Virologica Sinica最新文献

英文中文

Characterization of a SARS-CoV-2 infection model in golden hamsters with diabetes mellitus 糖尿病金仓鼠SARS-CoV-2感染模型的建立

IF 5.5 3区医学 Q1 Medicine

Virologica Sinica

Pub Date : 2025-06-01 Epub Date: 2025-05-17 DOI: 10.1016/j.virs.2025.05.001

Hao-Feng Lin , Ren-Di Jiang , Rui-Xin Qin , Bing Yao , Wen-Tao Zeng , Yun Gao , Ai-Min Shi , Jian-Min Li , Mei-Qin Liu

Being widespread across the globe, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) keeps evolving and generating new variants and continuously poses threat to public health, especially to the population with chronic comorbidities. Diabetes mellitus is one of high-risk factors for severe outcome of coronavirus disease 2019 (COVID-19). Establishment of animal models that parallel the clinical and pathological features of COVID-19 complicated with diabetes is thus highly essential. Here, in this study, we constructed leptin receptor gene knockout hamsters with the phenotype of diabetes mellitus (db/db), and revealed that the diabetic hamsters were more susceptible to SARS-CoV-2 and its variants than wild-type hamsters. SARS-CoV-2 and its variants induced a stronger immune cytokine response in the lungs of diabetic hamsters than in wild-type hamsters. Comparative histopathology analyses also showed that infection of SARS-CoV-2 and the variants caused more severe lung tissue injury in diabetic hamsters, and may induce serious complications such as diabetic kidney disease and cardiac lesions. Our findings demonstrated that despite the decreased respiratory pathogenicity, the SARS-CoV-2 variants were still capable of impairing other organs such as kidney and heart in diabetic hamsters, suggesting that the risk of evolving SARS-CoV-2 variants to diabetic patients should never be neglected. This hamster model may help better understand the pathogenesis mechanism of severe COVID-19 in patients with diabetes. It will also aid in development and testing of effective therapeutics and prophylactic treatments against SARS-CoV-2 variants among these high-risk populations.

严重急性呼吸综合征冠状病毒2型（SARS-CoV-2）在全球广泛传播，不断演变并产生新的变体，不断对公众健康构成威胁，特别是对患有慢性合并症的人群。糖尿病是2019冠状病毒病（COVID-19）严重结局的高危因素之一。因此，建立符合新冠肺炎合并糖尿病临床和病理特征的动物模型是非常必要的。在本研究中，我们构建了具有糖尿病表型（db/db）的瘦素受体基因敲除仓鼠，发现糖尿病型仓鼠比野生型仓鼠更容易感染SARS-CoV-2及其变体。SARS-CoV-2及其变体在糖尿病仓鼠的肺部诱导的免疫细胞因子反应比野生型仓鼠更强。比较组织病理学分析还显示，感染SARS-CoV-2及其变体可导致糖尿病仓鼠更严重的肺组织损伤，并可能诱发糖尿病肾病和心脏病变等严重并发症。我们的研究结果表明，尽管呼吸致病性降低，但SARS-CoV-2变异仍然能够损害糖尿病仓鼠的其他器官，如肾脏和心脏，这表明SARS-CoV-2变异对糖尿病患者的风险绝不应被忽视。该仓鼠模型可能有助于更好地了解糖尿病患者重症COVID-19的发病机制。它还将有助于在这些高风险人群中开发和测试针对SARS-CoV-2变体的有效疗法和预防性治疗。

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引用次数: 0

Human endogenous retrovirus W family envelope protein (ERVWE1) regulates macroautophagy activation and micromitophagy inhibition via NOXA1 in schizophrenia 人内源性逆转录病毒W家族包膜蛋白（ERVWE1）通过NOXA1调控精神分裂症大自噬激活和微自噬抑制。

IF 5.5 3区医学 Q1 Medicine

Virologica Sinica

Pub Date : 2025-06-01 Epub Date: 2025-05-24 DOI: 10.1016/j.virs.2025.05.007

Jiahang Zhang , Huiling Wang , Xing Xue , Xiulin Wu , Wenshi Li , Zhao Lv , Yaru Su , Mengqi Zhang , Kexin Zhao , Xu Zhang , Chen Jia , Fan Zhu

The human endogenous retrovirus type W envelope glycoprotein (ERVWE1), located at chromosome 7q21–22, has been implicated in the pathophysiology of schizophrenia. Our previous studies have shown elevated ERVWE1 expression in schizophrenia patients. Growing evidence suggests that autophagy dysfunction contributes to schizophrenia, yet the relationship between ERVWE1 and autophagy remains unclear. In this study, bioinformatics analysis of the human prefrontal cortex RNA microarray dataset (GSE53987) revealed that differentially expressed genes were predominantly enriched in autophagy-related pathways. Clinical data further demonstrated that serum levels of microtubule-associated protein 1 light chain 3β (LC3B), a key marker of macroautophagy, were significantly elevated in schizophrenia patients compared to controls, and positively correlated with ERVWE1 expression. Cellular and molecular experiments suggested that ERVWE1 promoted macroautophagy by increasing the LC3B II/I ratio, enhancing autophagosome formation, and reducing sequestosome 1 (SQSTM1) expression via upregulation of NADPH oxidase activator 1 (NOXA1). Concurrently, NOXA1 downregulated the expression of key micromitophagy-related genes, including PTEN-induced kinase 1 (PINK1), Parkin RBR E3 ubiquitin-protein ligase (Parkin), and the pyruvate dehydrogenase E1 subunit α 1 (PDHA1). As a result, ERVWE1, via NOXA1, inhibited micromitophagy by suppressing the expression of PINK1, Parkin, and PDHA1, thereby leading to impaired production of mitochondrial-derived vesicles (MDVs). Mechanistically, ERVWE1 enhanced NOXA1 transcription by upregulating upstream transcription factor 2 (USF2). In conclusion, ERVWE1 promotes macroautophagy and inhibits micromitophagy through USF2-NOXA1 axis, providing novel mechanistic insight into the role autophagy dysregulation in schizophrenia. These findings suggest that targeting autophagy pathways may offer novel therapeutic strategies for schizophrenia treatment.

位于染色体7q21-22的人类内源性逆转录病毒型W包膜糖蛋白（ERVWE1）与精神分裂症的病理生理有关。我们之前的研究表明，ERVWE1在精神分裂症患者中表达升高。越来越多的证据表明，自噬功能障碍有助于精神分裂症，但ERVWE1与自噬之间的关系尚不清楚。在这项研究中，对人类前额叶皮层RNA微阵列数据集（GSE53987）的生物信息学分析显示，差异表达基因主要富集在自噬相关通路中。临床数据进一步表明，与对照组相比，精神分裂症患者血清巨噬的关键标志物微管相关蛋白1轻链3β (LC3B)水平显著升高，且与ERVWE1表达呈正相关。细胞和分子实验表明，ERVWE1通过上调NADPH氧化酶激活物1 (NOXA1)，提高LC3B /I比值，增强自噬体形成，降低固溶体1 （SQSTM1）表达，从而促进大细胞自噬。同时，NOXA1下调微丝自噬相关关键基因的表达，包括pten诱导的激酶1 （PINK1）、Parkin RBR E3泛素蛋白连接酶（Parkin）和丙酮酸脱氢酶E1亚基α 1 （PDHA1）。因此，ERVWE1通过NOXA1通过抑制PINK1、Parkin和PDHA1的表达来抑制微丝自噬，从而导致线粒体源性囊泡（mdv）的产生受损。在机制上，ERVWE1通过上调上游转录因子2 （USF2）来增强NOXA1的转录。综上所述，ERVWE1通过USF2-NOXA1轴促进大自噬并抑制微自噬，为自噬失调在精神分裂症中的作用提供了新的机制见解。这些发现表明，靶向自噬途径可能为精神分裂症治疗提供新的治疗策略。

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引用次数: 0

Decoding the virome reveals diverse novel viruses in tree shrews (Tupaia belangeri) in Yunnan Province 解码病毒组揭示了云南省树鼩（图帕亚belangeri）中多种新型病毒。

IF 5.5 3区医学 Q1 Medicine

Virologica Sinica

Pub Date : 2025-06-01 DOI: 10.1016/j.virs.2025.05.011

Zhong-Hao Lian , Zhi You , Pei-Yu Han , Ye Qiu , Yun-Zhi Zhang , Xing-Yi Ge

Viruses circulating in small mammals possess the potential to infect humans. Tree shrews are a group of small mammals inhabiting widely in forests and plantations, but studies on viruses in tree shrews are quite limited. Herein, viral metagenomic sequencing was employed to detect the virome in the tissue and swab samples from seventy-six tree shrews that we collected in Yunnan Province. As the results, genomic fragments belonging to eighteen viral families were identified, thirteen of which contain mammalian viruses. Through polymerase chain reaction (PCR) and Sanger sequencing, twelve complete genomes were determined, including five parvoviruses, three torque teno viruses (TTVs), two adenoviruses, one pneumovirus, and one hepacivirus, together with three partial genomes, including two hepatitis E viruses and one paramyxovirus. Notably, the three TTVs, named TSTTV-HNU1, TSTTV-HNU2, and TSTTV-HNU3, may compose a new genus within the family Anelloviridae. Notably, TSParvoV-HNU5, one of the tree shrew parvoviruses detected, was likely to be a recombination of two murine viruses. Divergence time estimation further revealed the potential cross-species-transmission history of the tree shrew pneumovirus TSPneV-HNU1. Our study provides a comprehensive exploration of viral diversity in wild tree shrews, significantly enhancing our understanding of their roles as natural virus reservoirs.

在小型哺乳动物中传播的病毒有可能感染人类。树鼩是一种广泛生活在森林和人工林中的小型哺乳动物，但对树鼩病毒的研究相当有限。本文采用病毒宏基因组测序方法对云南省采集的76只树鼩组织和拭子样本中的病毒进行检测。结果，鉴定出了18个病毒科的基因组片段，其中13个含有哺乳动物病毒。通过聚合酶链反应（PCR）和Sanger测序，确定了12个完整基因组，包括5个细小病毒（parvovirus）、3个torque teno病毒（TTVs）、2个腺病毒、1个肺炎病毒和1个肝炎病毒，以及3个部分基因组，包括2个戊型肝炎病毒和1个副粘病毒。值得注意的是，被命名为TSTTV-HNU1、TSTTV-HNU2和TSTTV-HNU3的三个ttv可能组成了一个新的属。值得注意的是，发现的树鼩细小病毒之一TSParvoV-HNU5很可能是两种鼠病毒的重组。发散时间估计进一步揭示了树鼩肺炎病毒TSPenV-HNU1潜在的跨种传播史。我们的研究提供了对野生树鼩病毒多样性的全面探索，显著增强了我们对它们作为天然病毒宿主作用的理解。

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引用次数: 0

Differential susceptibility of immunodeficient mice to MPXV infection and the impact of various inoculation routes 免疫缺陷小鼠对MPXV感染的差异易感性及不同接种途径的影响。

IF 5.5 3区医学 Q1 Medicine

Virologica Sinica

Pub Date : 2025-06-01 Epub Date: 2025-04-07 DOI: 10.1016/j.virs.2025.04.001

Xiaohan Wang , Shaowen Shi , Xiaoxuan Nie , Yongyang Sun , Jinglei Hu , Manlin He , Wenhao Ren , Yuxing Wang , Zhendong Guo , Gonghe Li , Changbo Ou , Xiao Li , Zongzheng Zhao

Monkeypox virus (MPXV), a member of the Orthopoxvirus genus, caused a large-scale global outbreak in 2022. Developing mouse models for MPXV infection is crucial for advancing research on vaccines and therapeutic interventions. To address this, we conducted a comparative study on the susceptibility of six mouse strains—severe combined immune-deficiency (SCID), nude, genetically diabetic (db/db) and obese (ob/ob), C57BL/6J, and BALB/c—to MPXV infection. Mouse strains were infected with MPXV via intranasal inoculation, and body weight changes and mortality were monitored post-infection. Additionally, the tissue distribution of MPXV and the pathological changes in the lung tissues of the infected mice were evaluated. The results demonstrated that SCID and nude mice exhibited significant weight loss following MPXV infection, with 100 % mortality observed in SCID mice, while no mortality occurred in nude mice. In contrast, the other mouse strains showed no significant weight loss or mortality. Notably, the viral load in the lung tissues of SCID and nude mice was the highest among the tested strains. Furthermore, we investigated the impact of different inoculation routes—intranasal (I.N.), intraperitoneal (I.P.), and intravenous (I.V.)—on the pathogenicity of MPXV in mice. The results revealed that the intravenous route induced more pronounced pathogenic effects compared to the intranasal and intraperitoneal routes. In summary, this study provides valuable insights into the development of MPXV-infected mouse models, offering a foundation for further research on MPXV pathogenesis and therapeutic drug development.

猴痘病毒（MPXV）是正痘病毒属的一员，在2022年引起了大规模的全球疫情。开发MPXV感染的小鼠模型对于推进疫苗和治疗干预的研究至关重要。为了解决这个问题，我们对6种小鼠品系——严重联合免疫缺陷（SCID）、裸鼠、遗传性糖尿病（db/db）和肥胖（ob/ob）、C57BL/6J和BALB/c——对MPXV感染的易感性进行了比较研究。通过鼻内接种MPXV感染小鼠品系，监测感染后的体重变化和死亡率。观察MPXV的组织分布及感染小鼠肺组织的病理变化。结果表明，MPXV感染后，SCID和裸鼠体重明显减轻，SCID小鼠死亡率为100%，而裸鼠没有死亡。相比之下，其他小鼠品系没有表现出明显的体重减轻或死亡率。值得注意的是，SCID和裸鼠肺组织的病毒载量最高。此外，我们研究了不同的接种途径-鼻内（I.N.），腹腔（I.P.）和静脉(I.V.)-对小鼠MPXV致病性的影响。结果表明，与鼻内和腹腔途径相比，静脉途径诱导的致病作用更明显。综上所述，本研究为MPXV感染小鼠模型的建立提供了有价值的见解，为进一步研究MPXV的发病机制和治疗药物的开发提供了基础。

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引用次数: 0

Issue Cover 覆盖问题

IF 5.5 3区医学 Q1 Medicine

Virologica Sinica

Pub Date : 2025-06-01 Epub Date: 2025-07-15 DOI: 10.1016/S1995-820X(25)00073-2

引用次数: 0

Corrigendum to “Evaluating the performance of the PREDAC method in flu vaccine recommendations over the past decade (2013–2023)” [Virol. Sin. 40 (2025) 288–291] “评估过去十年（2013-2023）PREDAC方法在流感疫苗推荐中的表现”的勘误表性研究。罪恶，40 (2025)288-291 [j]。

IF 5.5 3区医学 Q1 Medicine

Virologica Sinica

Pub Date : 2025-06-01 Epub Date: 2025-06-21 DOI: 10.1016/j.virs.2025.06.001

Yousong Peng , Lei Yang , Weijuan Huang , Mi Liu , Xiao Ding , Xiangjun Du , Yuelong Shu , Taijiao Jiang , Dayan Wang

引用次数: 0

Nucleophosmin 1 inhibits the replication of influenza A virus by competitively binding viral RNA with viral proteins 核磷蛋白1通过竞争性结合病毒RNA与病毒蛋白抑制甲型流感病毒的复制。

IF 5.5 3区医学 Q1 Medicine

Virologica Sinica

Pub Date : 2025-06-01 Epub Date: 2025-05-08 DOI: 10.1016/j.virs.2025.04.007

Yingying Yu , Qian Wang , Yanli Wei , Junwen Liu , Guangwen Wang , Zhengxiang Wang , Wentao Shen , Lu Han , Chengjun Li , Cao-Qi Lei , Shuai Xu , Qiyun Zhu

Influenza A viruses (IAVs) are single-stranded negative-sense RNA viruses that continually challenge animal and human health. In IAV-infected cells, host RNA-binding proteins play key roles in the life cycle of IAV by directly binding to viral RNA. Here, we examined the role of the host RNA-binding protein nucleophosmin-1 (NPM1) in IAV replication. We found that, as a nucleolar phosphoprotein, NPM1 directly binds to viral RNA (vRNA) and inhibits the replication of various subtypes of IAV. NPM1 binding to vRNA competitively reduces the assembly of the viral ribonucleoprotein complex and the viral polymerase activity, thereby reducing the generation of progeny viral RNA and virions. The RNA-binding activity of NPM1, with the key residues T199, T219, T234, and T237, is essential for its anti-influenza function. Taken together, our findings demonstrate that NPM1 acts as an RNA-binding protein and interacts with IAV vRNA to suppress viral replication.

甲型流感病毒（iav）是单链负义RNA病毒，不断威胁动物和人类的健康。在IAV感染的细胞中，宿主RNA结合蛋白通过直接与病毒RNA结合，在IAV的生命周期中发挥关键作用。在这里，我们研究了宿主rna结合蛋白核磷蛋白-1 （NPM1）在IAV复制中的作用。我们发现，NPM1作为一种核仁磷酸化蛋白，可直接与病毒RNA （vRNA）结合，抑制多种IAV亚型的复制。NPM1与vRNA的结合竞争性地降低了病毒核糖核蛋白复合物的组装和病毒聚合酶的活性，从而减少了子代病毒RNA和病毒粒子的产生。NPM1与关键残基T199、T219、T234和T237的rna结合活性对其抗流感功能至关重要。综上所述，我们的研究结果表明NPM1作为一种rna结合蛋白，与IAV vRNA相互作用，抑制病毒复制。

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引用次数: 0

Host factor RBM25 promotes HBV replication through Yin Yang 1-mediated cccDNA transcription 宿主因子RBM25通过阴阳1介导的cccDNA转录促进HBV复制。

IF 5.5 3区医学 Q1 Medicine

Virologica Sinica

Pub Date : 2025-06-01 Epub Date: 2025-05-22 DOI: 10.1016/j.virs.2025.05.004

Yukun Li , Tianhao Mao , Liwei Zheng , Zhao Zhou , Qianqian Jiang , Xinyu Du , Ziyuan Ma , Xin Liu , Ting Zhang , Guochao Wei , Lin Wang , Yongzhen Liu , Xiaojing Zhang , Shourong Liu , Xiangmei Chen , Fengmin Lu

The persistence of covalently closed circular DNA (cccDNA) in hepatitis B virus (HBV)-infected hepatocytes remains a major obstacle to effective antiviral treatment. Understanding the molecular mechanisms regulating HBV cccDNA transcription is essential for developing novel therapeutic strategies. In this study, we investigated the role of RNA binding motif protein 25 (RBM25) in HBV replication, focusing on its interaction with cccDNA and its regulation of host transcription factors. The results demonstrated that RBM25 knockdown markedly inhibited HBV replication, reducing levels of HBV DNA, hepatitis B e antigen (HBeAg), hepatitis B surface antigen (HBsAg), HBV RNA, and L-HBs in HBV-replicating and infected cell models. Consistent results were observed in a mouse model hydrodynamically injected with 1.2 × HBV plasmid. Conversely, RBM25 overexpression significantly enhanced HBV replication. Mechanistically, RBM25 promoted HBV promoter activities by binding to cccDNA through its RE/RD and PWI domains. This effect was mediated by increased Yin Yang 1 (YY1) expression, which enhanced acetylation of cccDNA-bound histones, promoting HBV transcription. Furthermore, RBM25 expression was upregulated and translocated to the nucleus following core protein expression and accumulation, while overexpression of RBM25 promoted core protein degradation. In conclusion, this study demonstrates that RBM25 is a novel host factor that enhances HBV replication by upregulating YY1-dependent transcriptional activation of cccDNA. It also reveales a reciprocal regulatory mechanism between the HBV core protein and RBM25, which helps sustain HBV replication.

在乙型肝炎病毒（HBV）感染的肝细胞中，共价闭合环状DNA （cccDNA）的持续存在仍然是有效抗病毒治疗的主要障碍。了解调节HBV cccDNA转录的分子机制对于开发新的治疗策略至关重要。在本研究中，我们研究了RNA结合基序蛋白25 （RBM25）在HBV复制中的作用，重点研究了其与cccDNA的相互作用及其对宿主转录因子的调控。结果表明，RBM25敲低显著抑制HBV复制，降低HBV复制和感染细胞模型中HBV DNA、乙型肝炎e抗原（HBeAg）、乙型肝炎表面抗原（HBsAg）、HBV RNA和l - hbbs的水平。在水动力注射1.2×HBV质粒的小鼠模型中观察到一致的结果。相反，RBM25过表达显著增强HBV复制。机制上，RBM25通过其RE/RD和PWI结构域与cccDNA结合，促进HBV启动子活性。这种作用是由阴阳1 （YY1）表达增加介导的，YY1表达增强cccdna结合组蛋白的乙酰化，促进HBV转录。此外，随着核心蛋白的表达和积累，RBM25表达上调并易位至细胞核，而过表达RBM25促进核心蛋白降解。总之，本研究表明RBM25是一种新的宿主因子，通过上调yy1依赖性cccDNA的转录激活来增强HBV复制。它还揭示了HBV核心蛋白和RBM25之间的互惠调节机制，这有助于维持HBV的复制。

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引用次数: 0

Viral pseudo-enzyme facilitates KSHV lytic replication via suppressing PFAS-mediated RTA deamidation 病毒伪酶通过抑制pfas介导的RTA脱酰胺促进KSHV裂解复制。

IF 5.5 3区医学 Q1 Medicine

Virologica Sinica

Pub Date : 2025-06-01 Epub Date: 2025-04-12 DOI: 10.1016/j.virs.2025.04.005

Yang Xu , Qiushi Zhang , Guoli Hou , Liang Hu , Tiaoyi Xiao , Xinyu Liang , Deliang Li , Junhua Li

Deamidation, a type of post-translational modification commonly considered a hallmark of protein “aging” and function decay, is increasingly recognized for its pivotal role in regulating biological processes and viral infection. Our previous study has demonstrated that the deamidation of replication and transcription activator (RTA), a master regulator of ubiquitous and oncogenic Kaposi's sarcoma-associated herpesvirus (KSHV), mediated by phosphoribosylformylglycinamidine synthetase (PFAS), hinders its nuclear import and transcriptional activity. Here we report that the viral glutamine amidotransferase (vGAT) pseudo-enzyme is exploited to facilitate KSHV lytic infection by inhibiting RTA deamidation. To be more specific, vGAT interacts with both RTA and cellular PFAS, and inhibits PFAS-mediated RTA deamidation, thus facilitating RTA nuclear localization and suppressing nuclear factor-kappa B (NF-κB) signaling activation, as well as augmenting RTA-mediated transcriptional activation of viral open reading frames (ORFs). In addition, vGAT appears to regulate the deamidation process of several viral ORFs of KSHV. Collectively, these findings unveil that a viral pseudo-enzyme is exploited to enhance viral infection via deamidation regulation.

脱酰胺是一种翻译后修饰，通常被认为是蛋白质“老化”和功能衰退的标志，它在调节生物过程和病毒感染方面的关键作用越来越得到认可。我们之前的研究表明，由磷酸核糖基甲酰基甘氨酸合成酶（PFAS）介导的复制和转录激活因子（RTA）的脱酰胺化阻碍了其核输入和转录活性。RTA是普遍存在的致癌卡波西肉瘤相关疱疹病毒（KSHV）的主要调节因子。本文报道利用病毒谷氨酰胺氨基转移酶（vGAT）伪酶抑制RTA脱酰胺，促进KSHV裂解感染。更具体地说，vGAT与RTA和细胞PFAS相互作用，抑制PFAS介导的RTA脱酰胺，从而促进RTA核定位，抑制核因子κB （NF-κB）信号激活，并增强RTA介导的病毒开放阅读框（orf）的转录激活。此外，vGAT似乎调节了几种KSHV病毒orf的脱酰胺过程。总的来说，这些发现揭示了一种病毒伪酶通过脱酰胺调节来增强病毒感染。

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引用次数: 0

A noninfectious pseudovirus system for an emerging orthoflavivirus 新出现的正黄病毒的非传染性假病毒系统。

IF 5.5 3区医学 Q1 Medicine

Virologica Sinica

Pub Date : 2025-06-01 Epub Date: 2025-04-23 DOI: 10.1016/j.virs.2025.04.006

Yanfan Shi , Yu He , Xiaoli Wang , Zhen Wu , Tao Wang , Mingshu Wang , Renyong Jia , Dekang Zhu , Mafeng Liu , Xinxin Zhao , Qiao Yang , Ying Wu , Shaqiu Zhang , Juan Huang , Xumin Ou , Di Sun , Anchun Cheng , Shun Chen

引用次数: 0

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