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      Pathophysiology of acute respiratory syndrome coronavirus 2 infection: a systematic literature review to inform EULAR points to consider

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          Abstract

          Background

          The SARS-CoV-2 pandemic is a global health problem. Beside the specific pathogenic effect of SARS-CoV-2, incompletely understood deleterious and aberrant host immune responses play critical roles in severe disease. Our objective was to summarise the available information on the pathophysiology of COVID-19.

          Methods

          Two reviewers independently identified eligible studies according to the following PICO framework: P (population): patients with SARS-CoV-2 infection; I (intervention): any intervention/no intervention; C (comparator): any comparator; O (outcome) any clinical or serological outcome including but not limited to immune cell phenotype and function and serum cytokine concentration.

          Results

          Of the 55 496 records yielded, 84 articles were eligible for inclusion according to question-specific research criteria. Proinflammatory cytokine expression, including interleukin-6 (IL-6), was increased, especially in severe COVID-19, although not as high as other states with severe systemic inflammation. The myeloid and lymphoid compartments were differentially affected by SARS-CoV-2 infection depending on disease phenotype. Failure to maintain high interferon (IFN) levels was characteristic of severe forms of COVID-19 and could be related to loss-of-function mutations in the IFN pathway and/or the presence of anti-IFN antibodies. Antibody response to SARS-CoV-2 infection showed a high variability across individuals and disease spectrum. Multiparametric algorithms showed variable diagnostic performances in predicting survival, hospitalisation, disease progression or severity, and mortality.

          Conclusions

          SARS-CoV-2 infection affects both humoral and cellular immunity depending on both disease severity and individual parameters. This systematic literature review informed the EULAR ‘points to consider’ on COVID-19 pathophysiology and immunomodulatory therapies.

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          Most cited references100

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          A new coronavirus associated with human respiratory disease in China

          Emerging infectious diseases, such as severe acute respiratory syndrome (SARS) and Zika virus disease, present a major threat to public health 1–3 . Despite intense research efforts, how, when and where new diseases appear are still a source of considerable uncertainty. A severe respiratory disease was recently reported in Wuhan, Hubei province, China. As of 25 January 2020, at least 1,975 cases had been reported since the first patient was hospitalized on 12 December 2019. Epidemiological investigations have suggested that the outbreak was associated with a seafood market in Wuhan. Here we study a single patient who was a worker at the market and who was admitted to the Central Hospital of Wuhan on 26 December 2019 while experiencing a severe respiratory syndrome that included fever, dizziness and a cough. Metagenomic RNA sequencing 4 of a sample of bronchoalveolar lavage fluid from the patient identified a new RNA virus strain from the family Coronaviridae, which is designated here ‘WH-Human 1’ coronavirus (and has also been referred to as ‘2019-nCoV’). Phylogenetic analysis of the complete viral genome (29,903 nucleotides) revealed that the virus was most closely related (89.1% nucleotide similarity) to a group of SARS-like coronaviruses (genus Betacoronavirus, subgenus Sarbecovirus) that had previously been found in bats in China 5 . This outbreak highlights the ongoing ability of viral spill-over from animals to cause severe disease in humans.
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            Pathophysiology, Transmission, Diagnosis, and Treatment of Coronavirus Disease 2019 (COVID-19): A Review

            The coronavirus disease 2019 (COVID-19) pandemic, due to the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has caused a worldwide sudden and substantial increase in hospitalizations for pneumonia with multiorgan disease. This review discusses current evidence regarding the pathophysiology, transmission, diagnosis, and management of COVID-19.
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              Impaired type I interferon activity and inflammatory responses in severe COVID-19 patients

              Coronavirus disease 2019 (COVID-19) is characterized by distinct patterns of disease progression suggesting diverse host immune responses. We performed an integrated immune analysis on a cohort of 50 COVID-19 patients with various disease severity. A unique phenotype was observed in severe and critical patients, consisting of a highly impaired interferon (IFN) type I response (characterized by no IFN-β and low IFN-α production and activity), associated with a persistent blood viral load and an exacerbated inflammatory response. Inflammation was partially driven by the transcriptional factor NF-κB and characterized by increased tumor necrosis factor (TNF)-α and interleukin (IL)-6 production and signaling. These data suggest that type-I IFN deficiency in the blood could be a hallmark of severe COVID-19 and provide a rationale for combined therapeutic approaches.
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                Author and article information

                Journal
                RMD Open
                RMD Open
                rmdopen
                rmdopen
                RMD Open
                BMJ Publishing Group (BMA House, Tavistock Square, London, WC1H 9JR )
                2056-5933
                2021
                11 February 2021
                11 February 2021
                : 7
                : 1
                Affiliations
                [1 ]Institute of Infection, Immunity and Inflammation, College of Medical Veterinary and Life Sciences, University of Glasgow , Glasgow, UK
                [2 ]departmentDepartment of Medicine , Rheumatology Unit, University of Perugia , Perugia, Italy
                [3 ]INSERM U1184, Center for Immunology of Viral Infections and Autoimmune Diseases, Paris-Sud University, Paris-Saclay University , Le Kremlin-Bicêtre, France
                [4 ]Department of Rheumatology, AP-HP, Paris-Sud University Hospitals, Le Kremlin Bicêtre Hospital , Le Kremlin-Bicêtre, France
                [5 ]University of Paris, Assistance Publique-Hôpitaux de Paris, Cochin Hospital , Paris, France
                [6 ]departmentINSERM U970 , PARCC , Paris, Île-de-France, France
                [7 ]departmentLeeds Institute of Rheumatic and Musculoskeletal Medicine , University of Leeds, NIHR Leeds Biomedical Research Centre , Leeds, West Yorkshire, UK
                [8 ]departmentLeeds Biomedical Research Centre , Leeds Teaching Hospitals NHS Trust , Leeds, West Yorkshire, UK
                [9 ]departmentMedical Education , Library & Evidence Research Centre, Leeds Teaching Hospitals NHS Trust , Leeds, UK
                [10 ]departmentChapel Allerton Hospital , Leeds Institute of Rheumatic and Musculoskeletal Medicine, University of Leeds, NIHR Leeds Biomedical Research Centre , Leeds, UK
                [11 ]departmentCentre for Rheumatology , National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre (BRC), University College London Hospitals (UCLH) NHS Foundation Trus , London, UK
                [12 ]departmentDepartment of Rheumatology , Northwick Park Hospital, London North West University Healthcare NHS Trust , London, UK
                [13 ]departmentCentre for Rheumatology & Department of Neuromuscular Diseases , University College London , London, UK
                Author notes
                [Correspondence to ] Dr Aurélie Najm; aurelie.najm@ 123456gmail.com
                Article
                rmdopen-2020-001549
                10.1136/rmdopen-2020-001549
                7880117
                33574116
                abb510ee-a98f-4cbc-8391-be9100e4e34d
                © Author(s) (or their employer(s)) 2021. Re-use permitted under CC BY-NC. No commercial re-use. See rights and permissions. Published by BMJ.

                This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See:  http://creativecommons.org/licenses/by-nc/4.0/.

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                Funding
                Funded by: Institute of Infection, Inflammation and Immunity. College of Medical Veterinary and Life Sciences. University of Glasgow;
                Funded by: European League Against Rheumatism (CLI122);
                Funded by: National Institute for Health Research (NIHR) University College London Hospitals (UCLH) Biomedical Research Centre (BRC);
                Categories
                Infections
                1506
                2474
                2430
                Original research
                Custom metadata
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                covid-19,cytokines,inflammation,polymorphism,genetic,t-lymphocyte subsets

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