Journal of General Virology最新文献

{"title":"Structural insights into the nuclear import of ovine gammaherpesvirus 2 ORF73 LANA homologue.","authors":"Babu Kanti Nath, Renate H M Schwab, Crystall M D Swarbrick, Silvia Pavan, Nazia Rahman, Brian P McSharry, Shane R Raidal, Daryl Ariawan, Ole Tietz, Shubhagata Das, Gualtiero Alvisi, Jade K Forwood","doi":"10.1099/jgv.0.002250","DOIUrl":"https://doi.org/10.1099/jgv.0.002250","url":null,"abstract":"<p><p>Ovine gammaherpesviruses 2 (OvGHV2), a member of the <i>Macavirus</i> genus within the <i>Orthoherpesviridae</i> family, causes lymphoproliferative diseases in susceptible species, most notably sheep-associated malignant catarrhal fever. Research on OvGHV2 has been hindered by the absence of a permissive cell culture system, limiting investigations into viral replication, entry mechanisms and cell tropism. This challenge constrains progress towards understanding OvGHV2 pathogenesis and developing effective vaccines or therapeutics. We investigated the molecular mechanisms underlying OvGHV2 infection, focusing on the nuclear trafficking pathways of the latency-associated nuclear antigen (LANA), encoded by ORF73. In other gammaherpesviruses, LANA is known to mediate viral episome maintenance, chromatin tethering and latency through its nuclear localization. We identified and functionally characterized a novel bipartite nuclear localization signal (NLS) within the C-terminal region of OvGHV2 LANA and elucidated its interactions with host nuclear import receptors. Using high-resolution crystallography and quantitative binding assays, we mapped the key residues responsible for binding to importin alpha (IMP<i>α</i>) and demonstrated isoform-specific variations in binding affinity. Confocal microscopy revealed that the OvGHV2 LANA predominantly localizes to the nucleus through an IMP<i>α</i>/<i>β</i>1-dependent pathway, as mutation or inhibition of the NLS significantly reduced nuclear accumulation. Interestingly, partial nuclear localization under these conditions suggests an additional IMP<i>α</i>/<i>β</i>1-independent nuclear import mechanism. Collectively, our biochemical and structural analyses confirm that the identified NLS is essential for IMP<i>α</i>-mediated nuclear import of OvGHV2 LANA. These findings provide new insights into OvGHV2 host interactions and establish a molecular basis for developing targeted antiviral strategies against ovine gammaherpesvirus 2 infection.</p>","PeriodicalId":15880,"journal":{"name":"Journal of General Virology","volume":"107 4","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13089313/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Identification of the nucleolar localization signal in <i>Autographa californica</i> multiple nucleopolyhedrovirus multifunctional protein Ac16.","authors":"Guoqing Chen, Yihong Wu, Jing Yang, Haoran Wang, Xinxin Zhang, Guozhong Feng","doi":"10.1099/jgv.0.002246","DOIUrl":"10.1099/jgv.0.002246","url":null,"abstract":"<p><p><i>Autographa californica</i> multiple nucleopolyhedrovirus (AcMNPV) Ac16 (BV/ODV-E26) is a multifunctional protein found exclusively in group I NPV genomes. Here, we report a novel role for Ac16 in nucleolar localization. Using protein truncation and subcellular localization analysis, we characterized that the residues 78-113 of Ac16 contain nuclear (NLS) and nucleolar (NoLS) localization signals. Further multiple point mutation analysis within this region demonstrated that two basic-amino-acid-rich clusters, ⁷⁸HKKKLRH⁸⁴ and ¹⁰⁸KKTTHR¹¹³, function as NLSs, and together, they constitute a functional NoLS. However, Ac16 itself was not observed to localize to nucleoli, while it displayed an overlapping distribution with IE1 during AcMNPV infection. Co-expression assay revealed that IE1, an Ac16-interacting protein, alters the subcellular localization of Ac16, and this effect is independent of the Ac16 NoLS. By yeast two-hybrid library screening, vacuolar (H⁺)-ATPase subunit D (SfVhaD) was identified as a candidate interaction partner of Ac16, which was further confirmed by co-immunoprecipitation. Ac16 affected the localization of SfVhaD; both proteins predominantly colocalized in nucleoli in transient co-expression assays, while they primarily colocalized within the virogenic stroma during AcMNPV infection. Together, these data suggest that Ac16 contains a functional NoLS and may facilitate the transport of its interaction partners from nucleoli to viral replication centres during AcMNPV infection.</p>","PeriodicalId":15880,"journal":{"name":"Journal of General Virology","volume":"107 4","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13043108/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147592322","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sexual transmission of hepatitis E virus via vaginal and rectal routes in a rabbit model.","authors":"Manyu Li, Wenjun Wan, Zeyu Song, Wenwen Sun, Qiyu He, Haiwei Zhou","doi":"10.1099/jgv.0.002231","DOIUrl":"10.1099/jgv.0.002231","url":null,"abstract":"<p><p>Hepatitis E virus (HEV) is a major cause of acute hepatitis worldwide. While faecal-oral transmission is well-established, the potential for sexual transmission remains unclear. This study aimed to investigate whether HEV can be transmitted through sexual routes using a rabbit model. A total of 80 rabbits were inoculated intravaginally or intrarectally with HEV, compared to intravenous challenge. To assess hormonal influence, rabbits were pre-treated with medroxyprogesterone acetate (MPA) or pregnant mare serum gonadotrophin (PMSG) prior to vaginal inoculation. Also, 12 pregnant rabbits were injected with HEV by vaginal and intravenous routes, respectively, to evaluate adverse outcomes. Viral shedding, seroconversion, viral loads in tissues, histopathology and vaginal microbiota were analysed. Our results showed that HEV can be transmitted through both vaginal and rectal routes, establishing productive but less efficient infections than intravenous inoculation. Crucially, the MPA dramatically enhanced vaginal susceptibility, leading to prolonged viral shedding, higher systemic viral loads and 100% seroconversion, compared to partial infection in PMSG-treated and untreated controls. Vaginal infection in pregnant rabbits resulted in significant adverse outcomes, including abortion (66.7%) and vertical transmission. Furthermore, vaginal inoculation altered the local microbiota and transcriptome, suggesting a remodelled genital tract microenvironment. Our study provided the first direct experimental evidence that HEV can be sexually transmitted via vaginal and rectal routes. The progesterone-mediated enhancement of susceptibility and the severe pregnancy outcomes highlighted its public health risk, particularly for women.</p>","PeriodicalId":15880,"journal":{"name":"Journal of General Virology","volume":"107 4","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13043109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147592589","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hendra virus genotypes 1 and 2 differ in V protein-mediated immune evasion.","authors":"Melanie N Tripp, Stephen M Rawlinson, Sarah J Edwards, Cassandra T David, Glenn A Marsh, Kim Halpin, Gregory W Moseley","doi":"10.1099/jgv.0.002256","DOIUrl":"https://doi.org/10.1099/jgv.0.002256","url":null,"abstract":"<p><p>Hendra virus (HeV) is a highly pathogenic virus endemic to Australia that causes lethal infections in horses and humans following spillover from bat reservoirs. There are two known genotypes: genotype 1 and 2 (HeV-g1 and HeV-g2). Both have caused lethal disease in horses, but HeV-g1 causes a more severe disease than HeV-g2 in non-human primates. The molecular mechanisms underlying these differences are poorly understood. The capacity of viruses to evade the interferon (IFN)-mediated antiviral innate immune response is important in infection and disease, and in HeV, the virulence factor V protein is a key mediator and one of the most divergent proteins between the genotypes. We compared the IFN antagonist functions of the V proteins of HeV-g1 and HeV-g2, finding that HeV-g1-V was more potent than HeV-g2-V in antagonizing the induction of type-I IFN; we further found that the proteins differ in nucleocytoplasmic localization. Consistent with these findings, HeV-g1 suppressed type-I IFN production more effectively than HeV-g2 during infection. These data reveal differences in the fundamental biology of HeV genotypes, which may be significant to pathogenesis.</p>","PeriodicalId":15880,"journal":{"name":"Journal of General Virology","volume":"107 4","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13098992/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Double-edged sword: flavivirus NS1 enhances human plasmin-mediated fibrinolysis while being targeted for cleavage and inactivation.","authors":"Lucas Mendes-Monteiro, Pedro Henrique Carneiro, Jonas N Conde, Joice L Menezes, Matheus Silva de Souza, Pedro F de Carvalho, Eugenio D Hottz, Eva Harris, Diego Allonso, Ronaldo Mohana-Borges","doi":"10.1099/jgv.0.002253","DOIUrl":"10.1099/jgv.0.002253","url":null,"abstract":"<p><p>Dengue virus (DENV) is the most prevalent arbovirus in the world, being transmitted to humans through the bite of infected <i>Aedes</i> mosquitoes. Symptomatic individuals may develop a haemorrhagic fever leading to plasma leakage, hypovolaemic shock and death. A key player in viral pathogenesis is the non-structural protein 1 (NS1), which is secreted by infected cells and disrupts platelet and endothelial barrier function, contributing to plasma extravasation. Importantly, dengue patients present abnormal haemostasis, with concomitant activation of both coagulation and fibrinolytic systems correlating with disease severity. However, a direct role played by NS1 in fibrinolysis has never been shown. Here, we investigated the interaction between NS1 and plasminogen, the precursor of the fibrinolytic enzyme plasmin, aiming to characterize its implications in clot turnover during infection. We showed that binding of plasminogen to NS1 is dependent on lysine-binding sites in plasminogen, implicating NS1 as a plasmin substrate. We also demonstrated that NS1 is cleaved by plasmin, which, in turn, blocks its effect on endothelial glycocalyx layer disruption and endothelial hyperpermeability. Using euglobulin clot lysis assays, we showed that DENV NS1 enhances fibrin clot lysis and that this effect is conserved for other flaviviruses, including Zika and West Nile viruses. Altogether, we identified a novel mechanism by which NS1 might contribute to bleeding disorders, highlighting the relevance of the plasminogen/plasmin system for DENV pathogenesis in humans.</p>","PeriodicalId":15880,"journal":{"name":"Journal of General Virology","volume":"107 4","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13135474/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ICTV Virus Taxonomy Profile: <i>Satyavativiridae</i> 2026.","authors":"Apoorva Prabhu, Christian Rinke","doi":"10.1099/jgv.0.002249","DOIUrl":"https://doi.org/10.1099/jgv.0.002249","url":null,"abstract":"<p><p>Members of the family <i>Satyavativiridae</i> are dsDNA viruses associated with the host <i>Poseidoniales</i>, a marine archaeal lineage. Genomes assigned to this group have been identified via long-read sequencing of brackish estuarine samples. These viruses represent a novel viral lineage in the order <i>Adrikavirales</i> distinct from other <i>Poseidoniales</i> viruses known as 'magroviruses', a collective term derived from Marine Group II Euryarchaeota (former name of <i>Poseidoniales</i>) viruses. The family includes the genus <i>Vyasavirus</i> and the species <i>Vyasavirus brisbanense</i>. The virus genome is a linear dsDNA of 87 kbp and encodes proteins involved in the morphogenesis of virions, which are predicted to be composed of an icosahedral capsid and helical tail, characteristic of members of the class <i>Caudoviricetes</i>. This is a summary of the International Committee on Taxonomy of Viruses Report on the family <i>Satyavativiridae</i>, which is available at ictv.global/report/satyavativiridae.</p>","PeriodicalId":15880,"journal":{"name":"Journal of General Virology","volume":"107 4","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13108676/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147773384","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"ICTV Virus Taxonomy Profile: <i>Apasviridae</i> 2026.","authors":"Apoorva Prabhu, Christian Rinke","doi":"10.1099/jgv.0.002230","DOIUrl":"10.1099/jgv.0.002230","url":null,"abstract":"<p><p>The family <i>Apasviridae</i> includes dsDNA viruses associated with the marine archaeal lineage <i>Poseidoniales</i>. Members of this family have been identified using metagenomic analyses of brackish estuarine samples and are related to other 'magroviruses' infecting <i>Poseidoniales</i> archaea. The family belongs to the order <i>Magrovirales</i> and includes the genus <i>Agnivirus</i> and the species <i>Agnivirus brisbanense</i>. Viruses in the family possess a linear dsDNA genome of about 108 kbp and encode modules for DNA replication and virion morphogenesis, such as those relating to the formation of an icosahedral capsid and a helical tail, characteristic of members of the class <i>Caudoviricetes</i>. This is a summary of the International Committee on Taxonomy of Viruses (ICTV) Report on the family <i>Apasviridae</i>, which is available at ictv.global/report/apasviridae.</p>","PeriodicalId":15880,"journal":{"name":"Journal of General Virology","volume":"107 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12999244/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147473444","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Limited transmission of V180I genetic Creutzfeldt-Jakob disease in knock-in mice models.","authors":"Kenta Teruya, Shirou Mohri, Tetsuyuki Kitamoto","doi":"10.1099/jgv.0.002224","DOIUrl":"10.1099/jgv.0.002224","url":null,"abstract":"<p><p>Differentiating Creutzfeldt-Jakob disease (CJD) with the V180I mutation from other types of dementia is extremely difficult. Additionally, its differentiation is sometimes determined after performing neurosurgery, which is associated with a high risk of V180I prion contamination; however, the infectivity of the V180I prion has not been properly investigated. Especially in East Asia, this issue must be addressed to respond effectively to accidental contamination that leads to iatrogenic CJD. The results of our transmission experiments involving various humanized knock-in mice clearly indicate that the transmissibility of tissue from V180I genetic CJD cases is significantly limited.</p>","PeriodicalId":15880,"journal":{"name":"Journal of General Virology","volume":"107 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12999274/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147481142","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evaluating how infectious bursal disease virus (IBDV) infection influences influenza H3N8 challenge in chickens.","authors":"Salik Nazki, Chandana Tennakoon, Vishwanatha R A P Reddy, Yana Chen, Jean-Remy Sadeyen, Andrew J Brodrick, Munir Iqbal, Holly Shelton, Andrew J Broadbent","doi":"10.1099/jgv.0.002235","DOIUrl":"10.1099/jgv.0.002235","url":null,"abstract":"<p><p>Infectious bursal disease virus (IBDV) causes an endemic immunosuppressive disease in chickens. Prior exposure to IBDV influences the pathogenesis and shedding of chicken strains of influenza A virus (IAV), but its effect on waterfowl strains is poorly understood. To address this, we inoculated 14-day-old specific pathogen-free chickens with low pathogenicity avian influenza strain A/Mallard/Alberta/156/01 (H3N8) and compared the replication, shedding, pathogenesis, transmission and intra-host evolution between immunocompetent chickens and chickens that had IBDV-mediated immune dysregulation due to a prior infection with strain F52/70 at 2 days of age. The IAV replicated in the upper respiratory tract, and the virus was shed from the oropharyngeal cavity, but there was no shedding from the cloaca and no transmission to sentinel chickens. IAV replication in chickens was associated with amino acid substitutions in the polymerase complex and HA. Prior IBDV infection had no significant effect on IAV pathogenicity, replication or shedding and had a modest effect on IAV diversity, increasing the number of amino acid substitutions from an average of 2.50 substitutions per sample (sd±1.83) in the Mock/IAV group to 4.75 (sd±1.81) in the IBDV/IAV group (<i>P</i><0.01). Taken together, our data suggest that IBDV is unlikely to play a major role in the spillover or spread of waterfowl IAV strains in chicken flocks, although it could expand IAV diversity. This information is useful for informing preventative measures for controlling IAV in poultry flocks.</p>","PeriodicalId":15880,"journal":{"name":"Journal of General Virology","volume":"107 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12978164/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147433363","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Local citrus sudden death-associated virus infection in <i>Nicotiana benthamiana</i> induces chloroplast structural changes and HR-like responses that do not restrict systemic virus movement.","authors":"Sayuri Iwasaki, Dennis van Oevelen, Alba Pérez-Sánchez, Nell Lakatsch, Robin van der Helm, Lena Michailidou, Nadya N Icksan, Bradley Shibata, Emilyn E Matsumura","doi":"10.1099/jgv.0.002252","DOIUrl":"10.1099/jgv.0.002252","url":null,"abstract":"<p><p>The use of infectious clones to establish virus infections in well-established model plants has allowed us to greatly advance our understanding of virus-host interactions, providing controlled systems to study viruses that naturally infect complex hosts such as fruit trees. Citrus sudden death-associated virus (CSDaV) is a <i>Marafivirus</i> associated with citrus sudden death disease in Brazil, yet its molecular interactions in citrus or model plant hosts remain poorly characterized. In this work, we investigated the interaction between CSDaV and the model plant <i>Nicotiana benthamiana</i>. We show that CSDaV establishes a symptomless systemic infection in <i>N. benthamiana</i> plants, while inducing a hypersensitive response (HR)-like cell death preceded by chloroplast abnormalities in locally inoculated leaves. Immunogold labelling showed that CSDaV virions were localized near or inside altered chloroplasts in locally inoculated leaves. Membranous vesicles at the periphery of chloroplasts were also observed, suggesting chloroplast-associated replication. However, trans-complementation assays in which the viral RNA-dependent RNA polymerase rescued replication of a non-replicative CSDaV did not confirm a clear association between the replication complex and chloroplasts. Expression analyses showed that while <i>HIN1</i>, an HR-associated gene, was upregulated in CSDaV locally infected leaves, reactive oxygen species (ROS) levels and <i>CAT1</i>, a gene encoding a ROS-scavenging enzyme, were significantly reduced in the same CSDaV-infected tissues compared to controls, suggesting an ROS-independent HR-like reaction. Furthermore, the salicylic acid (SA) pathway genes <i>PR1</i> and <i>ICS1</i> were not induced, suggesting suppression of SA-mediated systemic resistance. These findings demonstrate <i>N. benthamiana</i> as a systemic host plant for CSDaV and suggest an infection strategy that couples localized HR-like responses with systemic defence suppression.</p>","PeriodicalId":15880,"journal":{"name":"Journal of General Virology","volume":"107 3","pages":""},"PeriodicalIF":4.3,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13035172/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147574368","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}