Virologica Sinica最新文献

{"title":"ZNF598 enhances FAT10-mediated non-covalent stabilization of Tat to promote HIV-1 transcription and replication.","authors":"Hongyun Shi, Panpan Quan, Chaohui Tang, Yubao Hou, Huihan Wang, Yingchao Wang, Hong Wang, Wenyan Zhang","doi":"10.1016/j.virs.2026.07.007","DOIUrl":"10.1016/j.virs.2026.07.007","url":null,"abstract":"<p><p>Human immunodeficiency virus type 1 (HIV-1) Tat is essential for efficient viral transcription and replication, and its stability is tightly controlled by host factors. In our previous study, we showed that ZNF598 stabilizes Tat and promotes HIV-1 replication through an E3 ligase activity-independent mechanism. Here, we identify FAT10 as a critical mediator of this effect. FAT10 knockout in HEK293T cells or FAT10 knockdown in Jurkat T-cell infection models markedly impaired the ability of ZNF598 to suppress Tat K48-linked ubiquitination, increase Tat abundance, and enhance HIV-1 replication. Mechanistically, FAT10 reduced Tat K48-linked ubiquitination, stabilized Tat, and promoted HIV-1 transcription and replication. Direct GST pull-down assays further demonstrated that FAT10 directly binds Tat in vitro, and this interaction was retained by a FAT10 mutant lacking the C-terminal diglycine motif, supporting a predominantly non-covalent mechanism rather than canonical FAT10ylation. Consistently, ZNF598 enhanced the FAT10-Tat interaction, whereas ZNF598 knockdown attenuated FAT10-mediated Tat stabilization and proviral effects. In addition, the N-terminal 1-32 amino acids of Tat were required for responsiveness to both ZNF598 and FAT10. Finally, FAT10 expression was increased in HIV-1-infected cells and in CD4⁺ T cells from HIV-infected individuals, where it was associated with clinical markers of disease activity and viral load. Together, these findings define a ZNF598-FAT10-Tat regulatory axis that promotes HIV-1 transcription and replication.</p>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2026-07-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148537289","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatitis B virus promotes hepatocellular carcinoma progression by disrupting NSUN2/YBX1-mediated m5C modification of PTEN mRNA","authors":"Mengxian Lin,&nbsp;Kunqi Chen,&nbsp;Hang Li,&nbsp;Xinjian Lin,&nbsp;Shuxiang Wu,&nbsp;Xu Lin","doi":"10.1016/j.virs.2026.03.001","DOIUrl":"10.1016/j.virs.2026.03.001","url":null,"abstract":"<div><div>Hepatitis B virus (HBV) has been implicated in hepatocellular carcinoma (HCC) progression, partly through regulation of the tumor suppressor phosphatase and tensin homolog (PTEN). Although transcriptional regulation of PTEN by HBV is well characterized, its post-transcriptional regulation remains poorly understood. Because RNA 5-methylcytosine (m⁵C) modification influences post-transcriptional gene control and cancer development, we investigated whether HBV modulates PTEN through m⁵C. Methylated RNA immunoprecipitation (MeRIP)–quantitative polymerase chain reaction showed a marked reduction in m⁵C on <em>PTEN</em> mRNA in HBV-producing cells. MeRIP sequencing further identified decreased m⁵C within the PTEN coding sequence region (chr10:89717747–89717771) in HBV-producing HepAD38/tetracycline-off cells, with chr10:89717756 emerging as a critical site where HBV suppresses m⁵C enrichment and PTEN expression. Mechanistically, the m⁵C “writer” NOP2/Sun RNA methyltransferase 2 (NSUN2) and the “reader” Y-box binding protein 1 (YBX1) stabilized <em>PTEN</em> mRNA in an m⁵C-dependent manner. HBV disrupted this pathway, decreasing <em>PTEN</em> mRNA stability via NSUN2- and YBX1-mediated m⁵C. Overexpression of NSUN2 or YBX1 attenuated HBV-driven proliferation, migration, and invasion, and these effects were partially reversed by the PTEN inhibitor VO-Ohpic. The small hepatitis B surface antigen and hepatitis B X protein downregulated NSUN2 and YBX1, linking viral proteins to PTEN suppression. Further, HBV is associated with reduced NSUN2 expression in HBV transgenic (HBV-Tg) mice, HBV-infected primary human hepatocytes as well as HBV-positive clinical HCC specimens, supporting the physiological and clinical relevance of this finding. Together, these findings identify the NSUN2/YBX1/PTEN axis as a potential therapeutic target in HBV-associated HCC.</div></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":"41 3","pages":"Pages 543-560"},"PeriodicalIF":4.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147459841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antiviral activity of Saponin C from Liriope muscari against influenza A virus and SARS-CoV-2","authors":"Yuhan Gong,&nbsp;Junwen Liu,&nbsp;Wenxuan Ding,&nbsp;Yuxing Yan,&nbsp;Xue Hu,&nbsp;Gary Wong,&nbsp;Huaijie Jia,&nbsp;Zhengxiang Wang,&nbsp;Xin Li,&nbsp;Jiayi Chen,&nbsp;Xin Zhang,&nbsp;Chao Shan,&nbsp;Shuai Xu,&nbsp;Xiaoxia Wang","doi":"10.1016/j.virs.2026.06.002","DOIUrl":"10.1016/j.virs.2026.06.002","url":null,"abstract":"<div><div>Saponin C (also known as DT-13) is the dominant ingredient extracted from the tuber of <em>Liriope muscari</em> (Decne.) L. H. Bailey, which exhibits multiple pharmacological activities, including anti-tumor, anti-thrombotic, cardioprotective and anti-inflammatory effects. However, its antiviral potential remains unexplored. This study aimed to investigate the inhibitory activity and underlying mechanisms of Saponin C against both influenza A virus (IAV) and SARS-CoV-2. <em>In vitro</em> experiments demonstrated that Saponin C dose-dependently inhibited IAV replication in MDCK and A549 cells. Time-of-addition assay revealed that Saponin C targeted the post-entry stages of IAV replication by impairing viral ribonucleoprotein (vRNP) function. This was evidenced by the suppression of viral polymerase activity, reduction of viral RNA synthesis, and delayed nuclear export of vRNP. The <em>in vivo</em> efficacy was further validated in a lethal H1N1 mouse model, where both prophylactic and therapeutic administration of Saponin C significantly improved the survival rate of infected mice, reduced viral loads in lung tissues, and attenuated virus-induced pulmonary inflammation in a dose-dependent manner. Beyond IAV, Saponin C also effectively inhibited SARS-CoV-2 infection by blocking viral entry, specifically through interfering with the binding of viral spike protein to the human ACE2 receptor and suppressing spike-mediated membrane fusion. Collectively, these findings demonstrate that Saponin C possesses antiviral potential against IAV and SARS-CoV-2, and may thus serve as a promising therapeutic agent for the treatment of respiratory viral infections.</div></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":"41 3","pages":"Pages 662-675"},"PeriodicalIF":4.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148164836","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic efficacy of a K1-specific bacteriophage against hypervirulent Klebsiella pneumoniae in a mouse infection model","authors":"Xiaona Yan,&nbsp;Mengmeng Su,&nbsp;Sixiang Xu,&nbsp;Xiangkuan Zheng,&nbsp;Xiaoyue Li,&nbsp;Peifan Liu,&nbsp;Yilin Fang,&nbsp;Libin Tan,&nbsp;Long Chen,&nbsp;Hong Du,&nbsp;Panpan Tong,&nbsp;Yuxia Zhang,&nbsp;Qinghai Ren,&nbsp;Wei Zhang","doi":"10.1016/j.virs.2026.06.003","DOIUrl":"10.1016/j.virs.2026.06.003","url":null,"abstract":"<div><div><em>Klebsiella pneumoniae</em> is an important opportunistic pathogen in both humans and animals. Controlling it has become increasingly difficult due to the rapid spread of antimicrobial resistance. In this study, we isolated and characterized a novel lytic bacteriophage, vB_Kp_Z1, and evaluated its therapeutic efficacy against K1-serotype <em>K. pneumoniae</em>. Host range analysis showed that vB_Kp_Z1 was strictly specific to K1 strains, as confirmed across multiple prevalent capsular types. The <em>in vivo</em> efficacy of vB_Kp_Z1 was assessed using intraperitoneal infection models in mice. Two hypervirulent K1 strains were used: a pigeon-derived strain (KP1897) and a human clinical strain (KP177). Phage treatment significantly improved survival compared with phosphate-buffered saline-treated controls. It provided complete protection in KP1897-infected mice and achieved an 87.5% survival rate in KP177-infected mice. In addition, phage administration markedly reduced bacterial loads in the blood, liver, and lungs, indicating effective control of systemic dissemination. These findings demonstrate that vB_Kp_Z1 is a K1-specific bacteriophage with therapeutic potential against hypervirulent <em>K. pneumoniae</em>, including strains from different host species.</div></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":"41 3","pages":"Pages 676-687"},"PeriodicalIF":4.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148177021","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Crimean-Congo hemorrhagic fever: An emerging threat in Europe","authors":"Mohammad Fereidouni (محمد فریدونی),&nbsp;Jens H. Kuhn,&nbsp;David B. Pecor,&nbsp;Dmitry A. Apanaskevich (Апанаскевич Дмитрий Александрович),&nbsp;Kurtesh Sherifi,&nbsp;Jelena Protić (Jелена Протић),&nbsp;Teodora Karevska (Теодора Каревска),&nbsp;Golubinka Boshevska (Голубинка Бошевска),&nbsp;María Paz Sánchez-Seco,&nbsp;Anna Papa (Άννα Παπά),&nbsp;Maryam Keshtkar-Jahromi (مریم کشتکار جهرمی)","doi":"10.1016/j.virs.2025.12.006","DOIUrl":"10.1016/j.virs.2025.12.006","url":null,"abstract":"<div><div>Crimean-Congo hemorrhagic fever (CCHF), caused by Crimean-Congo hemorrhagic fever virus (CCHFV), is endemic in Africa, Asia, and Europe. However, CCHF epidemiology and epizootiology have been poorly defined in Europe. Here, we summarize the current knowledge of CCHFV distribution in (non-Russian) Europe, including countries previously not considered to be at risk. We collected data on CCHF cases, human/vertebrate animal anti-CCHFV seroprevalence, CCHFV vector (<em>Hyalomma</em> tick), and CCHFV isolation from ticks and classified countries into five risk levels using a One Health approach. From 1944 through Feb 2025, more than 2000 recorded CCHF cases were identified in Europe, mostly from southern/eastern countries/regions, primarily Bulgaria (at least 1623), Kosovo (at least 339), Ukraine (at least 336), Croatia (at least 200), Albania (at least 146), and Republic of Moldova (at least 60). Albania, Bulgaria, Greece, Kosovo, and Spain were categorized as level 1 (reported CCHF cases, presence of robust surveillance systems). North Macedonia, Portugal, and Ukraine/Crimea were assigned to level 2 (reported CCHF cases in the absence of robust established surveillance). Bosnia and Herzegovina, Croatia, France, Hungary, Italy, Montenegro, Republic of Moldova, Romania, and Slovenia were assigned to level 3 due to evidence of CCHFV circulation in absence of recent CCHF cases. Thirty-four countries were assigned to level 4 (presence of <em>Hyalomma</em> ticks) or level 5 (no data). This work provides information on CCHFV distribution and burden with list of at-risk areas to inform international and local public health agencies to establish or strengthen surveillance systems.</div></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":"41 3","pages":"Pages 493-512"},"PeriodicalIF":4.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145775483","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immune profile and mitochondrial alterations driven by age and HIV infection: Associations with T-cell senescence in people with HIV receiving suppressive antiretroviral therapy","authors":"Junyan Jin,&nbsp;Xin Zhang,&nbsp;Qianqian Xu,&nbsp;Wei Xia,&nbsp;Hongxia Yan,&nbsp;Hao Wu,&nbsp;Christiane Moog,&nbsp;Tong Zhang,&nbsp;Bin Su","doi":"10.1016/j.virs.2026.05.001","DOIUrl":"10.1016/j.virs.2026.05.001","url":null,"abstract":"<div><div>Antiretroviral therapy (ART) has significantly extended the life expectancy of people with HIV (PWH), rendering population ageing and immunosenescence prominent clinical priorities. T-cell senescence is linked to mitochondrial dysfunction and drives age-related immune remodelling, yet how HIV infection and ageing jointly shape CD4⁺ and CD8⁺ T-cell immunophenotypes and mitochondrial remodelling remains unclear. This cross-sectional study included 61 PWH on suppressive ART for ≥ 12 months and 61 age- and sex-matched HIV-negative men who have sex with men, stratified into younger (≤ 35 years) and older (≥ 50 years) groups. Multiparameter flow cytometry was used to profile CD4⁺ and CD8⁺ T-cell differentiation, stemness, activation/exhaustion, and metabolic phenotypes, together with mitochondrial mass and membrane potential. We found that ageing and HIV infection were associated with T-cell remodelling, characterized by expanded late-differentiated phenotypes and reduced stem-like, homeostatic and costimulatory CD4⁺ and CD8⁺ T-cell subsets, as indicated by upregulated CD57 and CX3CR1 and downregulated CD45RA⁺CD31⁺, FOXO1, and CD28. Notably, younger PWH had an ageing-like CD4⁺ T-cell profile, with higher CD57, CX3CR1 and TIGIT expression than younger HIV-negative individuals. In contrast, HIV-related CD8⁺ T-cell perturbations (KLRG1, CXCR3, NKG2C and CD95) were more pronounced in older PWH. PWH exhibited increased mitochondrial mass and membrane potential in both total and senescent-like CD4⁺ and CD8⁺ T cells, particularly in CD8⁺ T cells from older PWH. In CD4⁺ T cells, KLRG1 and CX3CR1 expression correlated positively with age, and inversely with CD4⁺ T-cell counts and CD4/CD8 ratio. By contrast, FOXO1 expression in CD8⁺ T cells was inversely associated with age, late-differentiation markers, and ART duration in PWH. Overall, age is a major driver of T-cell immunosenescence, and HIV infection modulates and exacerbates these alterations. Mitochondrial stress, FOXO1 downregulation and immune network remodelling support a multifaceted model of HIV-associated immune ageing that may contribute to heterogeneous immune reconstitution in PWH, highlighting potential targets to mitigate immune ageing.</div></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":"41 3","pages":"Pages 561-573"},"PeriodicalIF":4.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147949751","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"RNF26 bridges ER stress and autophagy in the clearance of MERS envelope protein","authors":"Ziyue Li,&nbsp;Yang Wang,&nbsp;Jingbo Qie,&nbsp;Shuangqu Li,&nbsp;Zhaobing Gao,&nbsp;Hin Chu,&nbsp;Bingqing Xia","doi":"10.1016/j.virs.2026.06.005","DOIUrl":"10.1016/j.virs.2026.06.005","url":null,"abstract":"<div><div>Coronavirus envelope (E) proteins are small, highly conserved viroporins essential for virion assembly and pathogenicity. Despite extensive characterization of their ion channel activity, how host cells sense and dispose of excessive viral membrane proteins remains poorly understood. Here we show that expression of the MERS-CoV E protein triggers pronounced ER stress and autophagy activation in human cells. The E protein is selectively degraded through an RNF26-dependent autophagy-lysosome pathway, and inhibition of autophagy or loss of RNF26 function leads to E accumulation and sustained unfolded protein response. Mechanistically, RNF26, an ER-anchored E3 ubiquitin ligase, promotes RING-dependent clearance of the viral protein through an ER protein quality control-associated pathway linked to autophagy and ER stress adaptation. Disruption of this process establishes a self-amplifying ER stress–autophagy feedback loop that exacerbates proteotoxicity. These findings define a membrane homeostatic conflict between viral viroporins and the host defense machinery, and identify RNF26 as a potential therapeutic target for mitigating viroporin-induced cytotoxicity through host-directed intervention.</div></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":"41 3","pages":"Pages 612-623"},"PeriodicalIF":4.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148212710","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"First complete genomic sequencing of recent canine rabies viruses in Sierra Leone suggests cross-border transmission of Africa 2H subclade","authors":"Sheng Sun,&nbsp;Abdul Gudush Jalloh,&nbsp;Jinxia Zhang,&nbsp;Shuo Yu,&nbsp;Xiankai Liu,&nbsp;Weidi Xu,&nbsp;Yan Liu,&nbsp;Changchun Tu,&nbsp;Ye Feng","doi":"10.1016/j.virs.2026.06.010","DOIUrl":"10.1016/j.virs.2026.06.010","url":null,"abstract":"","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":"41 3","pages":"Pages 728-731"},"PeriodicalIF":4.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148273144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The guanosine nucleotide analog bemnifosbuvir inhibits hepatitis E virus infection in cell and organoid models","authors":"Kuan Liu,&nbsp;Yang Wang,&nbsp;Xincheng Li,&nbsp;Yilan Zhao,&nbsp;Luc J.W. van der Laan,&nbsp;Pengfei Li,&nbsp;Qiuwei Pan","doi":"10.1016/j.virs.2026.05.010","DOIUrl":"10.1016/j.virs.2026.05.010","url":null,"abstract":"","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":"41 3","pages":"Pages 716-719"},"PeriodicalIF":4.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148164918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A C-type single-domain antibody with protective efficacy against H1N1 via respiratory administration","authors":"Bihao Wu,&nbsp;Haiwei Zhang,&nbsp;Xiangxing He,&nbsp;Zhe Zhang,&nbsp;Xiaohui Liu,&nbsp;Rui Gong","doi":"10.1016/j.virs.2026.05.007","DOIUrl":"10.1016/j.virs.2026.05.007","url":null,"abstract":"<div><div>Influenza A viruses, particularly H1N1, pose a significant public health threat, highlighting the continued need for novel prophylactics and therapeutics. Monoclonal antibodies are promising, but conventional IgGs face challenges in respiratory delivery due to their large size. This study presents A1-B7, a C-type single-domain antibody (C-sdAb) based on a scaffold derived from a human IgG1 CH2 domain, targeting the hemagglutinin (HA) of H1N1 influenza virus. A1-B7 potently neutralizes multiple H1N1 subtypes <em>in vitro</em>. Both prophylactic intranasal administration and therapeutic aerosol inhalation of A1-B7 confer complete protection and reduce live virus in the lungs to undetectable levels. Structural prediction and epitope mapping reveal that A1-B7 binds a conserved stem-region epitope, engaging the HA2 A-helix and a hydrophobic groove. A1-B7 can block low-pH induced conformational change of HA. These findings establish A1-B7 as a promising candidate for further development as a convenient, respiratory tract delivered countermeasure against influenza.</div></div>","PeriodicalId":23654,"journal":{"name":"Virologica Sinica","volume":"41 3","pages":"Pages 688-699"},"PeriodicalIF":4.7,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148057277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}