Salt Tolerance in Machilus faberi: Elucidating Growth and Physiological Adaptations to Saline Environments.

Adversity stress is the main environmental factor limiting plant growth and development, including salt and other stress factors. This study delves into the adaptability and salt tolerance mechanisms of Machilus faberi Hemsl, a species with potential for cultivation in salinized areas. We subjected the plants to various salt concentrations to observe their growth responses and to assess key physiological and biochemical indicators. The results revealed that under high salt concentrations (500 and 700 mmol-1/L), symptoms such as leaf yellowing, wilting, and eventual death were observed. Notably, plant height and shoot growth ceased on the 14th day of exposure. Chlorophyll content (a, b, total a + b, and the a/b ratio) initially increased but subsequently decreased under varying levels of salt stress. Similarly, the net photosynthetic rate, stomatal conductance, leaf water content, and root activity significantly declined under these conditions. Moreover, we observed an increase in malondialdehyde levels and relative conductivity, indicative of cellular damage and stress. The activity of superoxide dismutase and ascorbate peroxidase initially increased and then diminished with prolonged stress, whereas peroxidase activity consistently increased. Levels of proline and soluble protein exhibited an upward trend, contrasting with the fluctuating pattern of soluble sugars, which decreased initially but increased subsequently. In conclusion, M. faberi exhibits a degree of tolerance to salt stress, albeit with growth limitations when concentrations exceed 300 mmol-1/L. These results shed light on the plant's mechanisms of responding to salt stress and provide a theoretical foundation for its cultivation and application in salt-affected regions.

Genome-Wide Analysis of the bHLH Gene Family in Loropetalum chinense var. rubrum: Identification, Classification, Evolution, and Diversity of Expression Patterns under Cultivation.

The basic helix-loop-helix (bHLH) transcription factor family is the second-largest transcription factor family in plants. Members of this family are involved in the processes of growth and development, secondary metabolic biosynthesis, signal transduction, and plant resistance. Loropetalum chinense var. rubrum is a critical woody plant with higher ornamental and economic values, which has been used as ornamental architecture and traditional Chinese herbal medicine plants. However, the bHLH transcription factors in Loropetalum chinense var. rubrum (L. chinense var. rubrum) have not yet been systematically demonstrated, and their role in the biosynthesis of anthocyanin is still unclear. Here, we identified 165 potential LcbHLHs genes by using two methods, and they were unequally distributed on chromosomes 1 to 12 of the genome of L. chinense var. rubrum. Based on an evolutionary comparison with proteins from Arabidopsis and Oryza sativa, these bHLH proteins were categorized into 21 subfamilies. Most LcbHLHs in a particular subfamily had similar gene structures and conserved motifs. The Gene Ontology annotation and Cis-elements predicted that LcbHLHs had many molecular functions and were involved in processes of plant growth, including the biosynthesis of flavonoids and anthocyanins. Transcriptomic analysis revealed different expression patterns among different tissues and cultivars of L. chinense var. rubrum. Many LcbHLHs were expressed in the leaves, and only a few genes were highly expressed in the flowers. Six LcbHLHs candidate genes were identified by bioinformatics analysis and expression analysis. Further Real-time quantitative PCR analysis and protein interaction network analysis showed that LcbHLH156, which is one of the candidate proteins belonging to the IIIf subfamily, could interact with proteins related to anthocyanin synthesis. Therefore, LcbHLH156 was transiently expressed in L. chinense var. rubrum to verify its function in regulating anthocyanin synthesis. Compared with the control group, red pigment accumulation appeared at the wound after injection, and the total anthocyanin content increased at the wound of leaves. These results lay a foundation for the research of the regulation mechanism of leaf colors in L. chinense var. rubrum and also provide a basis for the function of the LcbHLH family.

Transcriptome profiling highlights regulated biological processes and type III interferon antiviral responses upon Crimean-Congo hemorrhagic fever virus infection.

Crimean-Congo hemorrhagic fever virus (CCHFV) is a biosafety level-4 (BSL-4) pathogen that causes Crimean-Congo hemorrhagic fever (CCHF) characterized by hemorrhagic manifestation, multiple organ failure and high mortality rate, posing great threat to public health. Despite the recently increasing research efforts on CCHFV, host cell responses associated with CCHFV infection remain to be further characterized. Here, to better understand the cellular response to CCHFV infection, we performed a transcriptomic analysis in human kidney HEK293 â€‹cells by high-throughput RNA sequencing (RNA-seq) technology. In total, 496 differentially expressed genes (DEGs), including 361 up-regulated and 135 down-regulated genes, were identified in CCHFV-infected cells. These regulated genes were mainly involved in host processes including defense response to virus, response to stress, regulation of viral process, immune response, metabolism, stimulus, apoptosis and protein catabolic process. Therein, a significant up-regulation of type III interferon (IFN) signaling pathway as well as endoplasmic reticulum (ER) stress response was especially remarkable. Subsequently, representative DEGs from these processes were well validated by RT-qPCR, confirming the RNA-seq results and the typical regulation of IFN responses and ER stress by CCHFV. Furthermore, we demonstrate that not only type I but also type III IFNs (even at low dosages) have substantial anti-CCHFV activities. Collectively, the data may provide new and comprehensive insights into the virus-host interactions and particularly highlights the potential role of type III IFNs in restricting CCHFV, which may help inform further mechanistic delineation of the viral infection and development of anti-CCHFV strategies.

Serum anti-mumps IgG antibody levels among children aged 0 to 4 years in Haishu District / 预防医学

Objective@#To investigate the serum anti-mumps IgG antibody levels among children aged 0 to 4 years in Haishu District, Ningbo City, Zhejiang Province, so as to provide insights into improvements for mumps vaccination program.@*Methods@#Children aged 0 to 4 years were sampled from Haishu District using a stratified random sampling method in 2016 (before adjustment of the mumps vaccination program) and 2022 (after adjustment of the mumps vaccination program). Participants' demographics were collected using questionnaires, and the coverage of mumps-containing vaccines was collected from the Ningbo Municipal Immunization Information System. Serum anti-mumps IgG antibody was measured using enzyme-linked immunosorbent assay (ELISA), and the seroprevalence of anti-mumps IgG antibody and geometric mean concentration (GMC) were estimated among children aged 0 to 4 years in 2016 and 2022.@*Results@#A total of 464 children were enrolled in 2016, including 250 boys (53.88%) and 214 girls (46.12%), and there were 301 children receiving mumps-containing vaccines (64.87%). The seroprevalence of anti-mumps IgG antibody were 48.08%, 34.44%, 81.11%, 84.44% and 84.44%, and GMC were 233.86, 351.77, 333.66, 362.29 and 410.72 U/mL. A total of 456 children were recruited in 2022, including 236 boys (51.75%) and 220 girls (48.25%), and there were 427 children receiving mumps-containing vaccines (93.64%). The seroprevalence of anti-mumps IgG antibody were 72.73%, 95.00%, 100.00%, 98.68% and 99.04%, and GMC were 524.05, 1 229.69, 1 623.64, 788.01 and 738.41 U/mL. Higher seroprevalence and GMC of anti-mumps IgG antibody was seen in 2022 than in 2016 among children at all age groups (P<0.05).@*Conclusion@#Following adjustment for vaccination programs, the seroprevalence and GMC of anti-mumps IgG antibody significantly increased among children at ages of 0 to 4 years in Haishu District.

STAT1 is associated with NK cell dysfunction by downregulating NKG2D transcription in chronic HBV-infected patients.

PURPOSE: Natural killer (NK) cells are key players in the immune system, however, the exact mechanism of NK cell dysfunction during HBV infection remains poorly defined. METHODS: Hepatitis B envelope antigen-negative (HBeAg-, n = 19) chronic hepatitis B infection (CHB) patients, HBeAg-positive (HBeAg+, n = 20) CHB patients, HBV-related hepatocellular carcinoma (HBV-HCC, n = 12) patients and healthy blood donors (HD, n = 20), were enrolled in our study. The phenotype and function of the corresponding NK cells of these subjects were then determined. NK cells were cocultured with HBV to assess whether HBV influences the activation of STAT1. Receptors, proliferation, apoptosis rate, and cytotoxicity of NK-92 cells were detected after STAT1 overexpression and knockdown. The relationship between STAT1 and NKG2D promoter was determined by luciferase assay. RESULTS: The levels of NKG2D and STAT1 were the lowest in the HBV-HCC group compared with the HD group, followed by the HBeAg+ group and then the HBeAg- group, respectively. Interestingly, STAT1 levels were positively correlated with NKG2D expression and HBeAg status. Furthermore, STAT1 directly bound to the NKG2D promoter to regulate the transcription and expression of NKG2D. Finally, the results also suggested that knockdown of STAT1 can inhibit proliferation, increase apoptosis rate of NK-92 cells and impair cytotoxicity of NK-92 cells. CONCLUSION: STAT1 is correlated with NK cell dysfunction by downregulating NKG2D transcription in HBV-infected patients. Our findings demonstrate that STAT1 is an important and positive regulator of NK cells, which could provide a potential immunotherapy target for CHB.

Host restriction of emerging high-pathogenic bunyaviruses via MOV10 by targeting viral nucleoprotein and blocking ribonucleoprotein assembly.

Bunyavirus ribonucleoprotein (RNP) that is assembled by polymerized nucleoproteins (N) coating a viral RNA and associating with a viral polymerase can be both the RNA synthesis machinery and the structural core of virions. Bunyaviral N and RNP thus could be assailable targets for host antiviral defense; however, it remains unclear which and how host factors target N/RNP to restrict bunyaviral infection. By mass spectrometry and protein-interaction analyses, we here show that host protein MOV10 targets the N proteins encoded by a group of emerging high-pathogenic representatives of bunyaviruses including severe fever with thrombocytopenia syndrome virus (SFTSV), one of the most dangerous pathogens listed by World Health Organization, in RNA-independent manner. MOV10 that was further shown to be induced specifically by SFTSV and related bunyaviruses in turn inhibits the bunyaviral replication in infected cells in series of loss/gain-of-function assays. Moreover, animal infection experiments with MOV10 knockdown corroborated the role of MOV10 in restricting SFTSV infection and pathogenicity in vivo. Minigenome assays and additional functional and mechanistic investigations demonstrate that the anti-bunyavirus activity of MOV10 is likely achieved by direct impact on viral RNP machinery but independent of its helicase activity and the cellular interferon pathway. Indeed, by its N-terminus, MOV10 binds to a protruding N-arm domain of N consisting of only 34 amino acids but proving important for N function and blocks N polymerization, N-RNA binding, and N-polymerase interaction, disabling RNP assembly. This study not only advances the understanding of bunyaviral replication and host restriction mechanisms but also presents novel paradigms for both direct antiviral action of MOV10 and host targeting of viral RNP machinery.

SARS-CoV-2 nsp1: Bioinformatics, Potential Structural and Functional Features, and Implications for Drug/Vaccine Designs.

The emerging coronavirus disease (COVID-19) caused by SARS-CoV-2 has led to social and economic disruption globally. It is urgently needed to understand the structure and function of the viral proteins for understanding of the viral infection and pathogenesis and development of prophylaxis and treatment strategies. Coronavirus non-structural protein 1 (nsp1) is a notable virulence factor with versatile roles in virus-host interactions and exhibits unique characteristics on sequence, structure, and function mode. However, the roles and characteristics of SARS-CoV-2 nsp1 are currently unclear. Here, we analyze the nsp1 of SARS-CoV-2 from the following perspectives: (1) bioinformatics analysis reveals that the novel nsp1 is conserved among SARS-CoV-2 strains and shares significant sequence identity with SARS-CoV nsp1; (2) structure modeling shows a 3D α/ß-fold of SARS-CoV-2 nsp1 highly similar to that of the SARS-CoV homolog; (3) by detailed, functional review of nsp1 proteins from other coronaviruses (especially SARS-CoV) and comparison of the protein sequence and structure, we further analyzed the potential roles of SARS-CoV-2 nsp1 in manipulating host mRNA translation, antiviral innate immunity and inflammation response and thus likely promoting viral infection and pathogenesis, which are merited to be tested in the future. Finally, we discussed how understanding of the novel nsp1 may provide valuable insights into the designs of drugs and vaccines against the unprecedented coronavirus pandemic.

miR-199a-5p targeted regulation of MAGT1 expression in the functional depletion of CD8+T cells in HBV infection.

Magnesium transporter 1 (MAGT1) is a key protein that regulates the level of free Mg2+ in cells. Previous studies found that the downregulation of MAGT1 expression in CD8+T cells of HBV patients was correlated with the decrease of intracellular magnesium. However, the expression of MAGT1 mRNA in the CD8+T cells from HBV patients was not significantly altered, indicating that the change in MAGT1 expression was accomplished through posttranscriptional regulation. Through bioinformatics and qRT-PCR detection, miR-199a-5p was found to have a target gene relationship with MAGT1. The expression levels of miR-199a-5p and MAGT1 in HBV infection were evaluated. Lentivirus assays were used to analyze the effects of miR-199a-5p upregulation and downregulation on the MAGT1 expression level and the immune system. Results showed no significant change in the expression of MAGT1 mRNA in HBV-infected cell lines, but the expression of MAGT1 was downregulated. Additionally, the expression level of miR-199a-5p was significantly increased. To this end, we predicted a target relationship between miR-199a-5p and MAGT1 by using TargetScan and verified this relationship through a luciferase activity reporter gene assay. As a result, MAGT1 was found to be the direct target of miR-199a-5p. The targeted inhibition of MAGT1 induced by miR-199a-5p overexpression led to the immune function depletion of CD8+T cells in HBV patients. Downregulating the expression level of miR-199a-5p could effectively improve the functional depletion of CD8+T cells. These findings indicate that miR-199a-5p and MAGT1 could potentially be used as biomarkers for the diagnosis and treatment of chronic HBV infection.

The Nonstructural Protein of Guertu Virus Disrupts Host Defenses by Blocking Antiviral Interferon Induction and Action.

Guertu virus (GTV) is a potentially highly pathogenic bunyavirus newly isolated in China, which is genetically related to the severe fever with thrombocytopenia syndrome virus (SFTSV) and Heartland virus (HRTV), two other emerging life-threatening bunyaviruses. Previous studies suggested that SFTSV and HRTV antagonize the interferon (IFN) system by targeting antiviral signaling proteins in different ways. However, whether and how GTV counteracts the host innate immunity are unclear. Here, we found that GTV strongly inhibits both IFN induction and action through its nonstructural protein (NSs). Different from the NSs of SFTSV and HRTV, GTV NSs (G-NSs) induced the formation of two distinctive cytoplasmic structures, compact inclusion bodies (IBs) and extended filamentous structures (FSs). Protein interaction and colocalization analyses demonstrated that G-NSs interacts with TBK1 (TANK binding kinase-1, the pivotal kinase for IFN induction) and STAT2 (signal transducer and activator of transcription 2, the essential transcription factor for IFN action) and irreversibly sequesters the host proteins into the viral IBs and FSs. Consistently, G-NSs thus inhibited phosphorylation/activation and nuclear translocation of IFN-regulatory factor 3 (IRF3, the substrate of TBK1), diminishing the IFN induction. Furthermore, G-NSs sequestration of STAT2 blocked phosphorylation/activation and nuclear translocation of STAT2, disabling IFN action and host antiviral state establishment. Collectively, this study shows the robust subversion of the two phases of the IFN antiviral system by GTV and unravels the respective molecular mechanisms, exhibiting some notable differences from those employed by SFTSV and HRTV, providing insights into the virus-host interactions and pathogenesis, and probably also benefiting the prevention and treatment of the related infectious diseases in the future.

Evolution of Pore Structure during Pressurized Dewatering and Effects on Moisture Readsorption of Lignite.

In this study, pressurized method was used to dry lignite at moderate temperature to change its pore structure but preserve its oxygen-containing functional groups. The effects of drying conditions (time, pressure, and temperature) on equilibrium moisture content (EMC) and pore structure of dewatered coals were investigated, and the correlations between pore structure and EMC were also evaluated. The pore structure parameters of raw coal and dewatered coals were measured by nitrogen adsorption experiments. The EMC of dewatered coals was obtained by gravimetric method. The results indicated that the porous structure of dewatered coal was jointly affected by three factors (drying time, pressure, and temperature) in the initial pressurized drying stage. The drying pressure exhibited obvious effect in the initial stage of drying lignite. Destruction of pores under pressure was prevented due to the water present in these pores. To further improve the pore structures of dehydrated coals obtained by high-pressure treatment, the temperature was increased to above 140 °C under 3 MPa; thus, a large number of macropores were evolved into mesopores. Furthermore, the experiments on water reabsorption by dewatered coals indicated that the EMC (0.15-0.18) of dehydrated coal was the lowest when the pressure was 3 MPa, temperature was 140-160 °C, and the time required was 30 min. The moisture readsorption contents of dehydrated coals were found to be positively correlated with its pore volume at high relative humidity. When the relative humidity was below 20%, they were related to specific surface areas or oxygen-containing functional groups. Therefore, pressure in the process of drying lignite was the main factor influencing the pore structure and the water reabsorption of dewatered coals, and the drying temperature was dominant under the pressurizing conditions.

Interferon-γ-Directed Inhibition of a Novel High-Pathogenic Phlebovirus and Viral Antagonism of the Antiviral Signaling by Targeting STAT1.

Severe fever with thrombocytopenia syndrome (SFTS) is a life-threatening infectious disease caused by a novel phlebovirus, SFTS virus (SFTSV). Currently, there is no vaccine or antiviral available and the viral pathogenesis remains largely unknown. In this study, we demonstrated that SFTSV infection results in substantial production of serum interferon-γ (IFN-γ) in patients and then that IFN-γ in turn exhibits a robust anti-SFTSV activity in cultured cells, indicating the potential role of IFN-γ in anti-SFTSV immune responses. However, the IFN-γ anti-SFTSV efficacy was compromised once viral infection had been established. Consistently, we found that viral nonstructural protein (NSs) expression counteracts IFN-γ signaling. By protein interaction analyses combined with mass spectrometry, we identified the transcription factor of IFN-γ signaling pathway, STAT1, as the cellular target of SFTSV for IFN-γ antagonism. Mechanistically, SFTSV blocks IFN-γ-triggered STAT1 action through (1) NSs-STAT1 interaction-mediated sequestration of STAT1 into viral inclusion bodies and (2) viral infection-induced downregulation of STAT1 protein level. Finally, the efficacy of IFN-γ as an anti-SFTSV drug in vivo was evaluated in a mouse infection model: IFN-γ pretreatment but not posttreatment conferred significant protection to mice against lethal SFTSV infection, confirming IFN-γ's anti-SFTSV effect and viral antagonism against IFN-γ after the infection establishment. These findings present a picture of virus-host arm race and may promote not only the understanding of virus-host interactions and viral pathogenesis but also the development of antiviral therapeutics.

[Sediment-water flux and processes of nutrients and gaseous nitrogen release in a China River Reservoir].

The key processes and fluxes of nutrients (N and P) and gaseous N (N2 and N2O) across the sediment-water interface in a river reservoir (Xipi) of the Jiulong River watershed in southeast China were studied. Intact core sediment incubation of nutrients exchange, in-situ observation and lab incubation of excess dissolved N2 and N2O (products of nitrification, denitrification and Anammox), and determination of physiochemical and microbe parameters were carried out in 2013 for three representative sites along the lacustrine zone of the reservoir. Results showed that ammonium and phosphate were generally released from sediment to overlying water [with averaged fluxes of N (479.8 ± 675.4) mg. (m2. d)-1 and P (4. 56 ± 0.54) mg. (m2 d) -1] , while nitrate and nitrite diffused into the sediment. Flood events in the wet season could introduce a large amount of particulate organic matter that would be trapped by the dam reservoir, resulting in the high release fluxes of ammonium and phosphate observed in the following low-flow season. No clear spatial variation of sediment nutrient release was found in the lacustrine zone of the reservoir. Gaseous N release was dominated by excess dissolved N2 (98% of total), and the N2 flux from sediment was (15.8 ± 12. 5) mg (m2. d) -1. There was a longitudinal and vertical variation of excess dissolved N2, reflecting the combined results of denitrification and Anammox occurring in anoxic sediment and fluvial transport. Nitrification mainly occurred in the lower lacustrine zone, and the enrichment of N2O was likely regulated by the ratio of ammonium to DIN in water.