Tina Uršič, Monika Jevšnik Virant, Rok Kogoj, Uros Krivec, Joanna Prusnik, Minca Mramor, Sara Lovšin, Miroslav Petrovec
{"title":"Enterovirus D68 circulation between 2014 and 2022 in Slovenian children","authors":"Tina Uršič, Monika Jevšnik Virant, Rok Kogoj, Uros Krivec, Joanna Prusnik, Minca Mramor, Sara Lovšin, Miroslav Petrovec","doi":"10.3389/fviro.2024.1335752","DOIUrl":"https://doi.org/10.3389/fviro.2024.1335752","url":null,"abstract":"<sec><title>Introduction</title><p>Enterovirus D68 (EV-D68) belongs to the <italic>Picornaviridae</italic> family, genus <italic>Enterovirus</italic>. It is mostly known as a respiratory virus causing upper and lower respiratory tract infections, but it is also rarely associated with a variety of central nervous system complications, with acute flaccid myelitis being reported most frequently. This study assesses the incidence, seasonality, clinical presentation, and molecular epidemiology of the EV-D68 strain in EV-positive children hospitalized between 2014 and 2022 at the largest pediatric medical center in Slovenia.</p></sec><sec><title>Methods</title><p>EV-D68 was detected using specific qRT-PCR, whereas partial VP1 sequences were obtained with Sanger sequencing, and further analyzed using the software CLC Main Workbench version 7 and MEGA version X.</p></sec><sec><title>Results</title><p>EV-D68 was detected in 154 out of 1,145 (13.4%) EV-positive children. In the two epidemic years, 2014 and 2016, EV-D68 was most frequently detected in the summer and early autumn, peaking in September. The median age of EV-D68–infected children was 3 years (IQR 1–3 years), with a female: male ratio of 1:1.17. Rhinorrhea was present in 74.0% of children, respiratory distress in 82.5%, and hypoxemia requiring supplemental oxygen in 44.1%. Out of 154 patients, 80.0% were hospitalized, with a median stay of 2 days (IQR 1–3 days). Lower respiratory tract infection was observed in 89.0% of EV-D68–positive patients, with bronchitis and bronchiolitis being most frequently diagnosed. No central nervous system manifestations of EV-D68 infection were observed in the study cohort. Phylogenetic analysis of partial VP1 sequences of EV-D68 revealed close similarity to the EV-D68 variants that were circulating in other European countries in these years.</p></sec><sec><title>Discussion</title><p>Slovenia faced two EV-D68 epidemics in 2014 and 2016; however, after 2016 only nine more cases were detected until the end of the study period. Based on the results of this study, EV-D68 was a frequent cause of lower respiratory tract infection among EV-positive patients. However, none of the patients we studied needed ICU treatment, and none developed acute flaccid paralysis. Our results indicate that EV-D68 is not present constantly, so additional monitoring studies should be conducted in the future to better understand the implications of this EV type in human disease.</p></sec>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"76 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139515061","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}
Ashwin Badrinath, Anais Gardere, Samantha L. Palermo, Kenneth S. Campbell, Anna Kloc
{"title":"Analysis of Parvovirus B19 persistence and reactivation in human heart layers","authors":"Ashwin Badrinath, Anais Gardere, Samantha L. Palermo, Kenneth S. Campbell, Anna Kloc","doi":"10.3389/fviro.2024.1304779","DOIUrl":"https://doi.org/10.3389/fviro.2024.1304779","url":null,"abstract":"<p>Heart disease is the leading cause of death worldwide. Myocarditis, or inflammation of the cardiac muscle, is estimated to cause up to 1.5 million cases annually, with viral infection being the most common disease culprit. Past studies have shown that Parvovirus B19 is routinely detected in endomyocardial biopsies. This virus has been linked to acute heart inflammation, which can cause cardiac muscle damage. However, because Parvovirus B19 can be found in the heart tissues in the absence of disease symptoms, it is unclear if the long-term presence of the virus contributes to, or initiates, heart disease. Here, we utilized a PCR-based detection assay to assess the presence of the B19V genome and its mRNA intermediates in human heart tissues. The analysis was carried out in three heart layers derived from one individual: epicardium, endocardium and myocardium. We showed the Parvovirus B19 genome presence variability in different heart layers. Similarly, viral transcriptional activity, assessed by the mRNA presence, was detected only in a few of the analyzed samples. Our results suggest that localized sites of Parvovirus B19 infection may exist within individual heart layers, which may have implication for the cardiac muscle inflammation.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"19 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139754276","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":"APOBEC3D excludes APOBEC3F from HIV-1 virions by competitive binding of RNA","authors":"Shreoshri Bhattacharjee, Amit Gaba, Linda Chelico","doi":"10.3389/fviro.2024.1343037","DOIUrl":"https://doi.org/10.3389/fviro.2024.1343037","url":null,"abstract":"<p>The human family of APOBEC3 enzymes are primarily studied as single-stranded DNA deoxycytidine deaminases that act as host restriction factors for a number of viruses and retroelements. The deamination of deoxycytidine to deoxyuridine causes inactivating mutations in target DNA and the nucleic acid binding ability may also cause deamination independent restriction. There are seven APOBEC3 enzymes in humans, named A-H, excluding E, each of which has restriction activity against a subset of viruses or retroelements. There are primarily four, APOBEC3D, APOBEC3F, APOBEC3G, and APOBEC3H that have been found to restrict replication of HIV-1, however their restriction activity varies and they have primarily been studied individually despite co-expression in the cells that HIV-1 infects. It is known that APOBEC3F hetero-oligomerizes with APOBEC3G and APOBEC3H and that this influences host restriction outcomes during HIV-1 infection in tissue culture. Here, we examined if APOBEC3F interacts with APOBEC3D and the functional outcomes. We found that <italic>APOBEC3D</italic> mRNA expression was similar to or higher than <italic>APOBEC3F</italic> mRNA in multiple donors, suggesting that the proteins would be co-expressed, allowing for interactions to occur. We determined that APOBEC3F and APOBEC3D interacted primarily through an RNA intermediate; however, this interaction resulted in APOBEC3D competitively excluding APOBEC3F from virions. Although HIV-1 restriction still occurred when APOBEC3F and APOBEC3D were co-expressed, it was due to primarily APOBEC3D-mediated deamination-independent restriction. The APOBEC3D-mediated exclusion of APOBEC3F from HIV-1 encapsidation could be recapitulated <italic>in vitro</italic> through RNA capture experiments in which APOBEC3D decreased or abrogated the ability of APOBEC3F to bind to HIV-1 protease or 5’UTR RNA, respectively. Overall, the data suggest that there are mechanisms at the protein level that segregate APOBEC3s into different virus particles.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"123 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2024-01-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139559888","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}
Yuuka Masuda, H. Nasser, Jiří Zahradník, Shuya Mitoma, Ryo Shimizu, Kayoko Nagata, A. Takaori-Kondo, Gideon Schreiber, Kotaro Shirakawa, Akatsuki Saito, Terumasa Ikeda, Jumpei Ito, Kei Sato
{"title":"Characterization of the evolutionary and virological aspects of mutations in the receptor binding motif of the SARS-CoV-2 spike protein","authors":"Yuuka Masuda, H. Nasser, Jiří Zahradník, Shuya Mitoma, Ryo Shimizu, Kayoko Nagata, A. Takaori-Kondo, Gideon Schreiber, Kotaro Shirakawa, Akatsuki Saito, Terumasa Ikeda, Jumpei Ito, Kei Sato","doi":"10.3389/fviro.2023.1328229","DOIUrl":"https://doi.org/10.3389/fviro.2023.1328229","url":null,"abstract":"Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) has substantially diversified during the pandemic, resulting in the successive emergence of variants characterized by various mutations. It has been observed that several epidemic variants, including those classified as variants of concern, share mutations at four key residues (L452R, T478K, E484K, and N501Y) within the receptor binding motif (RBM) region of the spike protein. However, the processes through which these four specific RBM mutations were acquired during the evolution of SARS-CoV-2, as well as the degree to which they enhance viral fitness, remain unclear. Moreover, the effect of these mutations on the properties of the spike protein is not yet fully understood. In this study, we performed a comprehensive phylogenetic analysis and showed that the four RBM mutations have been convergently acquired across various lineages throughout the evolutionary history of SARS-CoV-2. We also found a specific pattern in the order of acquisition for some of these mutations. Additionally, our epidemic dynamic modeling demonstrated that acquiring these mutations leads to an increase in the effective reproduction number of the virus. Furthermore, we engineered mutant spike proteins with all feasible combinations of the four mutations, and examined their properties to uncover the influence that these mutations have on viral characteristics. Our results provide insights into the roles these four mutations play in shaping the viral characteristics, epidemic proliferation, and evolutionary pathway of SARS-CoV-2.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"31 16","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138946868","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}
Susanne Dudman, Ingvild Klundby, Joakim Øverbø, Sanela Numanovic, Mariann Nilsen, Andreas Lind, Mona Holberg-Petersen, Elisabeth Toverud Landaas
{"title":"Trends in the enterovirus surveillance in Oslo, Norway before and during the COVID-19 pandemic","authors":"Susanne Dudman, Ingvild Klundby, Joakim Øverbø, Sanela Numanovic, Mariann Nilsen, Andreas Lind, Mona Holberg-Petersen, Elisabeth Toverud Landaas","doi":"10.3389/fviro.2023.1343781","DOIUrl":"https://doi.org/10.3389/fviro.2023.1343781","url":null,"abstract":"<sec><title>Background</title><p>Enteroviruses have the potential to cause both high morbidity and mortality especially in children. High season in Norway is between August and November, but this seasonality was interrupted by the COVID-19 pandemic.</p></sec><sec><title>Methods</title><p>In this study, we describe the enterovirus surveillance in Norway before and during the COVID-19 pandemic including the years from the start of 2016 until the end of 2022. Screening of enterovirus was performed by both laboratory developed methods and FilmArray<sup>®</sup> ME Panel. Relevant samples were typed, mostly by VP1 sequencing.</p></sec><sec><title>Results</title><p>Seventy-four percent of all cases occurred in infants under five years of age. A significant reduction in positive cases was observed during the peak years of the COVID-19 pandemic compared to the years before. Pre-pandemic, a wide range of types from all four enterovirus species were detected. During the years with COVID-19 infection control measures, significantly fewer enterovirus types were found along with a substantial reduction in the detection rate.</p></sec><sec><title>Conclusion</title><p>Enterovirus surveillance discovered a large amount of different types mainly affecting infants. The positivity rate was markedly reduced during the pandemic in 2020-2022 and fewer types occurred.</p></sec>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139396459","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":"Differential susceptibility of human microglia HMC3 cells and brain microvascular endothelial HBEC-5i cells to Mayaro and Una virus infection","authors":"Dalkiria Campos, Madelaine Sugasti-Salazar, Patricia Valdés-Torres, Paola Elaine Galán-Jurado, Dalel Zegarra, José González-Santamaría","doi":"10.3389/fviro.2023.1325282","DOIUrl":"https://doi.org/10.3389/fviro.2023.1325282","url":null,"abstract":"<p>Mayaro (MAYV) and Una (UNAV) are emerging alphaviruses circulating in the Americas. Earlier reports have revealed that MAYV infects different human cell lines, including synovial and dermal fibroblasts, chondrocytes, osteoblasts, astrocytes and pericytes, as well as neural progenitor cells. In this study we evaluated the susceptibility of immortalized human microglia HMC3 cells and brain microvascular endothelial HBEC-5i cells to MAYV and UNAV infection. Cytopathic effects, cell viability, viral progeny yields, and the presence of E1 and nsP1 proteins in HMC3 and HBEC-5i cells infected with several MAYV or UNAV strains were assessed using an inverted microscope, MTT assay, plaque-forming assays, and immunofluorescence or Western blot, respectively. Finally, the expression of immune response genes was analyzed using RT-qPCR. MAYV and UNAV demonstrated strong cytopathic effects and significantly reduced cell viability in HMC3 cells. Moreover, the HMC3 cells were efficiently infected regardless of the virus strain tested, and E1 and nsP1 viral proteins were detected. In contrast, only MAYV appeared to infect HBEC-5i cells, and minimal effects on cell morphology or viability were observed. Furthermore, the MAYV titer and viral protein levels were substantially lower in the infected HBEC-5i cells when compared to those of the infected microglia cells. Finally, unlike UNAV, MAYV elicited a strong expression of specific interferon-stimulated genes in microglia cells, along with pro-inflammatory cytokines implicated in the immune response. Collectively, these findings demonstrate that MAYV and UNAV are capable of infecting relevant human brain cells.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"79 1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139396220","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":"Processing of the Hepatitis E virus ORF1 nonstructural polyprotein","authors":"Yogesh A. Karpe","doi":"10.3389/fviro.2023.1327745","DOIUrl":"https://doi.org/10.3389/fviro.2023.1327745","url":null,"abstract":"<p>Hepatitis E viruses (HEV) Open Reading Frame 1 (ORF1) encodes a non-structural polyprotein. In most positive-sense RNA viruses found in animals, this non-structural polyprotein is cleaved by viral protease or host protease. However, the mechanism behind the processing of HEV polyprotein remains one of the most controversial questions in HEV biology. The role of putative HEV protease in processing is difficult to demonstrate. Recent studies have questioned the existence of HEV protease and suggested that pORF1 lacks protease activity. Conversely, studies also suggested the role of host proteases involved in the blood coagulation cascade, like thrombin, in processing the HEV pORF1 polyprotein. In summary, recent studies support the notion that pORF1 lacks protease activity and host proteases are responsible for processing pORF1. The present review compiles a thorough overview of contentious research on HEV’s papain-like cysteine protease (PCP) and highlights recent advancements in the field. We aim to discuss the challenges and opportunities in the field to focus on further research.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"26 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139101821","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":"APOBEC3 family proteins as drivers of virus evolution","authors":"Michael Jonathan, Terumasa Ikeda","doi":"10.3389/fviro.2023.1332010","DOIUrl":"https://doi.org/10.3389/fviro.2023.1332010","url":null,"abstract":"<p>The apolipoprotein B mRNA editing enzyme catalytic polypeptide-like (APOBEC) family consists of cytosine deaminases implicated in diverse and important biological functions. APOBEC3 (A3) proteins belong to the APOBEC/AID family, and they catalyze the deamination of cytosine to uracil in single-stranded DNA and, to a lesser extent, in RNA substrates. In humans, seven <italic>A3</italic> genes have been identified (<italic>A3A</italic>, <italic>A3B</italic>, <italic>A3C</italic>, <italic>A3D</italic>, <italic>A3F</italic>, <italic>A3G</italic>, and <italic>A3H</italic>). The introduction of lethal G-to-A or C-to-U mutations into certain viral genomes leads to virus inactivation. However, the mutagenic capability of A3 proteins could serve as a source of mutations to drive virus evolution. Therefore, recent studies have implied the role of A3 proteins in aiding the evolution of viruses, conferring them with severe manifestations such as drug resistance and/or immune evasion. In this review, we discuss in depth the interactions of A3 proteins with viruses that infect humans and our self-proteins.</p>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-12-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138716693","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}
Eric Asare Fenteng, Paul Poku Sampene Ossei, William Gilbert Ayibor, Tracy Narh-Bedu
{"title":"Beyond survival: unraveling the dynamics of Ebola virus resurgence in Sub-Saharan Africa and the remarkable journey of survivors","authors":"Eric Asare Fenteng, Paul Poku Sampene Ossei, William Gilbert Ayibor, Tracy Narh-Bedu","doi":"10.3389/fviro.2023.1227314","DOIUrl":"https://doi.org/10.3389/fviro.2023.1227314","url":null,"abstract":"Ebola virus disease (EVD) remains a significant public health threat, with sporadic outbreaks occurring in Sub-Saharan Africa. Survivors of EVD may experience various post-infection symptoms, collectively known as post-Ebola virus syndrome (PES), which include chronic arthralgia, uveitis, headache, and psychosocial stressors. In this review, we discuss the persistence of Ebola virus in survivors and its possible role in the reemergence of current outbreaks. We highlight that waning immunity of survivors enhances viral persistence and may lead to viral reactivation and recurrence of disease in previously affected tissues. The delicate equilibrium between diminished immune cell surveillance and limited viral replication may lead to enduring chronic inflammation. Our systematic review, based on an extensive survivor cohort, underscores the importance of continued research and preparedness efforts to combat future outbreaks through adequate surveillance and timely public health interventions. This review serves as a comprehensive guide to understanding the complexities of EVD survivorship, the challenges of PES, and the strategies to mitigate its impact.","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"9 6","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2023-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"136352049","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}
Michael A. Zeller, Zebulun W. Arendsee, Gavin J.D. Smith, Tavis K. Anderson
{"title":"classLog: Logistic regression for the classification of genetic sequences","authors":"Michael A. Zeller, Zebulun W. Arendsee, Gavin J.D. Smith, Tavis K. Anderson","doi":"10.3389/fviro.2023.1215012","DOIUrl":"https://doi.org/10.3389/fviro.2023.1215012","url":null,"abstract":"<sec><title>Introduction</title><p>Sequencing and phylogenetic classification have become a common task in human and animal diagnostic laboratories. It is routine to sequence pathogens to identify genetic variations of diagnostic significance and to use these data in realtime genomic contact tracing and surveillance. Under this paradigm, unprecedented volumes of data are generated that require rapid analysis to provide meaningful inference. </p></sec><sec><title>Methods</title><p>We present a machine learning logistic regression pipeline that can assign classifications to genetic sequence data. The pipeline implements an intuitive and customizable approach to developing a trained prediction model that runs in linear time complexity, generating accurate output rapidly, even with incomplete data. Our approach was benchmarked against porcine respiratory and reproductive syndrome virus (PRRSv) and swine H1 influenza A virus (IAV) datasets. Trained classifiers were tested against sequences and simulated datasets that artificially degraded sequence quality at 0, 10, 20, 30, and 40%. </p></sec><sec><title>Results</title><p>When applied to a poor-quality sequence data, the classifier achieved between >85% to 95% accuracy for the PRRSv and the swine H1 IAV HA dataset and this increased to near perfect accuracy when using the full dataset. The model also identifies amino acid positions used to determine genetic clade identity through a feature selection ranking within the model. These positions can be mapped onto a maximum-likelihood phylogenetic tree, allowing for the inference of clade defining mutations. </p></sec><sec><title>Discussion</title><p>Our approach is implemented as a python package with code available at <uri xlink:href=\"https://github.com/flu-crew/classLog\" xmlns:xlink=\"http://www.w3.org/1999/xlink\">https://github.com/flu-crew/classLog</uri>.</p></sec>","PeriodicalId":73114,"journal":{"name":"Frontiers in virology","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2023-11-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138531603","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}