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Autism spectrum disorder (ASD) is a neurodevelopmental disorder with highly heritable heterogeneity. Mutations of CUB and sushi multiple domains 3 (CSMD3) gene have been reported in individuals with ASD. However, the underlying mechanisms of CSMD3 for the onset of ASD remain unexplored. Here, using maleCSMD3knock-out (CSMD3−/−) mice, we found that genetic deletion ofCSMD3produced core autistic-like symptoms (social interaction deficits, restricted interests, and repetitive and stereotyped behaviors) and motor dysfunction in mice, indicating that theCSMD3gene can be considered as a candidate for ASD. Moreover, we discovered that the ablation ofCSMD3in mice led to abnormal cerebellar Purkinje cell (PC) morphology in Crus I/II lobules, including aberrant developmental dendritogenesis and spinogenesis of PCs. Furthermore, combiningin vivofiber photometry calcium imaging andex vivoelectrophysiological recordings, we showed that theCSMD3−/−mice exhibited an increased neuronal activity (calcium fluorescence signals) in PCs of Crus I/II lobules in response to movement activity, as well as an enhanced intrinsic excitability of PCs and an increase of excitatory rather than inhibitory synaptic input to the PCs, and an impaired long-term depression at the parallel fiber–PC synapse. These results suggest that CSMD3 plays an important role in the development of cerebellar PCs. Loss of CSMD3 causes abnormal PC morphology and dysfunction in the cerebellum, which may underlie the pathogenesis of motor deficits and core autistic-like symptoms inCSMD3−/−mice. Our findings provide novel insight into the pathophysiological mechanisms by whichCSMD3mutations cause impairments in cerebellar function that may contribute to ASD.SIGNIFICANCE STATEMENTAutism spectrum disorder (ASD) is a neurodevelopmental disorder with highly heritable heterogeneity. Advances in genomic analysis have contributed to numerous candidate genes for the risk of ASD. Recently, a novel giant geneCSMD3encoding a protein with CUB and sushi multiple domains (CSMDs) has been identified as a candidate gene for ASD. However, the underlying mechanisms ofCSMD3for the onset of ASD remain largely unknown. Here, we unravel that loss ofCSMD3results in abnormal morphology, increased intrinsic excitabilities, and impaired synaptic plasticity in cerebellar PCs, subsequently leading to motor deficits and ASD-like behaviors in mice. These results provide novel insight into the pathophysiological mechanisms by whichCSMD3mutations cause impairments in cerebellar function that may contribute to ASD.

As a selective β

The decline of nicotinamide adenine dinucleotide (NAD) occurs in a variety of human pathologies including neurodegeneration. NAD-boosting agents can provide neuroprotective benefits. Here, we report the discovery and development of a class of potent activators (NATs) of nicotinamide phosphoribosyltransferase (NAMPT), the rate-limiting enzyme in the NAD salvage pathway. We obtained the crystal structure of NAMPT in complex with the NAT, which defined the allosteric action of NAT near the enzyme active site. The optimization of NAT further revealed the critical role of K189 residue in boosting NAMPT activity. NATs effectively increased intracellular levels of NAD and induced subsequent metabolic and transcriptional reprogramming. Importantly, NATs exhibited strong neuroprotective efficacy in a mouse model of chemotherapy-induced peripheral neuropathy (CIPN) without any overt toxicity. These findings demonstrate the potential of NATs in the treatment of neurodegenerative diseases or conditions associated with NAD level decline.

This study was designed to analyze the causes of cervical adjacent segment degenerative disease (ASDis), evaluate the surgical outcomes of longitudinal spinous-splitting laminoplasty with coral bone (SLAC) during cervical reoperation, and accumulate data on reoperation with SLAC in a primary hospital. Based on the inclusion and exclusion criteria, we conducted a retrospective study involving 52 patients who underwent cervical reoperation for ASDis using SLAC at the spinal surgery department of the Beijing Jishuitan Hospital from 1998 to 2014. Among them, 39 were treated with anterior cervical fusion and internal fixation during the first operation (anterior cervical corpectomy with fusion [ACCF], n = 24; anterior cervical discectomy and fusion [ACDF], n = 11; and cervical disc arthroplasty [CDA], n = 4). Outcomes were the Japanese Orthopaedic Association (JOA) score, neck disability index (NDI) score, upper limb/neck and shoulder evaluated using a visual analogue scale (VAS), and rates of ASDis. In patients who underwent an anterior cervical approach in the first instance, the incidence of ASDis was significantly higher in the C

Aims:Analysis the changes of microorganisms during Chinese Feng-flavour Daqu fermentation, and the specific contribution of different environmental factors to Daqu microorganisms. Methods and Results: High throughput sequencing technology and SourceTracker software were used to analyze the microbial diversity of Feng-flavour Daqu before and after fermentation. 85 fungal and 105 bacterial were detected in the newly pressed Feng-flavour Daqu, while 33 fungal and 50 bacterial in the mature Daqu, and 202 fungal and 555 bacterial in the environmental samples. After fermentation, the microbial community structure of Daqu changed and decreased significantly. Conclusions: 94.7% of fungi come from raw materials and 1.8% from outdoor ground, 60.95% of bacteria come from indoor ground, 20.44% from raw materials, and 8.98% from tools. By comparing the changes of microorganisms in Daqu before and after fermentation, the microorganisms in mature Daqu may mainly come from not only the enhanced strains but also the environment. Significance and Impact of the Study: The source of main microorganisms in Feng-flavour Daqu and the influence of environmental factors on the quality of Daqu were clarified, which provided a basis for improving the quality of Feng-flavour Daqu.

Some of the bridges across the Yangtze River in the Three Gorges Reservoir area are in the curved section, and the collision prevention of bridges is a hot issue in the current industry. The system of ships sailing across bridges is a complex system in the discipline of transportation engineering. It is affected by ship conditions, channel conditions, meteorology and hydrology, navigation management and human factors. In order to grasp the influence of turbulent flow near the piers of bridges in curved river sections and oblique flow during variable water level periods on ships crossing bridges, it is necessary to carry out numerical simulation analysis. Methods: By establishing a simple physical model of the water area of the bridge pier, the turbulent flow field of the bridge pier was simulated in two dimensions by Fluent software. Then the turbulent flow characteristics of the single pier and the tandem double pier were compared, and the flow velocity on the upstream side of the bridge pier was used as a parameter to carry out numerical simulation. Finally, the flow-induced drift of the ship is quantitatively calculated in combination with the flow velocity. Conclusion: The two-dimensional simulation confirms that the turbulent width of the bridge pier increases with the increase of the flow velocity. The turbulent width of the tandem double pier is larger than that of the single pier, but the vorticity extending downstream is smaller than that of the single pier. The deflection moment and flow-induced drift of the ship crossing the bridge confirm the risk of ship collision. It is necessary to add a multi-function navigation mark to collect water flow parameters in time, and introduce LED visual navigation in the bridge area to improve the reliability of ship navigation in the bridge area of the curved river section.

Carbohydrate can be converted into fat by de novo lipogenesis, a process upregulated in fatty liver disease. Chemically, de novo lipogenesis involves polymerization and reduction of acetyl-CoA, using NADPH as the electron donor. The feedstocks used to generate acetyl-CoA and NADPH in lipogenic tissues remain, however, unclear. Here we show using stable isotope tracing in mice that de novo lipogenesis in adipose is supported by glucose and its catabolism via the pentose phosphate pathway to make NADPH. The liver, in contrast, derives acetyl-CoA for lipogenesis from acetate and lactate, and NADPH from folate-mediated serine catabolism. Such NADPH generation involves the cytosolic serine pathway in liver running in the opposite direction to that observed in most tissues and tumours, with NADPH made by the SHMT1-MTHFD1-ALDH1L1 reaction sequence. SHMT inhibition decreases hepatic lipogenesis. Thus, liver folate metabolism is distinctively wired to support cytosolic NADPH production and lipogenesis. More generally, while the same enzymes are involved in fat synthesis in liver and adipose, different substrates are used, opening the door to tissue-specific pharmacological interventions.

PurposeParkinson's disease (PD) is a serious neurodegenerative disease affecting the elderly. In general, the locomotion deficit, which seriously affects the daily life of patients with PD, usually occurs at a later stage. The mask face symptom meanwhile progressively worsens. However, facial muscle disorders and changes involved in the freezing mask are unclear.MethodIn this study, we recruited 35 patients with PD and 26 age- and sex-balanced controls to undergo phonation tests, while the built-in camera on the laptop recorded their facial expressions during the whole pronunciation process. Furthermore, FaceReader (version 7.0; Noldus Information Technology, Wageningen, Netherlands) was used to analyze changes in PD facial landmark movement and region movement.ResultsThe two-tailed Student's t-test showed that the changes in facial landmark movement among 49 landmarks were significantly lower in patients with PD than in the control group (P < 0.05). The data on facial region movement revealed that the eyes and upper lip of patients with PD differed significantly from those in the control group.ConclusionPatients with PD had defects in facial landmark movement and regional movement when producing a single syllable, double syllable, and multiple syllables, which may be related to reduced facial expressions in patients with PD.

Automatic segmentation and differentiation of retinal arteriole and venule (AV), defined as small blood vessels directly before and after the capillary plexus, are of great importance for the diagnosis of various eye diseases and systemic diseases, such as diabetic retinopathy, hypertension, and cardiovascular diseases. Optical coherence tomography angiography (OCTA) is a recent imaging modality that provides capillary-level blood flow information. However, OCTA does not have the colorimetric and geometric differences between AV as the fundus photography does. Various methods have been proposed to differentiate AV in OCTA, which typically needs the guidance of other imaging modalities. In this study, we propose a cascaded neural network to automatically segment and differentiate AV solely based on OCTA. A convolutional neural network (CNN) module is first applied to generate an initial segmentation, followed by a graph neural network (GNN) to improve the connectivity of the initial segmentation. Various CNN and GNN architectures are employed and compared. The proposed method is evaluated on multi-center clinical datasets, including 3×3 mm

Owing to narrow band gap and low toxicity, tin-lead (Sn-Pb) hybrid perovskites have shown great potential in photovoltaic applications, and the highest power conversion efficiency (PCE) of Sn-Pb perovskite solar cells (PSCs) has recently reached 23.6%. However, it is still challenging to prepare Sn-Pb films in open-air condition due to the Sn

Comorbid anxiety and depressive symptoms in chronic pain are a common health problem, but the underlying mechanisms remain unclear. Previously, we have demonstrated that sensitization of the CeA neurons via decreased GABAergic inhibition contributes to anxiety-like behaviors in neuropathic pain rats. In this study, by using male Sprague Dawley rats, we reported that the CeA plays a key role in processing both sensory and negative emotional-affective components of neuropathic pain. Bilateral electrolytic lesions of CeA, but not lateral/basolateral nucleus of the amygdala (LA/BLA), abrogated both pain hypersensitivity and aversive and depressive symptoms of neuropathic rats induced by spinal nerve ligation (SNL). Moreover, SNL rats showed structural and functional neuroplasticity manifested as reduced dendritic spines on the CeA neurons and enhanced LTD at the LA/BLA-CeA synapse. Disruption of GluA2-containing AMPAR trafficking and endocytosis from synapses using synthetic peptides, either pep2-EVKI or Tat-GluA2((3Y)), restored the enhanced LTD at the LA/BLA-CeA synapse, and alleviated the mechanical allodynia and comorbid aversive and depressive symptoms in neuropathic rats, indicating that the endocytosis of GluA2-containing AMPARs from synapses is probably involved in the LTD at the LA/BLA-CeA synapse and the comorbid aversive and depressive symptoms in neuropathic pain in SNL-operated rats. These data provide a novel mechanism for elucidating comorbid aversive and depressive symptoms in neuropathic pain and highlight that structural and functional neuroplasticity in the amygdala may be important as a promising therapeutic target for comorbid negative emotional-affective disorders in chronic pain. SIGNIFICANCE STATEMENT Several studies have demonstrated the high comorbidity of negative affective disorders in patients with chronic pain. Understanding the affective aspects related to chronic pain may facilitate the development of novel therapies for more effective management. Here, we unravel that the CeA plays a key role in processing both sensory and negative emotional-affective components of neuropathic pain, and LTD at the amygdaloid LA/BLA-CeA synapse mediated by GluA2-containing AMPAR endocytosis underlies the comorbid aversive and depressive symptoms in neuropathic pain. This study provides a novel mechanism for elucidating comorbid aversive and depressive symptoms in neuropathic pain and highlights that structural and functional neuroplasticity in the amygdala may be important as a promising therapeutic target for comorbid negative emotional-affective disorders in chronic pain.

The β2 adrenergic receptor (β2AR) is a member of G protein-coupled receptors (GPCRs) that mediate the majority of cellular responses to external stimuli. The agonists can cause smooth muscle relaxa...

β2-Adrenoceptor (β2-AR) agonists are widely used as bronchodilators. The emerge of ultralong acting β2-agonists is an important breakthrough in pulmonary medicine. In this review, we will provide mechanistic insights into the application of β2-agonists in asthma, chronic obstructive pulmonary disease (COPD), and heart failure (HF). Recent studies in β-AR signal transduction have revealed opposing functions of the β1-AR and the β2-AR on cardiomyocyte survival. Thus, β2-agonists and β-blockers in combination may represent a novel strategy for HF management. Allosteric modulation and biased agonism at the β2-AR also provide a theoretical basis for developing drugs with novel mechanisms of action and pharmacological profiles. Overlap of COPD and HF presents a substantial clinical challenge but also a unique opportunity for evaluation of the cardiovascular safety of β2-agonists. Further basic and clinical research along these lines can help us develop better drugs and innovative strategies for the management of these difficult-to-treat diseases.

Cervical cancer (CC) seriously threatens the health of women. Radiation therapy (RT) is the major treatment for CC. However, the recurrent CC can acquire resistance to RT. Thus, it is necessary to find a new method for reversing RT resistance in CC. It has been reported that microRNA-324-5p (miR-324-5p) can suppress the progression of multiple cancers. However, whether it can reverse resistance to RT in CC remains unclear. qRT-PCR and Western blotting were used to detect gene and protein expression in CC cells, respectively. Cell proliferation was tested by CCK-8 assay and colony formation assay. In addition, cell apoptosis was detected by flow cytometry. Transwell assays were performed to detect cell migration. Dual luciferase reporter assay and TargetScan were used to explore the targets of miR-324-5p. MiR-324-5p was downregulated in CC cells. Overexpression of miR-324-5p sensitized CC cells to RT. In addition, miR-324-5p mimics significantly induced apoptosis and inhibits the migration of CC cells in the presence of 137 Cs ionizing radiation. Furthermore, miR-324-5p sensitized CC cells to ionizing radiation by targeting ELAV-like RNA binding protein 1 (ELAVL1). MiR-324-5p overexpression affects the radiotherapy response of CC by targeting ELAVL1, which may serve as a new target for the treatment of CC.

FAM19A5/TAFA5 is a member of the family with sequence similarity 19 with unknown function in emotional and cognitive regulation. Here, we reported that FAM19A5 was highly expressed in the embryonic and postnatal mouse brain, especially in the hippocampus. Behaviorally, genetic deletion of Fam19a5 resulted in increased depressive-like behaviors and impaired hippocampus-dependent spatial memory. These behavioral alterations were associated with the decreased expression of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors and N-methyl-D-aspartic acid receptors, as well as significantly reduced glutamate release and neuronal activity in the hippocampus. Subsequently, these changes led to the decreased density of dendritic spines. In recent years, the roles of chronic stress participating in the development of depression have become increasingly clear, but the mechanism remains to be elucidated. We found that the levels of FAM19A5 in plasma and hippocampus of chronic stress-treated mice were significantly decreased whereas overexpression of human FAM19A5 selectively in the hippocampus could attenuate chronic stress-induced depressive-like behaviors. Taken together, our results revealed for the first time that FAM19A5 plays a key role in the regulation of depression and spatial cognition in the hippocampus. Furthermore, our study provided a new mechanism for chronic stress-induced depression, and also provided a potential biomarker for the diagnosis and a new strategy for the treatment of depression.

The highly virulent and antigenic variant of Pseudorabies virus (PRV) that emerged from classical Bartha-K61-vaccinated pig herds has caused substantial economic losses to the swine industry in China since 2011. A safe and more effective vaccine is most desirable. In this study, a gE/TK gene-deficient PRV, namely, HD/c, was constructed based on a PRV type II DX strain isolated from a commercial vaccine-immunized farm and the HD/c-based inactivated vaccine was formulated and evaluated for its safety, immunogenicity, and protective efficacy in mice and piglets. The resulting PRV HD/c strain has a similar growth curve to the parental DX strain. After vaccination, the inactivated HD/c vaccine did not cause any visible gross pathological or histopathological changes in the tissues of mice and piglets and provided rapid and potent protection against the challenge of the classical and variant PRVs at day 21 post-vaccination in mice. A single immunization of 10

Game animals are wildlife species traded and consumed as food and are potential reservoirs for SARS-CoV and SARS-CoV-2. We performed a meta-transcriptomic analysis of 1,941 game animals, representing 18 species and five mammalian orders, sampled across China. From this, we identified 102 mammalian-infecting viruses, with 65 described for the first time. Twenty-one viruses were considered as potentially high risk to humans and domestic animals. Civets (Paguma larvata) carried the highest number of potentially high-risk viruses. We inferred the transmission of bat-associated coronavirus from bats to civets, as well as cross-species jumps of coronaviruses from bats to hedgehogs, from birds to porcupines, and from dogs to raccoon dogs. Of note, we identified avian Influenza A virus H9N2 in civets and Asian badgers, with the latter displaying respiratory symptoms, as well as cases of likely human-to-wildlife virus transmission. These data highlight the importance of game animals as potential drivers of disease emergence.

Several studies have indicated that dysregulation of long non‑coding RNAs (lncRNAs) participates in the initiation and progression of cancer. The lncRNA MIR4435‑2HG was previously reported to act as an oncogene in human cancer, including liver cancer. However, its role in the pathogenesis in liver cancer is largely unclear. The present study aimed to reveal the molecular mechanism by which MIR4435‑2HG regulates liver cancer. The expression levels of MIR4435‑2HG in liver cancer and adjacent normal tissues were analyzed using The Cancer Genome Atlas database. MIR4435‑2HG expression was validated by reverse transcription‑quantitative polymerase chain reaction (RT‑qPCR) in cancer cells in vitro. The target genes of MIR4435‑2HG were predicted using bioinformatics analysis. Interactions between miR‑136‑5p, MIR4435‑2HG and B3GNT5 were detected using luciferase reporter assays, and their effects on cell viability, migration and invasion were assessed using Cell Counting Kit‑8, wound healing and Transwell assays. The effects of miR‑136‑5p and MIR4435‑2HG on B3GNT5 expression were confirmed by western blot analysis. The results revealed that MIR4435‑2HG expression was upregulated in primary liver cancer and liver cancer cell lines, and was positively associated with advanced tumor stage, metastasis and poor prognosis in patients with liver cancer. Knockdown of MIR4435‑2HG significantly inhibited the proliferation, migration and invasion of liver cancer cells. Furthermore, miR‑136‑5p was determined to be a direct target of MIR4435‑2HG and suppressed MIR4435‑2HG expression by binding with the seed region of the 3'‑UTR of MIR4435‑2HG in liver cancer cells. Functional studies showed that the inhibitory effects of MIR4435‑2HG knockdown on cell proliferation, migration and invasion were significantly rescued by inhibiting miR‑136‑5p. Furthermore, the target gene, B3GNT5, of miR‑136‑5p was confirmed by bioinformatics analysis and RT‑qPCR. In addition, B3GNT5 expression was regulated by the MIR4435‑2HG/miR‑136‑5p axis. In conclusion, the present study indicated that MIR4435‑2HG facilitated the progression of liver cancer via the MIR4435‑2HG/miR‑136‑5p/B3GNT5 axis, which demonstrated that MIR4435‑2HG may be a potential biomarker for the prognosis and treatment of liver cancer.

Long noncoding RNAs (lncRNAs) play critical roles in the tumorigenesis and progression of hepatocellular carcinoma (HCC). As the most common malignant cancer type in humans, HCC poses a great threat to human health. However, the function of lncRNA colorectal neoplasia differentially expressed (CRNDE) in HCC has not been extensively studied. The chief aim of the present study was to reveal the potential role of CRNDE in HCC. Expression levels of CRNDE in HCC tissues and cell lines were detected by reverse transcription-quantitative (RT-q) PCR, and Cell Counting kit 8, wound-healing and Transwell assays were used to evaluate the influences of CRNDE on in vitro cellular proliferation, migration and invasiveness, respectively. The interaction between CRNDE and microRNA (miR)-29c-3p was determined by dual-luciferase reporter assay, and rescue experiments were conducted to evaluate the interactive relationships between CRNDE and miR-29c-3p or nuclear autoantigenic sperm protein (NASP). CRNDE was found to be upregulated in HCC tissues and cells, and to be positively associated with the poor prognosis of patients with HCC. Furthermore, CRNDE-knockdown suppressed cell proliferation, migration and invasion abilities. Bioinformatics and RT-qPCR analysis indicated miR-29c-3p as a potential target of CRNDE. In line with previous reports, as a tumor suppressor, downregulated expression of miR-29c-3p was observed in HCC. In addition, the present study revealed that miR-29c-3p directly targeted NASP. NASP expression was markedly elevated following transfection with an miR-29c-3p inhibitor, while knocking down CRNDE inhibited NASP expression. Moreover, the effects of CRNDE and NASP on HCC cells were reversed by miR-29c-3p. Collectively, the results of the present study revealed that CRNDE was upregulated and exerted an oncogenic role in HCC by targeting miR-29c-3p, and that the upregulation of CRNDE also promoted NASP expression. These findings indicate a novel role for CRNDE in the progression of HCC.

Porcine deltacoronavirus (PDCoV) has been emerging in several swine-producing countries for years. In our study, 719 porcine diarrhoea samples from 18 provinces in China were collected for PDCoV and porcine epidemic diarrhoea virus (PEDV) detection. The epidemiological survey revealed that the positive rates of PDCoV, PEDV and coinfection were 13.07%, 36.72% and 4.73%, respectively. The entire spike (S) genes of eleven detected PDCoV strains were sequenced. Phylogenetic analysis showed that the majority of PDCoVs could be divided into three lineages: the China lineage, the USA/Japan/South Korea lineage and the Viet Nam/Laos/Thailand lineage. The China and the Viet Nam/Laos/Thailand lineages showed much greater genetic divergences than the USA/Japan/South Korea lineage. The present study detected one new monophyletic branch that contained three PDCoVs from China, and this branch was separated from the China lineage but closely related to the Viet Nam/Laos/Thailand lineage. The strain CH-HA2-2017, which belongs to this new branch, had a possible recombination event between positions 27 and 1234. Significant amino acid substitutions of PDCoV S proteins were analysed and displayed with a three-dimensional cartoon diagram. The visual spatial location of these substitutions gave a conformational-based reference for further studies on the significance of critical sites on the PDCoV S protein., Highlights • The majority of global PDCoVs could be divided into three lineages. • Three sequenced PDCoVs from China were closely related to the Viet Nam/Laos/Thailand lineage. • The China lineage showed the greatest genetic divergence. • One sequenced strain CH-HA2–2017 had a possible recombination event.

Objective: To mainly explore the effect of thalidomide combined with CHOP chemotherapy regimen on immunoglobulin, VEGF, lactate dehydrogenase, inflammatory factors and other related factors in patients with diffuse large B-cell lymphoma. Methods: A total of 83 patients with diffuse large B-cell lymphoma admitted to the Department of Hematology and Oncology in our hospital from December 2012 to December 2018 were collected. CHOP chemotherapy was given to 40 patients in the chemotherapy group. And 43 patients in the thalidomide group were treated with thalidomide combined with CHOP chemotherapy. Immunoglobulin IgG, IgA, IgM, vascular endothelial growth factor (VEGF), tumor necrosis factor (TNF-α), lactate dehydrogenase (LDH), β2 microglobulin (β2-MG), Th17 cell ratio and natural killer cell (NK) ratio were measured before and after treatment. Results: There were no significant differences in immunoglobulin, inflammatory cytokines and other related factors between the two groups before treatment (P>0.05). After 6 cycles of treatment, the levels of immunoglobulin IgG, IgA, IgM, VEGF, LDH, β2-MG and the ratio of NK cells in the chemotherapy group were significantly lower than those before treatment (P

Since late 2011, outbreaks of pseudorabies virus (PRV) have occurred in southern China causing major economic losses to the pig industry. We previously reported that variant PRV forms and recombination in China could be the source of continued epidemics. Here, we analyzed samples from intensive pig farms in eastern China between 2017 and 2019, and sequenced the main glycoproteins (gB, gC, gD, and gE) to study the evolution characteristics of PRV. Based on the gC gene, we found that PRV variants belong to clade 2 and detected a founder effect during by the PRV epidemic. In addition, we detected inter- and intra-clade recombination; in particular, inter-clade recombination in the gB genes of strains FJ-ZXF and FJ-W2, which were recombinant with clade 1 strains. We also found specific amino-acid changes and positively selected sites, possibly associated with functional changes. This analysis of the emergence of PRV in China illustrates the need for continuous monitoring and the development of vaccines against specific variants of PRV. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (10.1007/s12250-019-00140-1) contains supplementary material, which is available to authorized users.