV-1, and the inhibition effect of pGP was much stronger than that of GP. Conclusions GP exerts good hepatocyte protective efficacy not only by inhibiting the proliferation of DHAV-1 but also by inhibiting duck embryonic hepatocyte apoptosis induced by DHAV-1, and phosphorylation modification significantly improves the antiviral and the anti-apoptotic effects of GP. Therefore, pGP has the potential to be developed into a novel drug against DHAV-1 infection.