Frontiers in virology最新文献

{"title":"A fatal pediatric infection with a C1-like subgenogroup enterovirus A71: case study and enterovirus A71 epidemiology in Finland","authors":"Tea Nieminen, Anne J. Jääskeläinen, Erika Lindh, Soile Blomqvist, Carita Savolainen-Kopra","doi":"10.3389/fviro.2024.1381001","DOIUrl":"https://doi.org/10.3389/fviro.2024.1381001","url":null,"abstract":"Enterovirus A71 (EV-A71) is among the most neuropathogenic non-polio enterovirus types and, in rare instances, can lead to severe or even fatal outcomes, particularly in children under 5 years of age. This case study presents clinical and microbiological findings from the initial documented severe pediatric EV-A71 case in Finland, identified in May 2019. The near-complete genome sequence confirms that the EV-A71 strain belongs to the newly identified recombinant C1-like EV-A71 genetic lineage, which emerged in 2015 and has since been circulating in Europe, causing severe cases among children in various European countries. Enhanced environmental surveillance revealed widespread circulation of EV-A71 in Finland in 2019. However, the overall number of EV clinical cases remained lower than in previous years.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"59 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140592596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Persistent transgene expression in peripheral tissues one year post intravenous and intramuscular administration of AAV vectors containing the alphaherpesvirus latency-associated promoter 2","authors":"Carola J. Maturana, Esteban A. Engel","doi":"10.3389/fviro.2024.1379991","DOIUrl":"https://doi.org/10.3389/fviro.2024.1379991","url":null,"abstract":"<p>Significant progress has been made in enhancing recombinant adeno-associated virus (rAAV) for clinical investigation. Despite its versatility as a gene delivery platform, the inherent packaging constraint of 4.7 kb imposes restrictions on the range of diseases it can address. In this context, we present findings of an exceptionally compact and long-term promoter that facilitates the expression of larger genes compared to conventional promoters. This compact promoter originated from the genome of the alphaherpesvirus pseudorabies virus, latency-associated promoter 2 (LAP2, 404 bp). Promoter driving an mCherry reporter was packaged into single strand (ss) AAV8 and AAV9 vectors and injected into adult C57BL/6 mice at a dose of 5 x 1011 vg/mouse by single intravenous or intramuscular administration. An ssAAV8 and ssAAV9 vector with elongation factor-1α promoter (EF1α, 1264 bp) was injected side-by-side for comparison. After 400 days, we sacrificed the mice and examined mCherry expression in liver, kidney, heart, lung, spleen, pancreas, skeletal muscle, and brain. We found that LAP2 exhibited robust transgene expression across a wide range of cells and tissues comparable to the larger EF1α, which is currently recognized as a rather potent and ubiquitous promoter. The AAV8-LAP2 and AAV9-LAP2 constructs displayed strong transduction and transcription in liver, kidney, and skeletal muscle on both route of administration. However, no expression was detected in the heart, lung, spleen, pancreas, and brain. The outcomes of our investigation propose the viability of LAP2 for gene therapy applications demanding the expression of large or multiple therapeutic genes following a single viral-vector administration.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"26 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140311625","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Virological characteristics correlating with SARS-CoV-2 spike protein fusogenicity","authors":"MST Monira Begum, Kimiko Ichihara, Otowa Takahashi, Hesham Nasser, Michael Jonathan, Kenzo Tokunaga, Isao Yoshida, Mami Nagashima, Kenji Sadamasu, Kazuhisa Yoshimura, The Genotype to Phenotype Japan (G2P-Japan) Consortium, Kei Sato, Terumasa Ikeda, Keita Matsuno, Naganori Nao, Hirofumi Sawa, Shinya Tanaka, Masumi Tsuda, Lei Wang, Yoshikata Oda, Zannatul Ferdous, Kenji Shishido, Takasuke Fukuhara, Tomokazu Tamura, Rigel Suzuki, Saori Suzuki, Hayato Ito, Jumpei Ito, Yu Kaku, Naoko Misawa, Arnon Plianchaisuk, Ziyi Guo, Alfredo Jr. Hinay, Keiya Uriu, Yusuke Kosugi, Shigeru Fujita, Jarel Elgin Mendoza Tolentino, Luo Chen, Lin Pan6, Mai Suganami, Mika Chiba, Ryo Yoshimura, Kyoko Yasuda, Keiko Iida, Naomi Ohsumi, Adam Patrick Strange, Hiroyuki Asakura, Isao Yoshida, So Nakagawa, Akifumi Takaori-Kondo, Kotaro Shirakawa, Kayoko Nagata, Ryosuke Nomura, Yoshihito Horisawa, Yusuke Tashiro, Yugo Kawai, Kazuo Takayama, Rina Hashimoto, Sayaka Deguchi, Yukio Watanabe, Ayaka Sakamoto, Naoko Yasuhara, Takao Hashiguchi, Tateki Suzuki, Kanako Kimura, Jiei Sasaki, Yukari Nakajima, Hisano Yajima, Takashi Irie, Ryoko Kawabata, Kaori Tabata, Ryo Shimizu1, Yuka Mugita1, Takamasa Ueno, Chihiro Motozono, Mako Toyoda, Akatsuki Saito, Maya Shofa, Yuki Shibatani, Tomoko Nishiuchi","doi":"10.3389/fviro.2024.1353661","DOIUrl":"https://doi.org/10.3389/fviro.2024.1353661","url":null,"abstract":"<sec><title>Introduction</title><p>The severe acute respiratory syndrome coronavirus (SARS-CoV-2) spike (S) protein is essential in mediating membrane fusion of the virus with the target cells. Several reports demonstrated that SARS-CoV-2 S protein fusogenicity is reportedly closely associated with the intrinsic pathogenicity of the virus determined using hamster models. However, the association between S protein fusogenicity and other virological parameters remains elusive.</p></sec><sec><title>Methods</title><p>In this study, we investigated the virological parameters (e.g., S1/S2 cleavage efficiency, plaque size, pseudoviral infectivity, pseudovirus entry efficiency, and viral replication kinetics) of eleven previous variants of concern (VOCs) and variants of interest (VOIs) correlating with S protein fusogenicity.</p></sec><sec><title>Results and discussion</title><p>S protein fusogenicity was found to be strongly correlated with S1/S2 cleavage efficiency and plaque size formed by clinical isolates. However, S protein fusogenicity was less associated with pseudoviral infectivity, pseudovirus entry efficiency, and viral replication kinetics. Taken together, our results suggest that S1/S2 cleavage efficiency and plaque size could be potential indicators to predict the intrinsic pathogenicity and S protein fusogenicity of newly emerged SARS-CoV-2 variants.</p></sec>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"33 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140128279","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding chikungunya virus non-structural protein 3 interacting partners in THP-1 derived infected macrophages through proteomic profiling","authors":"Priyanshu Srivastava, Nimisha Mishra, Sakshi Chaudhary, Sujatha Sunil","doi":"10.3389/fviro.2024.1310161","DOIUrl":"https://doi.org/10.3389/fviro.2024.1310161","url":null,"abstract":"<sec><title>Introduction</title><p>Chikungunya virus (CHIKV), an alphavirus transmitted by mosquitoes, has instigated several epidemics in recent years, sparking intensive efforts to understand its biology. Despite progress, the understanding of CHIKV’s molecular interactions with host cell constituents, especially in susceptible cells such as macrophages remains limited.</p></sec><sec><title>Methods</title><p>We used a mass spectrometry platform to characterize the interactions between CHIKV-nsP3, a viral nonstructural protein, and proteins in human THP-1 macrophage cells.</p></sec><sec><title>Results and Discussion</title><p>Our findings revealed 196 high-confidence interactions primarily involving nsP3. Further, the sub-cellular localization, and pathways these interacting proteins might be involved in were deduced using computational methods. The interacting partners were further incorporated into a comprehensive host-virus interaction network derived from extensive literature on alphavirus-host interactions. Collectively, this study offers the first interaction map between CHIKV nsP3 protein and THP-1 cells, illuminating new probable roles of host cell proteins in CHIKV’s replication cycle.</p></sec>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"18 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140128339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The roles of HCV core protein and its binding host factor in virus assembly and release","authors":"Kyo Izumida, Eiji Morita","doi":"10.3389/fviro.2024.1383261","DOIUrl":"https://doi.org/10.3389/fviro.2024.1383261","url":null,"abstract":"<p>Hepatitis C virus (HCV) is a well-known virus that causes liver diseases such as liver cirrhosis and hepatocellular carcinoma. For several decades, numerous studies have been conducted to unravel the life cycle and molecular mechanisms of this virus with the aim of developing strategies to combat diseases caused by its infection. In this review, we summarize HCV assembly to budding, focusing on one of the structural proteins, the core, a viral capsid that binds both the viral genome and host membrane, along with the core-interacting host partners. The HCV core matures in the endoplasmic reticulum (ER), localizes at the lipid droplet (LD), and shuttles between the LD and ER to form viral particles. This process is controlled by many host factors known to binds core proteins, such as diacylglycerol acyltransferase-1 (DGAT-1), Rab18, μ subunit of the clathrin adaptor protein complex 2 (AP2M1), nuclear pore complex protein 98 (Nup98), Cortactin, group IVA phospholipase A2 (PLA2G4A) etc. Virion budding is thought to involve contributions from endosomal sorting complexes required for transport (ESCRT), similar to other envelope viruses. We delved into potential perspectives to enhance our understanding of the HCV mechanism by drawing insights from existing studies.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140155309","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA methylation in long COVID","authors":"Yangfan Xiao, Sten H. Vermund","doi":"10.3389/fviro.2024.1371683","DOIUrl":"https://doi.org/10.3389/fviro.2024.1371683","url":null,"abstract":"<p>Long COVID (also termed Post-acute sequelae of COVID-19 [PASC]) refers to the chronic symptoms that survivors may experience after severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection and acute coronavirus disease 2019 (COVID-19) disease. Long COVID represents a global public health, medical, and nursing challenge that affects millions of people. As an emerging and evolving syndrome, long COVID manifests with many combinations of clinical signs and symptoms that healthcare providers and scientists are cataloging and struggling to understand. In this mini-review, we introduce the epigenetic battlefield of DNA methylation (DNAm) on which the virus and the host interact. We suggest ways in which DNAm phenomena and markers induced by this virus-host interaction may help clarify the pathology and prognosis of long COVID. Knowledge of DNAm characteristics of long COVID patients is limited as of this writing (early-2024), investigators have noted both the partial reversibility and the potential long-lasting persistence of the DNAm markers induced by acute COVID-19. Long-term sequelae seen in other coronavirus diseases such as severe acute respiratory syndrome (SARS) and Middle East respiratory syndrome (MERS) are potential references for long COVID in an effort towards more precise diagnosis and disease characterization, better prediction of outcomes, and the use of epigenetic phenomena towards development of new drugs and immunotherapies.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"29 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140047248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ESCRT-III-dependent and -independent egress of herpesviruses","authors":"Jun Arii","doi":"10.3389/fviro.2024.1378054","DOIUrl":"https://doi.org/10.3389/fviro.2024.1378054","url":null,"abstract":"<p>Enveloped viruses complete their replication cycle by forming virions that bud from infected cells through membrane scission. The mechanisms by which this is achieved are less well-understood than the well-characterized membrane scission of vesicles budding inwards into the cytosol. The scission of vesicles that bud away from the cytosol is mediated by machinery of the endosomal sorting complexes required for transport (ESCRT)-III, which is highjacked by viruses of several different families. Other groups of viruses can bud independently of ESCRT-III activity. It has not been fully elucidated how the latter achieve this in the absence of host ESCRT-III, but it is known that some viral proteins directly mediate membrane scission. The <italic>Herpesviridae</italic> constitute a family of highly diverse viruses that bud at the inner nuclear membrane and cytoplasmic membranes in infected cells. Many investigators have attempted to determine the mechanism of membrane scission during herpesvirus budding, and have found this to be complex, not exactly conforming to either of the two methods. The present review attempts to synthesize the disparate findings into a model of herpesvirus egress based on both ESCRT-mediated and viral protein-mediated mechanisms.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"740 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140036973","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Changing rates but persisting seasons: patterns of enterovirus infections in hospitalizations and outpatient visits in Denmark 2015-2022","authors":"Caroline Klint Johannesen, Amanda Marie Egeskov-Cavling, Micha Phill Grønholm Jepsen, Theis Lange, Tyra Grove Krause, Ulrikka Nygaard, Thea K. Fischer","doi":"10.3389/fviro.2024.1346352","DOIUrl":"https://doi.org/10.3389/fviro.2024.1346352","url":null,"abstract":"<sec><title>Background</title><p>Enteroviruses (EV) constitute a diverse group of viruses manifesting a broad spectrum of clinical presentations in humans ranging from mild skin manifestations to more severe central nervous system (CNS) infection. Severe infections are reported with increased frequency globally, albeit the burden of diseases and the evolution of circulating viruses is largely unknown. We aimed to systematically explore contemporary trends in hospitalizations attributed to EV infections using national hospitalization discharge data.</p></sec><sec><title>Methods</title><p>We utilized the Danish National Patient Register which holds information on all contacts to Danish hospitals. We covered eight full years (2015-2022). Length-of-stay and administrative procedure codes were used to distinguish hospital admissions from outpatient visits. We utilized burden of disease estimates and distribution statistics.</p></sec><sec><title>Results</title><p>We identified 1029 hospitalizations and 1970 outpatient visits due to EV infections. The hospital admissions were primarily associated with CNS-infections (n=570, 55.4%) and skin (n=252, 24.5%), with variation over the studied period. The admitted patients were predominately children (43.8%) though patients were identified in all ages. The clinical manifestation was associated with age, with CNS infections dominating in the neonates and adults, and skin infections dominating in children 1-2 years (17.2%). Outpatient visits were predominantly observed among children 1-2 years (55.0%), presenting with skin symptoms (77.9%). We show a seasonal pattern of EV infections with summer/fall peaks and markedly impact on the EV hospitalization burden related to COVID-19 mitigation measures including national lockdown periods. 25% of hospital admissions occurred during 2020-2022.</p></sec><sec><title>Conclusion</title><p>EV infections caused both hospital admissions and outpatient visits in the period studied, predominately among children aged 1-2 years. Overall, skin infections dominated the outpatient visits, while the majority of hospital admissions were due to CNS infections. The pandemic period did not change the seasonal pattern of EV infections but notably lowered the number of admissions to hospital with CNS infection and raised the number of outpatient admissions with skin infection.</p></sec>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"43 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140009504","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emergence of enterovirus D68 in a Norwegian paediatric population 2012-2022","authors":"Elisabeth Toverud Landaas, Ingvild Klundby, Per Kristian Knudsen, Anne-Marte Bakken Kran, Susanne Dudman, Andreas Lind, Mona Holberg-Petersen","doi":"10.3389/fviro.2024.1358963","DOIUrl":"https://doi.org/10.3389/fviro.2024.1358963","url":null,"abstract":"<sec><title>Background</title><p>Enterovirus D68 (EV-D68) primarily causes respiratory infection, occasionally manifesting with neurological symptoms. Outbreak reports have been published from various countries including Norway, but a longitudinal study on EV-D68 prevalence in Northern Europe is lacking.</p></sec><sec><title>Methods</title><p>Respiratory samples from children ≤14 years received at Oslo University Hospital in the years 2012-2022 were examined for EV-D68. Samples from 2012-2015 were retrospectively screened using a semi-specific RT-PCR, with positive samples confirmed by an EV-D68 specific RT-PCR. Samples from 2016-2022 underwent routine diagnostics with the EV-D68 specific RT-PCR.</p></sec><sec><title>Results</title><p>Among the 22,911 samples tested, EV-D68 was detected in 338 samples (324 patients). Most EV-D68 cases occurred in August to December. The highest detection rate was recorded in 2014, 2016 and 2022 (6.0%, 7.8% and 6.6% of samples from August-December). Lower frequencies were observed in 2018 and 2019 (1.0% and 2.4%), and in the years before the 2014 outbreak (2012: 1.3%, 2013: 0.8%). Few cases were identified in 2020-2021. Children aged 0-1 years accounted for 40%, and 0-4 years for 78%, of the EV-D68 positive patients. Most of the patients with EV-D68 (83%) were hospitalised.</p></sec><sec><title>Discussion</title><p>Also in Norway, EV-D68 has caused outbreaks with significant disease burden, especially among the youngest children. The detection rate varies, with a trend towards biennial outbreaks, except for low numbers in 2018 and during the COVID-19 restrictions (2020-2021). Due to its potential for severe respiratory illness and significant neurological complications, conducting EV-D68 testing is essential both for diagnosing clinically suspected cases, and for monitoring the disease burden.</p></sec>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-02-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139977785","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Enterovirus-D68 – a reemerging non-polio enterovirus that causes severe respiratory and neurological disease in children","authors":"Cassandra S. Grizer, Kevin Messacar, Joseph J. Mattapallil","doi":"10.3389/fviro.2024.1328457","DOIUrl":"https://doi.org/10.3389/fviro.2024.1328457","url":null,"abstract":"<p>The past decade has seen the global reemergence and rapid spread of enterovirus D68 (EV-D68), a respiratory pathogen that causes severe respiratory illness and paralysis in children. EV-D68 was first isolated in 1962 from children with pneumonia. Sporadic cases and small outbreaks have been reported since then with a major respiratory disease outbreak in 2014 associated with an increased number of children diagnosed with polio-like paralysis. From 2014-2018, major outbreaks were reported every other year in a biennial pattern with &gt; 90% of the cases occurring in children under the age of 16. With the outbreak of SARS-CoV-2 and the subsequent COVID-19 pandemic, there was a significant decrease in the prevalence EV-D68 cases along with other respiratory diseases. However, since the relaxation of pandemic social distancing protocols and masking mandates the number of EV-D68 cases have begun to rise again-culminating in another outbreak in 2022. Here we review the virology, pathogenesis, and the immune response to EV-D68, and discuss the epidemiology of EV-D68 infections and the divergence of contemporary strains from historical strains. Finally, we highlight some of the key challenges in the field that remain to be addressed.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139773184","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}