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                  <text>Dominio científico: Coronavirus</text>
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                <text>De Novo Assembled Wheat Transcriptomes Delineate Differentially Expressed Host Genes in Response to Leaf Rust Infection.</text>
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                <text>Saket Chandra, Dharmendra Singh, Jyoti Pathak, Supriya Kumari, Manish Kumar, Raju Poddar, Harindra Singh Balyan, Puspendra Kumar Gupta, Kumble Vinod Prabhu, Kunal Mukhopadhyay</text>
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                <text>Pathogens like Puccinia triticina, the causal organism for leaf rust, extensively damages wheat production. The interaction at molecular level between wheat and the pathogen is complex and less explored. The pathogen induced response was characterized using mock- or pathogen inoculated near-isogenic wheat lines (with or without seedling leaf rust resistance gene Lr28). Four Serial Analysis of Gene Expression libraries were prepared from mock- and pathogen inoculated plants and were subjected to Sequencing by Oligonucleotide Ligation and Detection, which generated a total of 165,767,777 reads, each 35 bases long. The reads were processed and multiple k-mers were attempted for de novo transcript assembly; 22 k-mers showed the best results. Altogether 21,345 contigs were generated and functionally characterized by gene ontology annotation, mining for transcription factors and resistance genes. Expression analysis among the four libraries showed extensive alterations in the transcriptome in response to pathogen infection, reflecting reorganizations in major biological processes and metabolic pathways. Role of auxin in determining pathogenesis in susceptible and resistant lines were imperative. The qPCR expression study of four LRR-RLK (Leucine-rich repeat receptor-like protein kinases) genes showed higher expression at 24 hrs after inoculation with pathogen. In summary, the conceptual model of induced resistance in wheat contributes insights on defense responses and imparts knowledge of Puccinia triticina-induced defense transcripts in wheat plants.</text>
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                <text>DOI: 10.1371/journal.pone.0148453</text>
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                <text>PLoS ONE</text>
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                <text>Full-length genome sequences of porcine epidemic diarrhoea virus strain CV777; Use of NGS to analyse genomic and sub-genomic RNAs.</text>
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                <text>Thomas Bruun Rasmussen, Maria Beatrice Boniotti, Alice Papetti, Béatrice Grasland, Jean-Pierre Frossard, Akbar Dastjerdi, Marcel Hulst, Dennis Hanke, Anne Pohlmann, Sandra Blome, Wim H.M. van der Poel, Falko Steinbach, Yannick Blanchard, Antonio Lavazza, Anette Bøtner, Graham J Belsham</text>
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                <text>Porcine epidemic diarrhoea virus, strain CV777, was initially characterized in 1978 as the causative agent of a disease first identified in the UK in 1971. This coronavirus has been widely distributed among laboratories and has been passaged both within pigs and in cell culture. To determine the variability between different stocks of the PEDV strain CV777, sequencing of the full-length genome (ca. 28kb) has been performed in 6 different laboratories, using different protocols. Not surprisingly, each of the different full genome sequences were distinct from each other and from the reference sequence (Accession number AF353511) but they are &gt;99% identical. Unique and shared differences between sequences were identified. The coding region for the surface-exposed spike protein showed the highest proportion of variability including both point mutations and small deletions. The predicted expression of the ORF3 gene product was more dramatically affected in three different variants of this virus through either loss of the initiation codon or gain of a premature termination codon. The genome of one isolate had a substantially rearranged 5´-terminal sequence. This rearrangement was validated through the analysis of sub-genomic mRNAs from infected cells. It is clearly important to know the features of the specific sample of CV777 being used for experimental studies.</text>
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                <text>DOI: 10.1371/journal.pone.0193682</text>
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                <text>PLoS ONE</text>
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                  <text>Dominio científico: Coronavirus</text>
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      <name>Text</name>
      <description>A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.</description>
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        <description>The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.</description>
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                <text>Environmental persistence of porcine coronaviruses in feed and feed ingredients.</text>
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                <text>Michaela P Trudeau, Harsha Verma, Fernando Sampedro, Pedro E Urriola, Gerald C Shurson, Sagar M. Goyal</text>
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                <text>Porcine Epidemic Diarrhea Virus (PEDV), Porcine Delta Corona Virus (PDCoV), and Transmissible Gastroenteritis Virus (TGEV) are major threats to swine health and contaminated feed plays a role in virus transmission. The objective of our study was to characterize inactivation of PEDV, PDCoV, and TGEV in various feed ingredient matrices. Samples of complete feed, spray dried porcine plasma, meat meal, meat and bone meal, blood meal, corn, soybean meal, and corn dried distillers grains with solubles were weighed (5 g/sample) into scintillation vials and inoculated with 1 mL of PEDV, PDCoV, or TGEV. Samples were incubated at room temperature for up to 56 days. Aliquots were removed at various time points followed by preparing serial 10-fold dilutions and inoculating in cell cultures to determine the amount of surviving virus. Inactivation kinetics were determined using the Weibull model, which estimates a delta value indicating the time necessary to reduce virus concentration by 1 log. Delta values of various ingredients were compared and analyzed as to their nutrient composition. Soybean meal had the greatest delta value (7.50 days) for PEDV (P &lt; 0.06) as compared with all other ingredients. High delta values (P &lt; 0.001) were observed in soybean meal for PDCoV (42.04 days) and TGEV (42.00 days). There was a moderate correlation between moisture content and the delta value for PDCoV (r = 0.49, P = 0.01) and TGEV (r = 0.41, P = 0.02). There was also a moderate negative correlation between TGEV survival and ether extract content (r = -0.51, P = 0.01). In conclusion, these results indicate that the first log reduction of PDCoV and TGEV takes the greatest amount of time in soybean meal. In addition to this, moisture and ether content appear to be an important determinant of virus survival in feed ingredients.</text>
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                <text>DOI: 10.1371/journal.pone.0178094</text>
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                <text>PLoS ONE</text>
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              <description>An account of the resource</description>
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                  <text>Dominio científico: Coronavirus</text>
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                <text>Viral etiology of acute respiratory infections in hospitalized children in Novosibirsk City, Russia (2013 - 2017).</text>
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                <text>Olga Kurskaya, Tatyana Ryabichenko, Natalya Leonova, Weifeng Shi, Hongtao Bi, Kirill Sharshov, Eugenia Kazachkova, Ivan Sobolev, Elena Prokopyeva, Tatiana Kartseva, Alexander Alekseev, Alexander Shestopalov</text>
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                <text>BACKGROUND:Acute respiratory infections (ARIs) cause a considerable morbidity and mortality worldwide especially in children. However, there are few studies of the etiological structure of ARIs in Russia. In this work, we analyzed the etiology of ARIs in children (0-15 years old) admitted to Novosibirsk Children's Municipal Clinical Hospital in 2013-2017. METHODS:We tested nasal and throat swabs of 1560 children with upper or lower respiratory infection for main respiratory viruses (influenza viruses A and B, parainfluenza virus types 1-4, respiratory syncytial virus, metapneumovirus, four human coronaviruses, rhinovirus, adenovirus and bocavirus) using a RT-PCR Kit. RESULTS:We detected 1128 (72.3%) samples were positive for at least one virus. The most frequently detected pathogens were respiratory syncytial virus (358/1560, 23.0%), influenza virus (344/1560, 22.1%), and rhinovirus (235/1560, 15.1%). Viral co-infections were found in 163 out of the 1128 (14.5%) positive samples. We detected significant decrease of the respiratory syncytial virus-infection incidence in children with increasing age, while the reverse relationship was observed for influenza viruses. CONCLUSIONS:We evaluated the distribution of respiratory viruses in children with ARIs and showed the prevalence of respiratory syncytial virus and influenza virus in the etiological structure of infections. This study is important for the improvement and optimization of diagnostic tactics, control and prevention of the respiratory viral infections.</text>
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                <text>DOI: 10.1371/journal.pone.0200117</text>
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                <text>PLoS ONE</text>
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                <text>Diminished COX-2/PGE2-Mediated Antiviral Response Due to Impaired NOX/MAPK Signaling in G6PD-Knockdown Lung Epithelial Cells.</text>
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                <text>Hsin-Ru Lin, Yi-Hsuan Wu, Wei-Chen Yen, Chuen-Mao Yang, Daniel  Tsun-Yee Chiu</text>
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                <text>Glucose-6-phosphate dehydrogenase (G6PD) provides the reducing agent NADPH to meet the cellular needs for reductive biosynthesis and the maintenance of redox homeostasis. G6PD-deficient cells experience a high level of oxidative stress and an increased susceptibility to viral infections. Cyclooxygenase-2 (COX-2) is a key mediator in the regulation of viral replication and inflammatory response. In the current study, the role of G6PD on the inflammatory response was determined in both scramble control and G6PD-knockdown (G6PD-kd) A549 cells upon tumor necrosis factor-α (TNF-α) stimulation. A decreased expression pattern of induced COX-2 and reduced production of downstream PGE2 occurred upon TNF-α stimulation in G6PD-kd A549 cells compared with scramble control A549 cells. TNF-α-induced antiviral activity revealed that decreased COX-2 expression enhanced the susceptibility to coronavirus 229E infection in G6PD-kd A549 cells and was a result of the decreased phosphorylation levels of MAPK (p38 and ERK1/2) and NF-κB. The impaired inflammatory response in G6PD-kd A549 cells was found to be mediated through NADPH oxidase (NOX) signaling as elucidated by cell pretreatment with a NOX2-siRNA or NOX inhibitor, diphenyleneiodonium chloride (DPI). In addition, NOX activity with TNF-α treatment in G6PD-kd A549 cells was not up-regulated and was coupled with a decrease in NOX subunit expression at the transcriptional level, implying that TNF-α-mediated NOX signaling requires the participation of G6PD. Together, these data suggest that G6PD deficiency affects the cellular inflammatory response and the decreased TNF-α-mediated antiviral response in G6PD-kd A549 cells is a result of dysregulated NOX/MAPK/NF-κB/COX-2 signaling.</text>
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                <text>DOI: 10.1371/journal.pone.0153462</text>
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                <text>Structure activity relationship and modeling studies of inhibitors of lysine specific demethylase 1.</text>
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                <text>Chao Zhou, Fangrui Wu, Lianghao Lu, Liping Wei, Eric Pai, Yuan Yao, Yongcheng Song</text>
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                <text>Post-translational modifications of histone play important roles in gene transcription. Aberrant methylation of histone lysine sidechains have been often found in cancer. Lysine specific demethylase 1 (LSD1), which can demethylate histone H3 lysine 4 (H3K4) and other proteins, has recently been found to be a drug target for acute myeloid leukemia. To understand structure activity/selectivity relationships of LSD1 inhibitors, several series of cyclopropylamine and related compounds were synthesized and tested for their activities against LSD1 and related monoamine oxidase (MAO) A and B. Several cyclopropylamine containing compounds were found to be highly potent and selective inhibitors of LSD1. A novel series cyclopropylimine compounds also exhibited strong inhibitory activity against LSD1. Structure activity relationships (SAR) of these compounds are discussed. Docking studies were performed to provide possible binding models of a representative compound in LSD1 and MAO-A. Moreover, these modeling studies can rationalize the observed SARs and selectivity.</text>
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                <text>DOI: 10.1371/journal.pone.0170301</text>
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                <text>PLoS ONE</text>
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                  <text>Dominio científico: Coronavirus</text>
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      <name>Text</name>
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                <text>Comparative pathology of rhesus macaque and common marmoset animal models with Middle East respiratory syndrome coronavirus.</text>
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                <text>Pin Yu, Yanfeng Xu, Wei Deng, Lin-Lin Bao, Lan HUANG, Yuhuan Xu, Yanfeng Yao, Chuan Qin</text>
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                <text>Middle East respiratory syndrome (MERS), which is caused by a newly discovered coronavirus (CoV), has recently emerged. It causes severe viral pneumonia and is associated with a high fatality rate. However, the pathogenesis, comparative pathology and inflammatory cell response of rhesus macaques and common marmosets experimentally infected with MERS-CoV are unknown. We describe the histopathological, immunohistochemical, and ultrastructural findings from rhesus macaque and common marmoset animal models of MERS-CoV infection. The main histopathological findings in the lungs of rhesus macaques and common marmosets were varying degrees of pulmonary lesions, including pneumonia, pulmonary oedema, haemorrhage, degeneration and necrosis of the pneumocytes and bronchial epithelial cells, and inflammatory cell infiltration. The characteristic inflammatory cells in the lungs of rhesus macaques and common marmosets were eosinophils and neutrophils, respectively. Based on these observations, the lungs of rhesus macaques and common marmosets appeared to develop chronic and acute pneumonia, respectively. MERS-CoV antigens and viral RNA were identified in type I and II pneumocytes, alveolar macrophages and bronchial epithelial cells, and ultrastructural observations showed that viral protein was found in type II pneumocytes and inflammatory cells in both species. Correspondingly, the entry receptor DDP4 was found in type I and II pneumocytes, bronchial epithelial cells, and alveolar macrophages. The rhesus macaque and common marmoset animal models of MERS-CoV can be used as a tool to mimic the oncome of MERS-CoV infections in humans. These models can help to provide a better understanding of the pathogenic process of this virus and to develop effective medications and prophylactic treatments.</text>
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                <text>DOI: 10.1371/journal.pone.0172093</text>
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              <elementText elementTextId="832">
                <text>PLoS ONE</text>
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                  <text>Dominio científico: Coronavirus</text>
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                <text>Human Mycobacterium tuberculosis CD8 T Cell Antigens/Epitopes Identified by a Proteomic Peptide Library.</text>
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                <text>David M Lewinsohn, Gwendolyn M Swarbrick, Meghan E Cansler, Megan D Null, Veena Rajaraman, Marisa M Frieder, David R Sherman, Shannon McWeeney, Deborah A. Lewinsohn</text>
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                <text>Identification of CD8(+) T cell antigens/epitopes expressed by human pathogens with large genomes is especially challenging, yet necessary for vaccine development. Immunity to tuberculosis, a leading cause of mortality worldwide, requires CD8(+) T cell immunity, yet the repertoire of CD8 antigens/epitopes remains undefined. We used integrated computational and proteomic approaches to screen 10% of the Mycobacterium tuberculosis (Mtb) proteome for CD8 Mtb antigens. We designed a weighting schema based upon a Multiple Attribute Decision Making:framework to select 10% of the Mtb proteome with a high probability of containing CD8(+) T cell epitopes. We created a synthetic peptide library consisting of 15-mers overlapping by 11 aa. Using the interferon-γ ELISPOT assay and Mtb-infected dendritic cells as antigen presenting cells, we screened Mtb-specific CD8(+) T cell clones restricted by classical MHC class I molecules (MHC class Ia molecules), that were isolated from Mtb-infected humans, against this library. Three novel CD8 antigens were unambiguously identified: the EsxJ family (Rv1038c, Rv1197, Rv3620c, Rv2347c, Rv1792), PE9 (Rv1088), and PE_PGRS42 (Rv2487c). The epitopes are B5701-restricted EsxJ24-34, B3905-restricted PE953-67, and B3514-restricted PE_PGRS4248-56, respectively. The utility of peptide libraries in identifying unknown epitopes recognized by classically restricted CD8(+) T cells was confirmed, which can be applied to other intracellular pathogens with large size genomes. In addition, we identified three novel Mtb epitopes/antigens that may be evaluated for inclusion in vaccines and/or diagnostics for tuberculosis.</text>
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                <text>2013</text>
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                <text>DOI: 10.1371/journal.pone.0067016</text>
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              <elementText elementTextId="823">
                <text>PLoS ONE</text>
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                <text>THE MOLECULAR EVOLUTION OF THE MOST DANGEROUS EMERGING VIRUS INFECTIONS</text>
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                <text>Popov N.N., Kolotova TYu</text>
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            <description>An account of the resource</description>
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                <text>In this paper we reviewed what is known about the emerging viruses, the hosts that they originate in, and the molecular events that drive their emergence. When a pathogen crosses over from animals to humans, or an existing human disease suddenly increases in incidence, the infectious disease is said to be ‘emerging’. Most of the emerging pathogens originate from nonhuman animal species which has been termed natural reservoirs. The number of emerging infectious diseases has increased over the last few decades, driven by both anthropogenic and environmental factors such as population growth, urbanization, global travel and trade, intensification of livestock production. Now it has been believed that the emergence process may include four steps. On the first step the exposure of the humans to a novel virus occures. On the second step the subset of the viruses overcome the cross-species barrier. Host shifts have resulted in multiple human pandemics, such as HIV from chimps the H1N1, ‘‘spanish flu’’ from birds, SARS-CoV and virus Ebola from bats. Then some viruses enables to transmit from one human to another. And on the last step the viruses that are sufficiently transmissible between humans cause outbreaks and become endemic in human populations without the requirement of a natural reservoir. This review aims to discuss the molecular mechanisms that govern virus cross-species transmission and following stage, using the emergence of HIV, SARS-CoV, virus Ebola and influenza virus A as the models.Populations of many viruses harbour abundant genetic variability due to a combination of high mutation, recombination or reassortation rates and large population sizes. Mutations and recombinations has been associated with the increases in virulence, the evasion of host immunity and the evolution of resistance to antivirals. Genetic alterations in one species may results in the acquisition of variations that allow them to overcome cross species barriers and infect new hosts. Really, many recently emerged human diseases are caused by viruses that display active recombination or reassortment. The continual shuffling of genes of influenza A represents a example of the key role of reassortment for the new virus emergence. Available data demonstrate the possible origin of SARS-CoV from recombination of different bat SL-CoVs viruses strains. However in other cases the emergence of a specific virus cannot be directly attributed to its ability to recombine. For example, although SIV recombines at a high rate in natural reservoirs, there is no evidence that recombination assisted the cross-species transfer of the virus from the chimpanzee into humans. But mutagenesis and recombination actively shape the further molecular history of HIV in humans. Also it is not proved that recombination precede the cross-species jump of the Ebola virus. In summary, the available data suggest that although recombination, reassortment and mutagenesis is sometimes directly involved to the process of cross-species transmission, it is not a necessary precursor to successful viral emergence. Further investigations are required to reveal the role of genetic change in the history of virus emergence. We believe that comprehensive description of molecular evolution of new viruses has led to a better understanding of the causes and predictability of infection emergence.</text>
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                <text>2016</text>
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                <text>Emerging viruses, four stage of the emergence, Natural reservoir, recombination, reassotment, Mutagenesis, HIV-1, HIV-2, SIV, SARS-CoV, virus Ebola, influenza virus A</text>
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                <text>Anali Mečnikìvsʹkogo Institutu</text>
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                <text>Mechnikov Institute of Microbiology and immunology</text>
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                <text>Medicine (General)</text>
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                <text>EN, RU, UK</text>
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                  <text>Coronavirus</text>
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                  <text>Dominio científico: Coronavirus</text>
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                <text>First report of bovine rotavirus and bovine coronavirus seroprevalance in goats in Turkey</text>
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                <text>Gumusova Okur S., Yazici Z., Albayrak H., Çakiroglu D.</text>
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                <text>In this study, bovine coronavirus (BCV) and bovine rotavirus (BRV) seroprevalances were detected by ELISA in 107 goat blood serum samples obtained from five different provinces of Northern Turkey. The results of the study reflected 41.12% and 82.24% seropositivity against BCV and BRV, respectively, in the goat sera. BCV seroprevalance in mature goats is determined for the first time with this study. Furthermore, this is the first statement of BRV and BCV seroprevalances in the mature goat population in Turkey.</text>
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                <text>2007</text>
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                <text>BRV, BCV, ELISA, goat, Seroprevalance</text>
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                <text>DOI: 10.2298/VETGL0702075G</text>
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                <text>Veterinarski Glasnik</text>
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                <text>Faculty of Veterinary Medicine, Belgrade</text>
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                <text>Veterinary medicine</text>
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                <text>SR</text>
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