Early versus the traditional start of oral intake following esophagectomy for esophageal cancer: a systematic review and meta-analysis.

BACKGROUND: Nil by mouth is considered the standard of care during the first days following esophagectomy. However, with the routine implementation of enhanced recovery after surgery, early oral intake is more likely to be the preferred mode of nutrition following esophagectomy. The present study aims to evaluate the safety and effectiveness of early oral intake following esophagectomy for esophageal cancer. METHODS: Comprehensive literature searches were conducted using PubMed, Web of Science, Embase, and Cochrane Library. Weighted mean differences (WMD) and odds ratios (OR) with 95% confidence intervals (CI) were calculated as the effect sizes for continuous and dichotomous variables, respectively. RESULTS: Fourteen studies with a total of 1947 patients were included. Length of hospital stay (WMD = - 3.94, CI: - 4.98 to - 2.90; P < 0.001), the time to first flatus (WMD = - 1.13, CI: - 1.25 to - 1.01; P < 0.001) and defecation (WMD = - 1.26, CI: - 1.82 to - 0.71; P < 0.001) favored the early oral intake group. There was no statistically significant difference in mortality (OR = 1.23, CI: 0.45 to 3.36; P = 0.69). Early oral intake also did not increase the risk of pneumonia and overall postoperative complications. CONCLUSIONS: Current evidence indicates early oral intake following esophagectomy seems to be safe and effective. It may be the preferred mode of nutrition following esophagectomy. However, more high-quality studies are still needed to further validate this conclusion.

Comprehensive genome and transcriptome analysis of the dermatophyte Trichophyton schoenleinii reveals the candidate pathogenic genes.

BACKGROUND: Trichophyton schoenleinii is an anthropophilic dermatophyte that causes tinea favosa. Nowadays, it remains an important pathogen in some regions of the world, mainly epidemic in Africa and West Asia. Despite the medical importance of T. schoenleinii infections, a high-quality reference genome for T. schoenleinii is still unavailable, neither its transcriptomic profile. OBJECTIVES: The aim of the current study was to improve understanding of the underlying pathogenic mechanism of T. schoenleinii, and to define the candidate pathogenic genes of T. schoenleinii. METHODS: Comprehensive genomic analysis of T. schoenleinii was carried out by Illumina and PacBio sequencing platforms. Transcriptome profiles of T. schoenleinii cultured in vitro in two media containing either keratin or soy protein were determined using RNA sequencing (RNA-seq) technology. RESULTS: Here, we present the first draft genome sequence of T. schoenleinii strain T2s, which consists of 11 scaffolds containing 7474 predicted genes. Transcriptome analysis showed that genes involved in keratin hydrolysis have higher expression in T. schoenleinii grown in keratin medium, including genes encoding proteases, cysteine dioxygenase and acetamidase. Other genes with higher expression include genes encoding the components of the pH-responsive signal transduction pathways and transcription factors, many of which may play a role in pathogenicity. CONCLUSION: In summary, this study provides new insights into the pathogenic mechanism of T. schoenleinii and highlights candidate genes for further development of novel targets in disease diagnosis and treatment of tinea favosa.

ROS-induced NLRP3 inflammasome priming and activation mediate PCB 118- induced pyroptosis in endothelial cells.

Growing epidemiological evidence has shown that exposure to polychlorinated biphenyls (PCBs) is harmful to the cardiovascular system. However, how PCB 118-induced oxidative stress mediates endothelial dysfunction is not fully understood. Here, we explored whether and how PCB 118 exposure-induced oxidative stress leads to NLRP3 inflammasome-dependent pyroptosis in endothelial cells. As expected, PCB 118 was cytotoxic to HUVECs and induced caspase-1 activation and cell membrane disruption, which are characteristics of pyroptosis. Moreover, PCB 118-induced pyroptosis may have been due to the activation of the NLRP3 infammasomes. PCB 118 also induced excessive reactive oxygen species (ROS) in HUVECs. The ROS scavenger (±)-α-tocopherol and the NFκB inhibitor BAY11-7082 reversed the upregulation of NLRP3 expression and the increase in NLRP3 inflammasome activation induced by PCB 118 exposure in HUVECs. Additionally, PCB 118-induced oxidative stress and pyroptosis were dependent on Aryl hydrocarbon receptor (AhR) activation and subsequent cytochrome P450 1A1 upregulation, which we confirmed by using the AhR selective antagonist CH 223191. These data suggest that PCB 118 exposure induces NLRP3 inflammasome activation and subsequently leads to pyroptosis in endothelial cells in vitro and in vivo. AhR-mediated ROS production play a central role in PCB 118-induced pyroptosis by priming NFκB-dependent NLRP3 expression and promoting inflammasome activation.

Successful Treatment of Eczema-Like Mucormycosis in a Child by Combination of Intravenous Drip and Percutaneous Injection Amphotericin B.

We report a case of eczema-like cutaneous mucormycosis caused by Rhizopus arrhizus. A 4-year-old child was presented to our hospital with a history of gradually enlarging papule and plaque in the periumbilical area for nearly 4 years since 2 weeks after his birth, and it has been misdiagnosed as eczema for nearly 3 years. Based on histopathology examination, the fungus culture test and DNA sequencing, it was revealed that R. arrhizus should be the responsible fungus for skin infection. The patient was successfully cured by combination of intravenous drip and percutaneous injection amphotericin B for nearly 3 months, and no recrudescence was seen during a follow-up of 6-month observation.

Profiling analysis of 17ß-estradiol-regulated lncRNAs in mouse thymic epithelial cells.

Thymus is the primary organ for T cell differentiation and maturation. Many studies have demonstrated that estrogen plays a crucial role in thymic epithelial cell (TEC) proliferation during thymic involution. LncRNAs are involved in various biological processes; however, estrogen-mediated lncRNA expression in TECs has not been yet reported. To address this question, the mouse medullary thymic epithelial cell line 1 (MTEC1) was treated with 17ß-estradiol (E2). By using CCK8 assay and flow cytometry, we found that E2 was able to inhibit viability and proliferation of MTEC1 cells. The expression profiles of lncRNAs in MTEC1 cells with or without E2 treatment were then measured by RNA-Seq, and a total of 962 lncRNAs and 2,469 mRNAs were shown to be differentially expressed. The reliability of RNA-Seq was confirmed by quantitative RT-PCR. Correlation analysis was conducted to investigate the potential function of lncRNAs. According to gene ontology (GO) analysis, differentially expressed lncRNAs were mainly related to cell proliferation, cell cycle and cell apoptosis. KEGG pathway analysis indicated that these lncRNAs were associated with several pathways, namely immunological activity, metabolism and cytokine-cytokine receptor interaction. In conclusion, our study provided a novel direction for studying the relationship between lncRNAs and E2 in the thymus.

Transcriptional profiling analysis of Zearalenone-induced inhibition proliferation on mouse thymic epithelial cell line 1.

Zearalenone (ZEA) was a mycotoxin biosynthesized by a variety of Fusarium fungi via a polypeptide pathway. ZEA has significant toxic reaction on immune cells. Thymic epithelial cells (TECs) as a crucial constituent of thymic stroma can provide unique microenvironment for thymocyte maturation, but the mechanism of ZEA affecting the TECs is poorly understood. The basic data about gene expression differences for the ZEA on thymic epithelial cell line 1 (MTEC1) will help us to elucidate this mechanism. Here, cell viability and proliferation assay and transcriptome sequencing on MTEC1 treated with ZEA were performed. 4188 differentially expressed genes (DEGs) between ZEA treated and control groups were identified, confirmed and analyzed. Our results showed that 10-50µg/ml ZEA significantly inhibited MTEC1 proliferation and arrested cell cycle at G2/M phase. Gene ontology and KEGG pathway analysis revealed that Chemokine, JAK-STAT and Toll-like receptor signaling pathway, were involved in the cell cycle pathway. 16 key genes involved in the cell cycle processes were validated and the results suggested that Mitotic catastrophe (MC) may take part in ZEA inhibition of METC1 cell proliferation. These data highlighted the importance of cell cycle pathway in MTEC1 treated with ZEA, and will contribute to get the molecular mechanisms of ZEA inhibition of MTEC1 cell proliferation.

Successful Treatment by Surgery of a Primary Cutaneous Mucormycosis Caused by Mucor irregularis.

We report a case of primary cutaneous mucormycosis caused by Mucor irregularis. A 66-year-old man was presented to our hospital with a history of gradually enlarging plaque on the right leg for about a year. The identification of pathogen based on the fungus morphology and DNA sequencing revealed M. irregularis as the responsible fungus for skin lesion. The lesion was removed incidentally by a surgery procedure, and no recrudescence was seen during a follow-up of 24-month observation.

2,3',4,4',5-Pentachlorobiphenyl impairs insulin-induced NO production partly through excessive ROS production in endothelial cells.

Polychlorinated biphenyls (PCBs) have been reported to be associated with increased risk to hypertension, atherosclerosis, cardiovascular disease, etc. 2,3',4,4',5-Pentachlorobiphenyl, known as PCB-118, is a member of coplanar PCBs which renders their structure similar to polychlorinated dibenzo-p-dioxins (PCDDs) and has dioxin-like activity. In our current study, we investigated the effect of PCB-118 exposure on nitric oxide (NO) production and the underlying mechanisms in vitro. Exposure of PCB-118 impaired insulin-induced NO production and endothelial nitric oxide synthase (eNOS) activity in human umbilical vein endothelial cells (HUVECs) with no significant effect on cell viability. Furthermore, PCB-118 treatment induced oxidative stress. In addition, scavenging of reactive oxygen species (ROS) by 10 µM N-acetyl-l-cysteine (NAC) partly rescued impaired insulin-induced eNOS activities and NO productions induced by PCB-118 in HUVECs. Taken together, these results indicate that PCB-118 mediates lower eNOS activity and impairs insulin-induced NO production partly through excessive ROS production in endothelial cells.

PCB 118-induced endothelial cell apoptosis is partially mediated by excessive ROS production.

Endothelial cell apoptosis, which may alter the integrity of the endothelium and lead to plaque instability, plays a critical role in the development and pathogenesis of atherosclerosis. Exposure of polychlorinated biphenyls (PCBs) is associated with increased risk of atherosclerosis and cardiovascular disease. In our present study, we explored whether exposure to PCB 118 influences endothelial cell apoptosis in vitro and the underlying mechanisms involved. As expected, exposure to PCB 118 increased the intracellular reactive oxygen species (ROS) levels in HUVECs. Increases in apoptosis and Bax/Bcl-2 ratios were observed in PCB 118-treated HUVECs. N-acetyl-l-cysteine (NAC), a ROS scavenger, partially reduced PCB 118-induced apoptosis and Bax/Bcl-2 ratios in HUVECs. Taken together, PCB 118-induced endothelial cell apoptosis was partially initiated by excessive ROS production.

Preoperative Biometric Parameters Predict the Vault after ICL Implantation: A Retrospective Clinical Study.

PURPOSE: To investigate the correlation between the preoperative biometric parameters of the anterior segment and the vault after implantable Collamer lens (ICL) implantation via this retrospective study. DESIGN: Retrospective clinical study. METHODS: A total of 78 eyes from 41 patients who underwent ICL implantation surgery were included in this study. Preoperative biometric parameters, including white-to-white (WTW) diameter, central corneal thickness, keratometer, pupil diameter, anterior chamber depth, sulcus-to-sulcus diameter, anterior chamber area (ACA) and central curvature radius of the anterior surface of the lens (Lenscur), were measured. Lenscur and ACA were measured with Rhinoceros 5.0 software on the image scanned with ultrasound biomicroscopy (UBM). The vault was assessed by UBM 3 months after surgery. Multiple stepwise regression analysis was employed to identify the variables that were correlated with the vault. RESULTS: The results showed that the vault was correlated with 3 variables: ACA (22.4 ± 4.25 mm2), WTW (11.36 ± 0.29 mm) and Lenscur (9.15 ± 1.21 mm). The regressive equation was: vault (mm) = 1.785 + 0.017 × ACA + 0.051 × Lenscur - 0.203 × WTW. CONCLUSIONS: Biometric parameters of the anterior segment (ACA, WTW and Lenscur) can predict the vault after ICL implantation using a new regression equation.

Short-term and long-term outcomes of surgical treatment for HCC within Milan criteria with cirrhotic portal hypertension.

BACKGROUND/AIMS: To compare and assess the outcomes of liver resection, radiofrequency ablation and liver transplantation for patients with hepatocellular carcinoma (HCC) within Milan criteria and cirrhotic portal hypertension. METHODOLOGY: 248 patients with HCC within Milan criteria and cirrhotic portal hypertension who underwent surgical treatments (liver resection, radiofrequency ablation and liver transplantation were reviewed in this study. Patients were divided into three groups according to different surgical strategies: RST Group, RFA Group and LT Group. Pre- and intra-operative parameters were statistically analyzed. Postoperative outcomes including Hematological data and tumor data, complications, long-term survival rates and recurrence-free survival rates were compared. RESULTS: The incidence of postoperative complications that were classified according to Clavien-Dido Classification were 16.22% for RST Group, 9.09% for RFA Group and 53.85% for LT Group. The 1-, 2- and 3-year recurrence-free survival rate of three groups were 88%, 74%, 68% for RST Group, 60%, 39%, 35% for RFA Group and 97%, 89%, 87% for LT Group, respectively. CONCLUSION: Although the postoperative recurrence rate following RFA was higher than that of RST and LT, the long-term survival rates of three managements for patients with HCC within Milan criteria and portal hypertension were similar.

Reconsideration of liver transplantation for portal hypertension due to hepatitis B cirrhosis: a single center experience.

BACKGROUND/AIMS: Some patients with portal hypertension due to hepatitis B cirrhosis who were suitable for periesophagogastric devascularization with splenectomy (PDS) also met the indications of liver transplantation (LT), the study compared the effect of PDS and LT, and of PDS followed by LT when required. METHODOLOGY: Patients with portal hypertension due to hepatitis B cirrhosis were analyzed. Patients were organized into PDS or LT groups, and PDS followed by LT. RESULTS: The PDS group suffered from lower incidence of severe postoperative complications (p=0.007) and perioperative death (p=0.015) than group LT. The 1-, 3- and 5-year survival rates of the PDS and LT groups were 99.3%, 98.1% and 89.0%, and 91.1%, 85.4% and 79.0%, respectively (p=0.04). There were no significant differences in severe postoperative complications (p=1.000) or perioperative mortality (p=1.000) between the PDS followed by LT and the LT groups, and their 1-, 3- and 5-year survival rates were 91.2%, 82.1% and 82.1%, and 91.1%, 85.4% and 79.0%, respectively (p=0.694). CONCLUSION: For patients with portal hypertension due to hepatitis B cirrhosis, when they satisfy the indications for both PDS and LT, we appeal to perform PDS as bridging therapy for final liver transplantation.

Roles of Rho/Rock signaling pathway in silica-induced epithelial-mesenchymal transition in human bronchial epithelial cells.

OBJECTIVE: To investigate the roles of Rho/Rock signaling pathway in silica-induced Epithelial-mesenchymal transition (EMT) in human bronchial epithelial cells (BEC) in vitro. METHODS: Human BEC were incubated with silica with various concentrations for indicated times. Cell viability was assayed by MTT test. Morphologic Changes were observed by microscope. Mesenchymal marker α-smooth muscle actin (α-SMA), vimentin (Vim), and epithelial marker E-cadherin (E-cad) were analyzed by Western Blot. The pull-down assay was used to measure Rho activity. In the prevention experiments, the specific inhibitor for Rho effector ROCK (Y27632) was used to inhibit the activity of Rho. RESULTS: Human BEC stimulated with silica were converted from a "cobblestone" epithelial structure into an elongated fibroblast-like shape structure. Incubation of human BEC with silica induced de novo expression of α-SMA and Vim, and loss of E-cad. Also, silica treatment resulted in Rho activation in human BEC. Y27632 up-regulated the E-cad expression but attenuated α-SMA and Vim expression in silica-stimulated cells. CONCLUSION: The activation of Rho/ROCK signaling pathways is most likely involved in Silica-induced EMT in human bronchial epithelial cells.

Construction and Validation of a Novel Prognosis Model in Colon Cancer Based on Cuproptosis-Related Long Non-Coding RNAs.

Colon cancer (CC) is one of the most common (6%) malignancies and leading cause of cancer-associated death (more than 0.5 million) worldwide, which demands reliable prognostic biomarkers. Cuproptosis is a novel modality of regulated cell death triggered by the accumulation of intracellular copper. LncRNAs have been reported as prognostic signatures in different types of tumors. However, the correlation between cuproptosis-related lncRNAs (CRLs) and CC remains unclear. Data of CC patients were downloaded from public databases. The prognosis-associated CRLs were identified by co-expression analysis and univariate Cox. Least absolute shrinkage and selection operator were utilized to construct the CRLs-based prognostic signature in silico for CC patients. CRLs level was validated in human CC cell lines and patient tissues. ROC curve and Kaplan-Meier curve results revealed that high CRLs-risk score was associated with poor prognosis in CC patients. Moreover, the nomogram revealed that this model possessed a steady prognostic prediction capability with C-index as 0.68. More importantly, CC patients with high CRLs-risk score were more sensitive to eight targeted therapy drugs. The prognostic prediction power of the CRLs-risk score was further confirmed by cell lines, tissues and two independent CC cohorts. This study constructed a novel ten-CRLs-based prognosis model for CC patients. The CRLs-risk score is expected to serve as a promising prognostic biomarker and predict targeted therapy response in CC patients.

Role of MEG3 in Cellular Physiology of Atherosclerosis.

OBJECTIVE: To investigate the role of the lncRNA MEG3 (MEG3) in opposing the biochemical processes thought to be involved in the development of atherosclerosis (AS). METHODS: Thirty patients with AS and thirty healthy control subjects were enrolled in this study. The expression of MEG3, miR-200b-3p and ABCA1 was analyzed by RT-qPCR in the individuals and the macrophages-derived foam cells. Lipid accumulation was detected by oil red O staining. Cholesterol efflux was measured by ELISA assay in the foam cells. Expression of miR-200b-3p was identified by sequencing. Targeting relationships were determined by dual luciferase assay between MEG3 and miR-200b-3p, miR-200b-3p and ABCA1. RESULTS: In the patients with AS, MEG3 and ABCA1 expression were decreased and miR-200b-3p expression was upregulated. Foam cells transfected with an expression vector (pcDNA3.1) containing MEG3 (pcDNA3.1-MEG3) induced decrease of lipid accumulation and increase of cholesterol efflux compared to cells transfected with control plasmid alone. Foam cells transfected by pcDNA3.1-MEG3 also showed decreased miR-200b-3p and increased ABCA1 expression. Interestingly, co-expression of miR-200b-3p partially prevented these effects of MEG3 expression. CONCLUSION: Expression of MEG3 is downregulated in the patients with AS and foam cells. Overexpressed MEG3 may act as an anti-atherosclerotic factor by reducing lipid accumulation and accelerating cholesterol efflux through the miR-200b-3p/ABCA1 axis.

Safety of synchronous hepatectomy and splenectomy for patients with hepatocellular carcinoma and hypersplenism.

BACKGROUND/AIMS: To assess the surgical safety of synchronous hepatic resection and splenectomy for patients with hepatocellular carcinoma (HCC) and hypersplenism. METHODOLOGY: Patients with HCC and hypersplenism who underwent surgical treatment were included in this study. According to the difference of operations, patients were divided into two groups (group A, patients who underwent hepatic resection; group B, patients who underwent synchronous hepatic resection and hypersplenism). Pre- and intra-operative parameters were statistically analyzed. Postoperative outcomes including white blood cell and platelet count changes, surgical complications and long-term survival rates were compared. RESULTS: The pre- and intra-operative parameters of two groups were comparable except for preoperative white blood cell and platelet counts. The incidences of postoperative surgical complication were 53.33% for group A and 35.48% for group B (p=0.161). The 1- and 3-year survival rates of the two groups were 83%, 42% and 82%, 54%, respectively (p=0.313). CONCLUSIONS: Synchronous hepatic resection and splenectomy could increase the postoperative WBC and platelet level for patients with hepatocellular carcinoma and hypersplenism without increasing surgical risks.

A Novel m7G-Related Gene Signature Predicts the Prognosis of Colon Cancer.

Colon cancer (CC), one of the most common malignancies worldwide, lacks an effective prognostic prediction biomarker. N7-methylguanosine (m7G) methylation is a common RNA modification type and has been proven to influence tumorigenesis. However, the correlation between m7G-related genes and CC remains unclear. The gene expression levels and clinical information of CC patients were downloaded from public databases. Twenty-nine m7G-related genes were obtained from the published literature. Via unsupervised clustering based on the expression levels of m7G-related genes, CC patients were divided into three m7G clusters. Based on differentially expressed genes (DEGs) from the above three groups, CC patients were further divided into three gene clusters. The m7G score, a prognostic model, was established using principal component analysis (PCA) based on 15 prognosis-associated m7G genes. KM curve analysis demonstrated that the overall survival rate was remarkably higher in the high-m7G score group, which was much more significant in advanced CC patients as confirmed by subgroup analysis. Correlation analysis indicated that the m7G score was associated with tumor mutational burden (TMB), PD-L1 expression, immune infiltration, and drug sensitivity. The expression level of prognosis-related m7G genes was further confirmed in human CC cell lines and samples. This study established an m7G gene-based prognostic model (m7G score), which demonstrated the important roles of m7G-related genes during CC initiation and progression. The m7G score could be a practical biomarker to predict immunotherapy response and prognosis in CC patients.

Optimal level of 25-(OH)D in children in Nanjing (32°N Lat) during winter.

BACKGROUND: The optimal serum level of 25-hydroxyvitamin D (25-(OH)D) for bone health is still unclear, especially in children. Hypovitaminosis D is also re-emerging in developed and developing countries. The purpose of the present study was therefore to determine optimal serum 25-(OH)D level and preliminarily identify the vitamin D nutritional status in Nanjing children. METHODS: All subjects (76 healthy, 66 suffering from infectious diseases) aged 0-10 years were recruited during the period December 2007-March 2008. Venous blood samples were collected before breakfast and the levels of serum 25-(OH)D, parathyroid hormone (PTH), bone-specific alkaline phosphatase (BAP), calcium (Ca), phosphorus (P) were determined. The optimal level of serum 25-(OH)D was explored using the three response curves of 25-(OH)D versus PTH, 25-(OH)D versus BAP, and 25-(OH)D versus Ca×P product. RESULTS: For 25-(OH)D ≤ 50 nmol/L, PTH and BAP were both inversely correlated with 25-(OH)D (PTH, r=-0.864, P < 0.01; BAP, r=-0.856, P < 0.01). For 25-(OH)D > 50-60 nmol/L, levels of PTH and BAP remained steady. With regard to the Ca×P product, for 25-(OH)D ≤ 50 nmol/L, Ca×P product increased as 25-(OH)D increased (r= 0.037, P > 0.05). For 25-(OH)D > 50-60 nmol/L, Ca×P product remained steady. The mean serum level of 25-(OH)D was 80.5 ± 29.3 nmol/L (mean ± SD) in the healthy children, and 65.7 ± 32.3 nmol/L in the sick children. CONCLUSION: The optimal 25-(OH)D level may be 50-60 nmol/L for bone health in Nanjing children. The vitamin D nutritional status of Nanjing children is relatively good in winter.

[The influence of SiO2 on epithelial-mesenchymal transition (EMT) in human bronchial epithelial cells].

OBJECTIVE: To investigate SiO2-induced EMT in human bronchial epithelial cells HBE in vitro. METHODS: HBE cells were cultured and then stimulated with indicated doses of SiO2 (0, 50, 100, 200, 300 µg/ml). The morphological changes were observed by microscope. In addition, Western blot was per-formed to detect the expression of E-cad, α-SMA and Vim. The changes of migration ability were examined by wound-healing assay in vitro. RESULTS: (1) After exposure to SiO2, HBE cells lost contact with their neighbor and displayed a spindle-shape, fibroblast-like morphology. (2) Compared with the control, the E-cad (300 µg/ml group) expression downregulated 2.98 fold (P < 0.05), and the Vim (300 µg/ml group) and α-SMA (200 µg/ml group) expression upregulated 4.46 fold and 3.55 fold (P < 0.05). There were significant differences between 100, 200, 300 µg/ml groups and the control group (P < 0.05). (3) In the test group, the percentage of wound-healing areas/wound areas were larger than those in control group (P < 0.05). CONCLUSIONS: SiO2 could induce EMT in human bronchial epithelial cells.

A Method for the Analysis of African Swine Fever by Viral Metagenomic Sequencing.

In 2018, there was an outbreak of African swine fever (ASF) in China, which spread to other provinces in the following 3 years and severely damaged China's pig industry. ASF is caused by the African swine fever virus (ASFV). Given that the genome of the African swine fever virus is very complex and whole genome information is currently inadequate, it is important to efficiently obtain virus genome sequences for genomic and epidemiological studies. The prevalent ASFV strains have low genetic variability; therefore, whole genome sequencing analysis provides a basis for the study of ASFV. We provide a method for the efficient sequencing of whole genomes, which requires only a small number of tissues. The database construction method was selected according to the genomic types of ASFV, and the whole ASFV genome was obtained through data filtering, host sequence removal, virus classification, data assembly, virus sequence identification, statistical analysis, gene prediction, and functional analysis. Our proposed method will facilitate ASFV genome sequencing and novel virus discovery.