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                  <text>Coronavirus</text>
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                  <text>Dominio científico: Coronavirus</text>
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        <name>Dublin Core</name>
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                <text>Immune-Inflammatory Parameters in COVID-19 Cases: A Systematic Review and Meta-Analysis</text>
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                <text>Bo Chen, Qiang Sun, Jiaqi ZHU, Shuangshuang Li, Xudong Feng, Guo-Dong Cao, Mao-Ming Xiong</text>
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                <text>Background: The recent outbreak of coronavirus disease 2019 (COVID-19) has been rapidly spreading on a global scale and poses a great threat to human health. Acute respiratory distress syndrome, characterized by a rapid onset of generalized inflammation, is the leading cause of mortality in patients with COVID-19. We thus aimed to explore the effect of risk factors on the severity of the disease, focusing on immune-inflammatory parameters, which represent the immune status of patients.Methods: A comprehensive systematic search for relevant studies published up to April 2020 was performed by using the PubMed, Web of Science, EMBASE, and China National Knowledge Internet (CNKI) databases. After extracting all available data of immune-inflammatory indicators, we statistically analyzed the risk factors of severe and non-severe COVID-19 patients with a meta-analysis.Results: A total of 4,911 patients from 29 studies were included in the final meta-analysis. The results demonstrated that severe patients tend to present with increased white blood cell (WBC) and neutrophil counts, neutrophil-lymphocyte ratio (NLR), procalcitonin (PCT), C-reaction protein (CRP), erythrocyte sedimentation rate (ESR), and Interleukin-6 (IL-6) and a decreased number of total lymphocyte and lymphocyte subtypes, such as CD4+ T lymphocyte and CD8+ T lymphocyte, compared to the non-severe patients. In addition, the WBC count&amp;gt;10 × 109/L, lymphocyte count&amp;lt;1 × 109/L, PCT&amp;gt;0.5 ng/mL, and CRP&amp;gt;10 mg/L were risk factors for disease progression in patients with COVID-19 (WBC count&amp;gt;10 × 109/L: OR = 2.92, 95% CI: 1.96–4.35; lymphocyte count&amp;lt;1 × 109/L: OR = 4.97, 95% CI: 3.53–6.99; PCT&amp;gt;0.5 ng/mL: OR = 6.33, 95% CI: 3.97–10.10; CRP&amp;gt;10 mg/L: OR = 3.51, 95% CI: 2.38–5.16). Furthermore, we found that NLR, as a novel marker of systemic inflammatory response, can also help predict clinical severity in patients with COVID-19 (OR = 2.50, 95% CI: 2.04–3.06).Conclusions: Immune-inflammatory parameters, such as WBC, lymphocyte, PCT, CRP, and NLR, could imply the progression of COVID-19. NLR has taken both the levels of neutrophil and lymphocyte into account, indicating a more complete, accurate, and reliable inspection efficiency; surveillance of NLR may help clinicians identify high-risk COVID-19 patients at an early stage.</text>
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                <text>2020</text>
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                <text>Meta-analysis, risk factor, neutrophil/lymphocyte ratio, COVID-19, Immune-inflammatory parameters</text>
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                <text>DOI: 10.3389/fmed.2020.00301</text>
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                <text>Frontiers in Medicine</text>
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                <text>Frontiers Media S.A.</text>
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                <text>Medicine (General)</text>
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              <name>Title</name>
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                  <text>Coronavirus</text>
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              <name>Description</name>
              <description>An account of the resource</description>
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                  <text>Dominio científico: Coronavirus</text>
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        <name>Dublin Core</name>
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            <description>A name given to the resource</description>
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                <text>Immunization with SARS coronavirus vaccines leads to pulmonary immunopathology on challenge with the SARS virus.</text>
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            <description>An entity primarily responsible for making the resource</description>
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                <text>Chien-Te Tseng, Elena Sbrana, Naoko Iwata-Yoshikawa, Patrick C Newman, Tania Garron, Robert  L. Atmar, Clarence J. Peters, Robert B. Couch</text>
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            <description>An account of the resource</description>
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                <text>BACKGROUND:Severe acute respiratory syndrome (SARS) emerged in China in 2002 and spread to other countries before brought under control. Because of a concern for reemergence or a deliberate release of the SARS coronavirus, vaccine development was initiated. Evaluations of an inactivated whole virus vaccine in ferrets and nonhuman primates and a virus-like-particle vaccine in mice induced protection against infection but challenged animals exhibited an immunopathologic-type lung disease. DESIGN:Four candidate vaccines for humans with or without alum adjuvant were evaluated in a mouse model of SARS, a VLP vaccine, the vaccine given to ferrets and NHP, another whole virus vaccine and an rDNA-produced S protein. Balb/c or C57BL/6 mice were vaccinated i.m. on day 0 and 28 and sacrificed for serum antibody measurements or challenged with live virus on day 56. On day 58, challenged mice were sacrificed and lungs obtained for virus and histopathology. RESULTS:All vaccines induced serum neutralizing antibody with increasing dosages and/or alum significantly increasing responses. Significant reductions of SARS-CoV two days after challenge was seen for all vaccines and prior live SARS-CoV. All mice exhibited histopathologic changes in lungs two days after challenge including all animals vaccinated (Balb/C and C57BL/6) or given live virus, influenza vaccine, or PBS suggesting infection occurred in all. Histopathology seen in animals given one of the SARS-CoV vaccines was uniformly a Th2-type immunopathology with prominent eosinophil infiltration, confirmed with special eosinophil stains. The pathologic changes seen in all control groups lacked the eosinophil prominence. CONCLUSIONS:These SARS-CoV vaccines all induced antibody and protection against infection with SARS-CoV. However, challenge of mice given any of the vaccines led to occurrence of Th2-type immunopathology suggesting hypersensitivity to SARS-CoV components was induced. Caution in proceeding to application of a SARS-CoV vaccine in humans is indicated.</text>
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                <text>2012</text>
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                <text>DOI: 10.1371/journal.pone.0035421</text>
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                <text>PLoS ONE</text>
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                <text>Public Library of Science (PLoS)</text>
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                <text>Science, Medicine</text>
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            <description>A language of the resource</description>
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                <text>EN</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>Text</name>
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        <name>Dublin Core</name>
        <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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          <element elementId="50">
            <name>Title</name>
            <description>A name given to the resource</description>
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                <text>Immunofluorescence Assay for Serologic Diagnosis of SARS</text>
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            <name>Creator</name>
            <description>An entity primarily responsible for making the resource</description>
            <elementTextContainer>
              <elementText elementTextId="7313">
                <text>Paul K. S. Chan, King-Cheung Ng, Rickjason C. W. Chan, Rebecca K. Y. Lam, Viola C. Y. Chow, Mamie Hui, Alan Wu, Nelson Lee, Florence H.Y. Yap, Frankie W. T. Cheng, Joseph J. Y. Sung, John S. Tam</text>
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            <description>An account of the resource</description>
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                <text>We evaluated a virus-infected cell-based indirect immunofluorescence assay for detecting anti–severe acute respiratory syndrome-associated coronavirus (SARS-CoV) immunoglobulin (Ig) G antibody. All confirmed SARS cases demonstrated seroconversion or fourfold rise in IgG antibody titer; no control was positive. Sensitivity and specificity of this assay were both 100%. Immunofluorescence assay can ascertain the status of SARS-CoV infection.</text>
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            <description>A point or period of time associated with an event in the lifecycle of the resource</description>
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                <text>2004</text>
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            <name>Subject</name>
            <description>The topic of the resource</description>
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                <text>coronavirus, diagnosis, serology, Sensitivity, specificity, severe acute respiratory syndrome</text>
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            <description>An unambiguous reference to the resource within a given context</description>
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                <text>DOI: 10.3201/eid1003.030493</text>
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            <description>A related resource from which the described resource is derived</description>
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                <text>Emerging Infectious Diseases</text>
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            <description>An entity responsible for making the resource available</description>
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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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            <description>A language of the resource</description>
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                <text>EN</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>Immunogenicity of prime-boost protein subunit vaccine strategies against SARS-CoV-2 in mice and macaques</text>
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            <description>An entity primarily responsible for making the resource</description>
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                <text>Hyon-Xhi Tan, Jennifer A. Juno, Wen Shi Lee, Isaac Barber-Axthelm, Hannah G. Kelly, Kathleen M. Wragg, Robyn Esterbauer, Thakshila Amarasena, Francesca L. Mordant, Kanta Subbarao, Stephen J. Kent, Adam K. Wheatley</text>
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                <text>Current vaccine strategies for SARS-CoV-2 focus on eliciting neutralising antibodies to the spike protein (S), but differences in immunogenicity of full-length S versus receptor binding domain (RBD) only aren’t fully understood. Here, the authors show immunogenicity of different prime-boost strategies with S and/or RBD in mice and macaques.</text>
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                <text>2021</text>
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                <text>10.1038/s41467-021-21665-8</text>
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                <text>Epidemiology and Health</text>
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                <text>Korean Society of Epidemiology</text>
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                <text>Science</text>
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                <text>Immunoinformatics and Structural Analysis for Identification of Immunodominant Epitopes in SARS-CoV-2 as Potential Vaccine Targets</text>
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                <text>Sumit Mukherjee, Dmitry Tworowski, Rajesh Detroja, Sunanda  Biswas Mukherjee, Milana Frenkel-Morgenstern</text>
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                <text>A new coronavirus infection, COVID-19, has recently emerged, and has caused a global pandemic along with an international public health emergency. Currently, no licensed vaccines are available for COVID-19. The identification of immunodominant epitopes for both B- and T-cells that induce protective responses in the host is crucial for effective vaccine design. Computational prediction of potential epitopes might significantly reduce the time required to screen peptide libraries as part of emergent vaccine design. In our present study, we used an extensive immunoinformatics-based approach to predict conserved immunodominant epitopes from the proteome of SARS-CoV-2. Regions from SARS-CoV-2 protein sequences were defined as immunodominant, based on the following three criteria regarding B- and T-cell epitopes: (i) they were both mapped, (ii) they predicted protective antigens, and (iii) they were completely identical to experimentally validated epitopes of SARS-CoV. Further, structural and molecular docking analyses were performed in order to understand the binding interactions of the identified immunodominant epitopes with human major histocompatibility complexes (MHC). Our study provides a set of potential immunodominant epitopes that could enable the generation of both antibody- and cell-mediated immunity. This could contribute to developing peptide vaccine-based adaptive immunotherapy against SARS-CoV-2 infections and prevent future pandemic outbreaks.</text>
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                <text>HLA, covid-19, immunodominant epitope, SARS-CoV-2, vaccine target</text>
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                <text>10.3390/vaccines8020290</text>
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                <text>Korean Society of Epidemiology</text>
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                  <text>Dominio científico: Coronavirus</text>
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                <text>Immunologic Effects of Vitamin D on Human Health and Disease</text>
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                <text>Nipith Charoenngam, Michael  F. Holick</text>
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                <text>Vitamin D is responsible for regulation of calcium and phosphate metabolism and maintaining a healthy mineralized skeleton. It is also known as an immunomodulatory hormone. Experimental studies have shown that 1,25-dihydroxyvitamin D, the active form of vitamin D, exerts immunologic activities on multiple components of the innate and adaptive immune system as well as endothelial membrane stability. Association between low levels of serum 25-hydroxyvitamin D and increased risk of developing several immune-related diseases and disorders, including psoriasis, type 1 diabetes, multiple sclerosis, rheumatoid arthritis, tuberculosis, sepsis, respiratory infection, and COVID-19, has been observed. Accordingly, a number of clinical trials aiming to determine the efficacy of administration of vitamin D and its metabolites for treatment of these diseases have been conducted with variable outcomes. Interestingly, recent evidence suggests that some individuals might benefit from vitamin D more or less than others as high inter-individual difference in broad gene expression in human peripheral blood mononuclear cells in response to vitamin D supplementation has been observed. Although it is still debatable what level of serum 25-hydroxyvitamin D is optimal, it is advisable to increase vitamin D intake and have sensible sunlight exposure to maintain serum 25-hydroxyvitamin D at least 30 ng/mL (75 nmol/L), and preferably at 40–60 ng/mL (100–150 nmol/L) to achieve the optimal overall health benefits of vitamin D.</text>
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                <text>Immunomodulation, vitamin D, 25-hydroxyvitamin d, 1, immune function, 25- dihydroxyvitamin D, autoimmune disorders</text>
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                <text>10.3390/nu12072097</text>
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                <text>Biotemas</text>
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                <text>Universidade Federal de Santa Catarina</text>
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                <text>Nutrition. Foods and food supply</text>
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                  <text>Dominio científico: Coronavirus</text>
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                <text>Immunological Control of Viral Infections in Bats and the Emergence of Viruses Highly Pathogenic to Humans</text>
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                <text>Tony Schountz, Michelle L. Baker, John Butler, Vincent Munster</text>
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                <text>Bats are reservoir hosts of many important viruses that cause substantial disease in humans, including coronaviruses, filoviruses, lyssaviruses, and henipaviruses. Other than the lyssaviruses, they do not appear to cause disease in the reservoir bats, thus an explanation for the dichotomous outcomes of infections of humans and bat reservoirs remains to be determined. Bats appear to have a few unusual features that may account for these differences, including evidence of constitutive interferon (IFN) activation and greater combinatorial diversity in immunoglobulin genes that do not undergo substantial affinity maturation. We propose these features may, in part, account for why bats can host these viruses without disease and how they may contribute to the highly pathogenic nature of bat-borne viruses after spillover into humans. Because of the constitutive IFN activity, bat-borne viruses may be shed at low levels from bat cells. With large naive antibody repertoires, bats may control the limited virus replication without the need for rapid affinity maturation, and this may explain why bats typically have low antibody titers to viruses. However, because bat viruses have evolved in high IFN environments, they have enhanced countermeasures against the IFN response. Thus, upon infection of human cells, where the IFN response is not constitutive, the viruses overwhelm the IFN response, leading to abundant virus replication and pathology.</text>
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                <text>2017</text>
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                <text>bats, Chiroptera, zoonosis, antibody repertoire, emerging infectious disease, virus ecology</text>
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                <text>DOI: 10.3389/fimmu.2017.01098</text>
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                <text>Frontiers in Immunology</text>
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                <text>Frontiers Media S.A.</text>
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                <text>Immunologic diseases. Allergy</text>
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            <description>A language of the resource</description>
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                <text>Immunological Subpopulations Within Critically Ill COVID-19 Patients.</text>
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                <text>Julie Kay Wilson, Manu Shankar-Hari</text>
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                <text>10.1016/j.chest.2021.01.023</text>
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                <text>Chest</text>
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                <text>Immunology of Bats and Their Viruses:  Challenges and Opportunities</text>
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                <text>Bats are reservoir hosts of several high-impact viruses that cause significant human diseases, including Nipah virus, Marburg virus and rabies virus. They also harbor many other viruses that are thought to have caused disease in humans after spillover into intermediate hosts, including SARS and MERS coronaviruses. As is usual with reservoir hosts, these viruses apparently cause little or no pathology in bats. Despite the importance of bats as reservoir hosts of zoonotic and potentially zoonotic agents, virtually nothing is known about the host/virus relationships; principally because few colonies of bats are available for experimental infections, a lack of reagents, methods and expertise for studying bat antiviral responses and immunology, and the difficulty of conducting meaningful field work. These challenges can be addressed, in part, with new technologies that are  species-independent that can provide insight into the interactions of bats and viruses, which should clarify how the viruses persist in nature, and what risk factors might facilitate transmission to humans and livestock.</text>
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                <text>DOI: 10.3390/v6124880</text>
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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>
              <description>An account of the resource</description>
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                  <text>Dominio científico: Coronavirus</text>
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            <name>Title</name>
            <description>A name given to the resource</description>
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                <text>Immunomodulatory and Antiviral Activity of Metformin and Its Potential Implications in Treating Coronavirus Disease 2019 and Lung Injury</text>
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            <name>Creator</name>
            <description>An entity primarily responsible for making the resource</description>
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              <elementText elementTextId="83928">
                <text>Xianyang Chen, Huifang Guo, Li Qiu, Chengdong Zhang, Qiang Deng, Qibin Leng</text>
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            <name>Description</name>
            <description>An account of the resource</description>
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              <elementText elementTextId="83929">
                <text>The pandemic of coronavirus disease 2019 (COVID-19), a disease which causes severe lung injury and multiple organ damage, presents an urgent need for new drugs. The case severity and fatality of COVID-19 are associated with excessive inflammation, namely, a cytokine storm. Metformin, a widely used drug to treat type 2 diabetes (T2D) mellitus and metabolic syndrome, has immunomodulatory activity that reduces the production of proinflammatory cytokines using macrophages and causes the formation of neutrophil extracellular traps (NETs). Metformin also inhibits the cytokine production of pathogenic Th1 and Th17 cells. Importantly, treatment with metformin alleviates various lung injuries in preclinical animal models. In addition, a recent proteomic study revealed that metformin has the potential to directly inhibit SARS-CoV-2 infection. Furthermore, retrospective clinical studies have revealed that metformin treatment reduces the mortality of T2D with COVID-19. Therefore, metformin has the potential to be repurposed to treat patients with COVID-19 at risk of developing severe illness. This review summarizes the immune pathogenesis of SARS-CoV-2 and addresses the effects of metformin on inhibiting cytokine storms and preventing SARS-CoV-2 infection, as well as its side effects.</text>
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            <name>Date</name>
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                <text>2020</text>
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                <text>antiviral activity, SARS-CoV-2, Coronavirus disease 2019, cytokine storm, Metformin</text>
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            <name>Identifier</name>
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              <elementText elementTextId="83932">
                <text>10.3389/fimmu.2020.02056</text>
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            <name>Source</name>
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              <elementText elementTextId="83933">
                <text>Epidemiology and Health</text>
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          <element elementId="45">
            <name>Publisher</name>
            <description>An entity responsible for making the resource available</description>
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              <elementText elementTextId="83934">
                <text>Korean Society of Epidemiology</text>
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          </element>
          <element elementId="38">
            <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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              <elementText elementTextId="83935">
                <text>Immunologic diseases. Allergy</text>
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            </elementTextContainer>
          </element>
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  </item>
</itemContainer>
