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                  <text>Agricultura sostenible</text>
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                  <text>Dominio científico: Agricultura sostenible</text>
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                <text>Genetic Response of Common Bean to the Inoculation with Indigenous &lt;i&gt;Fusarium&lt;/i&gt; Isolates</text>
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                <text>Sara Mayo-Prieto, Pedro A. Casquero, Samuel Álvarez-García, Alejandra J. Porteous-Álvarez, Bonifacio Reinoso</text>
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                <text>Fungal species from the genus Fusarium are important soil-borne pathogens worldwide, causing significant economic losses in diverse crops. The need to find sustainable solutions against this disease has led to the development of new strategies—for instance, the use of biocontrol agents. In this regard, non-pathogenic Fusarium isolates have demonstrated their ability to help other plants withstand subsequent pathogen attacks. In the present work, several Fusarium isolates were evaluated in climatic chambers to identify those presenting low or non-pathogenic behavior. The inoculation with a low-pathogenic isolate of the fungus did not affect the development of the plant, contrary to the results observed in plants inoculated with pathogenic isolates. The expression of defense-related genes was evaluated and compared between plants inoculated with pathogenic and low-pathogenic Fusarium isolates. Low-pathogenic isolates caused a general downregulation of several plant defense-related genes, while pathogenic ones produced an upregulation of these genes. This kind of response to low-pathogenic fungal isolates has been already described for other plant species and fungal pathogens, being related to enhanced tolerance to later pathogen attacks. The results here presented suggest that low-pathogenic F. oxysporum and F. solani isolates may have potential biocontrol activity against bean pathogens via induced and systemic responses in the plant.</text>
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                <text>2020</text>
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                <text>&lt;i&gt;Phaseolus vulgaris&lt;/i&gt;, biocontrol, biodiversity, legume, qPCR, soil-borne pathogens</text>
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                <text>10.3390/jof6040228</text>
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                <text>Journal of Fungi</text>
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                <text>MDPI AG</text>
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                <text>Biology (General)</text>
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                <text>&lt;a href="https://www.mdpi.com/2309-608X/6/4/228" target="_blank" rel="noreferrer noopener"&gt;https://www.mdpi.com/2309-608X/6/4/228&lt;/a&gt;</text>
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                  <text>Coronavirus</text>
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                  <text>Dominio científico: Coronavirus</text>
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                <text>Genetic Variant of SARS-CoV-2 Isolates in Indonesia: Spike Glycoprotein Gene</text>
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            <description>An entity primarily responsible for making the resource</description>
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                <text>Arli Aditya Parikesit, Arif Nur Muhammad Ansori, Viol Dhea Kharisma, Sahal Sabilil Muttaqin, Yulanda Antonius</text>
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                <text>Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), a novel coronavirus and the primarycausative agent of coronavirus disease 2019 (COVID-19), first occurred in China and rapidly spreadworldwide. The government of the Republic of Indonesia confirmed its first two cases of COVID-19 inMarch 2020. COVID-19 is a serious illness with no efficacious antiviral medication or approved vaccinecurrently available. Therefore, there is a need to investigate the genome of SARS-CoV-2. In this study,we characterized SARS-CoV-2 spike glycoprotein genes from Indonesia to investigate their geneticcomposition and variability. Overall, ten SARS-CoV-2 spike glycoprotein gene sequences retrievedfrom GenBank (National Center for Biotechnology Information, USA) and the GISAID EpiCoV database(Germany) were compared. We analyzed nucleotide variants and amino acid changes using MolecularEvolutionary Genetics Analysis (MEGA) X and analyzed gene similarity using the LALIGN web server.Interestingly, we revealed several specific mutation sites, however, there were no significant changesin the genetic composition of SARS-CoV-2 spike glycoprotein genes, when compared to the WuhanHu-1 isolate from China. However, this is a preliminary study and we recommend that molecularepidemiology and surveillance programs against COVID-19 in Indonesia be improved.</text>
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                <text>2020</text>
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                <text>mutation, coronavirus, genetic composition, SARS-CoV-2, COVID-19</text>
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            <name>Identifier</name>
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                <text>DOI: 10.22207/JPAM.14.SPL1.35</text>
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            <description>A related resource from which the described resource is derived</description>
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                <text>Journal of Pure and Applied Microbiology</text>
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            <description>An entity responsible for making the resource available</description>
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                <text>Journal of Pure and Applied Microbiology</text>
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                <text>Microbiology</text>
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              <description>An account of the resource</description>
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                <text>Genetic Variant Severe Acute Respiratory Syndrome Coronavirus 2 Isolates in Thailand</text>
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              <elementText elementTextId="36229">
                <text>Viroj Wiwanitkit, Beuy Joob</text>
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                <text>2020</text>
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                <text>-</text>
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                <text>DOI: 10.22207/JPAM.14.SPL1.01</text>
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            <description>A related resource from which the described resource is derived</description>
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              <elementText elementTextId="36233">
                <text>Journal of Pure and Applied Microbiology</text>
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            <name>Publisher</name>
            <description>An entity responsible for making the resource available</description>
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              <elementText elementTextId="36234">
                <text>Journal of Pure and Applied Microbiology</text>
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                <text>Microbiology</text>
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              <name>Title</name>
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              <description>An account of the resource</description>
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                  <text>Dominio científico: Coronavirus</text>
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            <name>Title</name>
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                <text>Genetic variants of the human host influencing the coronavirus-associated phenotypes (SARS, MERS and COVID-19): rapid systematic review and field synopsis</text>
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            <description>An entity primarily responsible for making the resource</description>
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                <text>Emilio Di Maria, Andrea Latini, Paola Borgiani, Giuseppe Novelli</text>
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                <text>Abstract The COVID-19 pandemic has strengthened the interest in the biological mechanisms underlying the complex interplay between infectious agents and the human host. The spectrum of phenotypes associated with the SARS-CoV-2 infection, ranging from the absence of symptoms to severe systemic complications, raised the question as to what extent the variable response to coronaviruses (CoVs) is influenced by the variability of the hosts’ genetic background. To explore the current knowledge about this question, we designed a systematic review encompassing the scientific literature published from Jan. 2003 to June 2020, to include studies on the contemporary outbreaks caused by SARS-CoV-1, MERS-CoV and SARS-CoV-2 (namely SARS, MERS and COVID-19 diseases). Studies were eligible if human genetic variants were tested as predictors of clinical phenotypes. An ad hoc protocol for the rapid review process was designed according to the PRISMA paradigm and registered at the PROSPERO database (ID: CRD42020180860). The systematic workflow provided 32 articles eligible for data abstraction (28 on SARS, 1 on MERS, 3 on COVID-19) reporting data on 26 discovery cohorts. Most studies considered the definite clinical diagnosis as the primary outcome, variably coupled with other outcomes (severity was the most frequently analysed). Ten studies analysed HLA haplotypes (1 in patients with COVID-19) and did not provide consistent signals of association with disease-associated phenotypes. Out of 22 eligible articles that investigated candidate genes (2 as associated with COVID-19), the top-ranked genes in the number of studies were ACE2, CLEC4M (L-SIGN), MBL, MxA (n = 3), ACE, CD209, FCER2, OAS-1, TLR4, TNF-α (n = 2). Only variants in MBL and MxA were found as possibly implicated in CoV-associated phenotypes in at least two studies. The number of studies for each predictor was insufficient to conduct meta-analyses. Studies collecting large cohorts from different ancestries are needed to further elucidate the role of host genetic variants in determining the response to CoVs infection. Rigorous design and robust statistical methods are warranted.</text>
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                <text>2020</text>
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            <description>The topic of the resource</description>
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                <text>coronavirus, covid-19, genetic susceptibility, Genetic association, human host, genomic biomarker</text>
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            <name>Identifier</name>
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                <text>10.1186/s40246-020-00280-6</text>
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                <text>Epidemiology and Health</text>
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            <name>Publisher</name>
            <description>An entity responsible for making the resource available</description>
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                <text>Korean Society of Epidemiology</text>
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                <text>Medicine, Genetics</text>
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                  <text>Dominio científico: Coronavirus</text>
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                <text>Genetic variation in the Staphylococcus aureus 8325 strain lineage revealed by whole-genome sequencing.</text>
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                <text>Kristoffer T. Bæk, Dorte Frees, Adriana Renzoni, Christine Barras, Natalia Rodríguez, Caroline Manzano, William L Kelley</text>
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                <text>Staphylococcus aureus strains of the 8325 lineage, especially 8325-4 and derivatives lacking prophage, have been used extensively for decades of research. We report herein the results of our deep sequence analysis of strain 8325-4. Assignment of sequence variants compared with the reference strain 8325 (NRS77/PS47) required correction of errors in the 8325 reference genome, and reassessment of variation previously attributed to chemical mutagenesis of the restriction-defective RN4220. Using an extensive strain pedigree analysis, we discovered that 8325-4 contains 16 single nucleotide polymorphisms (SNP) arising prior to the construction of RN4220. We identified 5 indels in 8325-4 compared with 8325. Three indels correspond to expected Φ11, 12, 13 excisions, one indel is explained by a sequence assembly artifact, and the final indel (Δ63bp) in the spa-sarS intergenic region is common to only a sub-lineage of 8325-4 strains including SH1000. This deletion was found to significantly decrease (75%) steady state sarS but not spa transcript levels in post-exponential phase. The sub-lineage 8325-4 was also found to harbor 4 additional SNPs. We also found large sequence variation between 8325, 8325-4 and RN4220 in a cluster of repetitive hypothetical proteins (SA0282 homologs) near the Ess secretion cluster. The overall 8325-4 SNP set results in 17 alterations within coding sequences. Remarkably, we discovered that all tested strains of the 8325-4 lineage lack phenol soluble modulin α3 (PSMα3), a virulence determinant implicated in neutrophil chemotaxis, biofilm architecture and surface spreading. Collectively, our results clarify and define the 8325-4 pedigree and reveal clear evidence that mutations existing throughout all branches of this lineage, including the widely used RN6390 and SH1000 strains, could conceivably impact virulence regulation.</text>
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                <text>Genetic Variation of SARS Coronavirus in Beijing Hospital</text>
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                <text>Dong-ping XU, Zheng Zhang, Fuliang Chu, Yonggang Li, Lei JIN, Lingxia Zhang, George F. Gao, Fu-sheng WANG</text>
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                <text>To characterize genetic variation of severe acute respiratory syndrome–associated coronavirus (SARS-CoV) transmitted in the Beijing area during the epidemic outbreak of 2003, we sequenced 29 full-length S genes of SARS-CoV from 20 hospitalized SARS patients on our unit, the Beijing 302 Hospital. Viral RNA templates for the S-gene amplification were directly extracted from raw clinical samples, including plasma, throat swab, sputum, and stool, during the course of the epidemic in the Beijing area. We used a TA-cloning assay with direct analysis of nested reverse transcription–polymerase chain reaction products in sequence. One hundred thirteen sequence variations with nine recurrent variant sites were identified in analyzed S-gene sequences compared with the BJ01 strain of SARS-CoV. Among them, eight variant sites were, we think, the first documented. Our findings demonstrate the coexistence of S-gene sequences with and without substitutions (referred to BJ01) in samples analyzed from some patients.</text>
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                <text>DOI: 10.3201/eid1005.030875</text>
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                <text>Emerging Infectious Diseases</text>
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                <text>Centers for Disease Control and Prevention</text>
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                <text>Infectious and parasitic diseases, Medicine</text>
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                <text>Genetic variation of the human α-2-Heremans-Schmid glycoprotein (AHSG) gene associated with the risk of SARS-CoV infection.</text>
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                <text>Xiaohui Zhu, Yan Wang, Hongxing Zhang, Xuan Liu, Ting Chen, Ruifu Yang, Yu-ling SHI, Wu-Chun Cao, Ping Li, Qingjun Ma, Yun Zhai, Fu-chu HE, Gang-qiao ZHOU, Cheng Cao</text>
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                <text>Genetic background may play an important role in the process of SARS-CoV infection and SARS development. We found several proteins that could interact with the nucleocapsid protein of the SARS coronavirus (SARS-CoV). α-2-Heremans-Schmid Glycoprotein (AHSG), which is required for macrophage deactivation by endogenous cations, is associated with inflammatory regulation. Cytochrome P450 Family 3A (CYP4F3A) is an ω-oxidase that inactivates Leukotriene B4 (LTB4) in human neutrophils and the liver. We investigated the association between the polymorphisms of these two inflammation-associated genes and SARS development. The linkage disequilibrium (LD) maps of these two genes were built with Haploview using data on CHB+JPT (version 2) from the HapMap. A total of ten tag SNPs were selected and genotyped. In the Guangzhou cohort study, after adjusting for age and sex, two AHSG SNPs and one CYP4F3 SNP were found to be associated with SARS susceptibility: rs2248690 (adjusted odds ratio [AOR] 2.42; 95% confidence interval [CI] 1.30-4.51); rs4917 (AOR 1.84; 95% CI 1.02-3.34); and rs3794987 (AOR 2.01; 95% CI 1.10-3.68). To further validate the association, the ten tag SNPs were genotyped in the Beijing cohort. After adjusting for age and sex, only rs2248690 (AOR, 1.63; 95% CI, 1.30-2.04) was found to be associated with SARS susceptibility. The combined analysis of the two studies confirmed tag SNP rs2248690 in AHSG as a susceptibility variant (AOR 1.70; 95% CI 1.37-2.09). The statistical analysis of the rs2248690 genotype data among the patients and healthy controls in the HCW cohort, who were all similarly exposed to the SARS virus, also supported the findings. Further, the SNP rs2248690 affected the transcriptional activity of the AHSG promoter and thus regulated the AHSG serum level. Therefore, our study has demonstrated that the AA genotype of rs2268690, which leads to a higher AHSG serum concentration, was significantly associated with protection against SARS development.</text>
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                <text>DOI: 10.1371/journal.pone.0023730</text>
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                <text>Xiaohui Zhu, Yan Wang, Hongxing Zhang, Xuan Liu, Ting Chen, Ruifu Yang, Yuling Shi, Wuchun Cao, Ping Li, Qingjun Ma, Yun Zhai, Fuchu He, Gangqiao Zhou, Cheng Cao</text>
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                <text>Genetic background may play an important role in the process of SARS-CoV infection and SARS development. We found several proteins that could interact with the nucleocapsid protein of the SARS coronavirus (SARS-CoV). α-2-Heremans-Schmid Glycoprotein (AHSG), which is required for macrophage deactivation by endogenous cations, is associated with inflammatory regulation. Cytochrome P450 Family 3A (CYP4F3A) is an ω-oxidase that inactivates Leukotriene B4 (LTB4) in human neutrophils and the liver. We investigated the association between the polymorphisms of these two inflammation-associated genes and SARS development. The linkage disequilibrium (LD) maps of these two genes were built with Haploview using data on CHB+JPT (version 2) from the HapMap. A total of ten tag SNPs were selected and genotyped. In the Guangzhou cohort study, after adjusting for age and sex, two AHSG SNPs and one CYP4F3 SNP were found to be associated with SARS susceptibility: rs2248690 (adjusted odds ratio [AOR] 2.42; 95% confidence interval [CI] 1.30-4.51); rs4917 (AOR 1.84; 95% CI 1.02-3.34); and rs3794987 (AOR 2.01; 95% CI 1.10-3.68). To further validate the association, the ten tag SNPs were genotyped in the Beijing cohort. After adjusting for age and sex, only rs2248690 (AOR, 1.63; 95% CI, 1.30-2.04) was found to be associated with SARS susceptibility. The combined analysis of the two studies confirmed tag SNP rs2248690 in AHSG as a susceptibility variant (AOR 1.70; 95% CI 1.37-2.09). The statistical analysis of the rs2248690 genotype data among the patients and healthy controls in the HCW cohort, who were all similarly exposed to the SARS virus, also supported the findings. Further, the SNP rs2248690 affected the transcriptional activity of the AHSG promoter and thus regulated the AHSG serum level. Therefore, our study has demonstrated that the AA genotype of rs2268690, which leads to a higher AHSG serum concentration, was significantly associated with protection against SARS development.</text>
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                <text>Infectious bronchitis virus (IBV) causes a costly respiratory viral disease of chickens. The role of wild birds in the epidemiology of IBV is poorly understood. We detected diverse coronaviruses by PCR in wildfowl and wading birds in England. Sequence analysis showed some viruses to be related to IBV.</text>
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                <text>2009</text>
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          <element elementId="49">
            <name>Subject</name>
            <description>The topic of the resource</description>
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                <text>coronavirus, Infectious Bronchitis, IBV, wild birds, Viruses, Zoonoses</text>
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            <name>Identifier</name>
            <description>An unambiguous reference to the resource within a given context</description>
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              <elementText elementTextId="7129">
                <text>DOI: 10.3201/eid1507.090067</text>
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            </elementTextContainer>
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          <element elementId="48">
            <name>Source</name>
            <description>A related resource from which the described resource is derived</description>
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              <elementText elementTextId="7130">
                <text>Emerging Infectious Diseases</text>
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            <name>Publisher</name>
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                <text>Centers for Disease Control and Prevention</text>
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            <description>The spatial or temporal topic of the resource, the spatial applicability of the resource, or the jurisdiction under which the resource is relevant</description>
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                <text>Infectious and parasitic diseases, Medicine</text>
              </elementText>
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            <description>A language of the resource</description>
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                <text>EN</text>
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        <src>https://www.socictopen.socict.org/files/original/c857f4916d94846ed4afc2d025784320.pdf</src>
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            <element elementId="50">
              <name>Title</name>
              <description>A name given to the resource</description>
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                  <text>Coronavirus</text>
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              <name>Description</name>
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                  <text>Dominio científico: Coronavirus</text>
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                <text>Genetics and Pathogenesis of Feline Infectious Peritonitis Virus</text>
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            <name>Creator</name>
            <description>An entity primarily responsible for making the resource</description>
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                <text>Meredith A. Brown, Jennifer L. Troyer, Jill Pecon-Slattery, Melody E. Roelke, Stephen J. O’Brien</text>
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                <text>Feline coronavirus (FCoV) is endemic in feral cat populations and cat colonies, frequently preceding outbreaks of fatal feline infectious peritonitis (FIP). FCoV exhibits 2 biotypes: the pathogenic disease and a benign infection with feline enteric coronavirus (FECV). Uncertainty remains regarding whether genetically distinctive avirulent and virulent forms coexist or whether an avirulent form mutates in vivo, causing FIP. To resolve these alternative hypotheses, we isolated viral sequences from FCoV-infected clinically healthy and sick cats (8 FIP cases and 48 FECV-asymptomatic animals); 735 sequences from 4 gene segments were generated and subjected to phylogenetic analyses. Viral sequences from healthy cats were distinct from sick cats on the basis of genetic distances observed in the membrane and nonstructural protein 7b genes. These data demonstrate distinctive circulating virulent and avirulent strains in natural populations. In addition, 5 membrane protein amino acid residues with functional potential differentiated healthy cats from cats with FIP. These findings may have potential as diagnostic markers for virulent FIP-associated FCoV.</text>
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            <name>Date</name>
            <description>A point or period of time associated with an event in the lifecycle of the resource</description>
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                <text>2009</text>
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          <element elementId="49">
            <name>Subject</name>
            <description>The topic of the resource</description>
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                <text>coronavirus, infectious peritonitis, feline, Virulence, Genetic, Marker</text>
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            <name>Identifier</name>
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                <text>DOI: 10.3201/eid1509.081573</text>
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            <name>Source</name>
            <description>A related resource from which the described resource is derived</description>
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              <elementText elementTextId="9014">
                <text>Emerging Infectious Diseases</text>
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            <name>Publisher</name>
            <description>An entity responsible for making the resource available</description>
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              <elementText elementTextId="9015">
                <text>Centers for Disease Control and Prevention</text>
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            <name>Coverage</name>
            <description>The spatial or temporal topic of the resource, the spatial applicability of the resource, or the jurisdiction under which the resource is relevant</description>
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                <text>Infectious and parasitic diseases, Medicine</text>
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            <name>Language</name>
            <description>A language of the resource</description>
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                <text>EN</text>
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