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      SARS-Cov2 acute and post-active infection in the context of autoimmune and chronic inflammatory diseases

      research-article
      a , b , c , b , a , a , d , a , a , a , d , e , a , d , a , f , , a , b
      Journal of Translational Autoimmunity
      Elsevier
      SARS-Cov2, Infection, Rheumatoid arthritis, Systemic lupus erythematosus, Risk factors, Inflammation, ACE2, angiotensin converting enzyme 2, ACPA, anti-cyclic citrullinated peptide autoAb, ANA, antinuclear autoAb, aPL, antiphospholipid, AutoAb, autoantibodies, BAFF/BlySS, B-cell-activating factor/B lymphocyte stimulator, CCL, chemokine ligand, COVID-19, coronavirus disease 2019, DMARDs, disease-modifying anti-rheumatic drugs, E, envelope, HEp-2, human epithelioma cell line 2, IFN-I, interferon type I, IFNAR, IFN-alpha receptors, Ig, immunoglobulin, IL, interleukin, IRF, interferon regulatory factor, ISGs, IFN-stimulated genes, ITP, immune-thrombocytopenic purpura, Jak, Janus kinase, LDH, lactate dehydrogenase, M, membrane, mAb, monoclonal Ab, MDA-5, melanoma differentiation-associated protein, MERS-Cov, Middle East respiratory syndrome coronavirus, MIS-C, multisystem inflammatory syndrome in children, N, nucleocapsid, NET, nuclear extracellular traps, NF-κB, nuclear factor-kappa B, NK, natural killer, NLRP3, NOD-like receptor family, pyrin domain containing 3, ORF, open reading frame, PACS, post-active COVID-19 syndrome, PAD-4, peptidylarginine deiminase 4, PAMPs, pathogen-associated molecular patterns, pDC, plasmacytoid dendritic cells, PMN, polymorphonuclear leukocytes, PRRs, pattern recognition receptors, RA, rheumatoid arthritis, RBD, receptor binding domain, RF, rheumatoid factor, RIG-I, retinoic acid-inducible gene I, ROS, reactive oxygen species, rt-PCR, reverse transcription polymerase chain reaction, S, spike, SAD, systemic autoimmune disease, SARS-Cov2, severe acute respiratory coronavirus 2, SjS, primary Sjögren's syndrome, SLE, systemic lupus erythematosus, SSc, systemic sclerosis, ssRNA, single-stranded ribonucleic acid, STAT, signal transducer and activator of transcription, TCR, T cell receptor, TLR, Toll-like receptor, TMPRSS2, transmembrane serine protease 2, TNF, tumor necrosis factor, Treg, regulatory T cells, VDJ, variable, diversity and joining Ig genes

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          Abstract

          The clinical and immunological spectrum of acute and post-active COVID-19 syndrome overlaps with criteria used to characterize autoimmune diseases such as rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). Indeed, following SARS-Cov2 infection, the innate immune response is altered with an initial delayed production of interferon type I (IFN–I), while the NF-kappa B and inflammasome pathways are activated. In lung and digestive tissues, an alternative and extrafollicular immune response against SARS-Cov2 takes place with, consequently, an altered humoral and memory T cell response leading to breakdown of tolerance with the emergence of autoantibodies. However, the risk of developing severe COVID-19 among SLE and RA patients did not exceed the general population except in those having pre-existing neutralizing autoantibodies against IFN-I. Treatment discontinuation rather than COVID-19 infection or vaccination increases the risk of developing flares. Last but not least, a limited number of case reports of individuals having developed SLE or RA following COVID-19 infection/vaccination have been reported. Altogether, the SARS-Cov2 pandemic represents an unique opportunity to investigate the dangerous interplay between the immune response against infectious agents and autoimmunity, and to better understand the triggering role of infection as a risk factor in autoimmune and chronic inflammatory disease development.

          Highlights

          • SARS-Cov2 leads to a dysregulated immune response that mimics systemic autoimmune diseases.

          • Sera from acute and post-active COVID-19 syndrome may contain SLE and RA associated autoantibodies.

          • COVID-19 infection and vaccination impact on SLE and RA (incidence, flare) is limited.

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          Most cited references142

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          Clinical and immunologic features in severe and moderate Coronavirus Disease 2019

          Journal of Clinical Investigation
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            Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis

            Abstract Severe acute respiratory syndrome (SARS) is an acute infectious disease that spreads mainly via the respiratory route. A distinct coronavirus (SARS‐CoV) has been identified as the aetiological agent of SARS. Recently, a metallopeptidase named angiotensin‐converting enzyme 2 (ACE2) has been identified as the functional receptor for SARS‐CoV. Although ACE2 mRNA is known to be present in virtually all organs, its protein expression is largely unknown. Since identifying the possible route of infection has major implications for understanding the pathogenesis and future treatment strategies for SARS, the present study investigated the localization of ACE2 protein in various human organs (oral and nasal mucosa, nasopharynx, lung, stomach, small intestine, colon, skin, lymph nodes, thymus, bone marrow, spleen, liver, kidney, and brain). The most remarkable finding was the surface expression of ACE2 protein on lung alveolar epithelial cells and enterocytes of the small intestine. Furthermore, ACE2 was present in arterial and venous endothelial cells and arterial smooth muscle cells in all organs studied. In conclusion, ACE2 is abundantly present in humans in the epithelia of the lung and small intestine, which might provide possible routes of entry for the SARS‐CoV. This epithelial expression, together with the presence of ACE2 in vascular endothelium, also provides a first step in understanding the pathogenesis of the main SARS disease manifestations. Copyright © 2004 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.
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              Post-acute COVID-19 syndrome

              Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the pathogen responsible for the coronavirus disease 2019 (COVID-19) pandemic, which has resulted in global healthcare crises and strained health resources. As the population of patients recovering from COVID-19 grows, it is paramount to establish an understanding of the healthcare issues surrounding them. COVID-19 is now recognized as a multi-organ disease with a broad spectrum of manifestations. Similarly to post-acute viral syndromes described in survivors of other virulent coronavirus epidemics, there are increasing reports of persistent and prolonged effects after acute COVID-19. Patient advocacy groups, many members of which identify themselves as long haulers, have helped contribute to the recognition of post-acute COVID-19, a syndrome characterized by persistent symptoms and/or delayed or long-term complications beyond 4 weeks from the onset of symptoms. Here, we provide a comprehensive review of the current literature on post-acute COVID-19, its pathophysiology and its organ-specific sequelae. Finally, we discuss relevant considerations for the multidisciplinary care of COVID-19 survivors and propose a framework for the identification of those at high risk for post-acute COVID-19 and their coordinated management through dedicated COVID-19 clinics.
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                Author and article information

                Contributors
                Journal
                J Transl Autoimmun
                J Transl Autoimmun
                Journal of Translational Autoimmunity
                Elsevier
                2589-9090
                12 April 2022
                2022
                12 April 2022
                : 5
                : 100154
                Affiliations
                [a ]Central Research Laboratory, Kazan State Medical Academy, Kazan, Russia
                [b ]Institute of Fundamental Medicine and Biology, Kazan (Volga Region) Federal University, Kazan, Russia
                [c ]Institute of Fundamental Medicine, Kazan (Volga Region) Federal University, Kazan, Russia
                [d ]Institute of Environmental Sciences, Kazan (Volga Region) Federal University, Kazan, Russia
                [e ]Kazan State Academy of Veterinary Medicine Named After N.E. Bauman, Kazan, Russia
                [f ]Laboratory of Immunology, CHU Purpan Toulouse, INSERM U1291, CNRS U5051, University Toulouse III, Toulouse, France
                Author notes
                []Corresponding author. Institut Fédératif de Biologie, Laboratoire d'immunologie, CHU Purpan, 330 avenue de Grande Bretagne, 31000, Toulouse, France. renaudineau.y@ 123456chu-toulouse.fr
                Article
                S2589-9090(22)00015-6 100154
                10.1016/j.jtauto.2022.100154
                9005220
                35434592
                e251f4b5-ee75-4dc2-9541-6bb937cad931
                © 2022 The Authors

                This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

                History
                : 19 February 2022
                : 31 March 2022
                Categories
                VSI: Autoimmune disorder

                sars-cov2,infection,rheumatoid arthritis,systemic lupus erythematosus,risk factors,inflammation,ace2, angiotensin converting enzyme 2,acpa, anti-cyclic citrullinated peptide autoab,ana, antinuclear autoab,apl, antiphospholipid,autoab, autoantibodies,baff/blyss, b-cell-activating factor/b lymphocyte stimulator,ccl, chemokine ligand,covid-19, coronavirus disease 2019,dmards, disease-modifying anti-rheumatic drugs,e, envelope,hep-2, human epithelioma cell line 2,ifn-i, interferon type i,ifnar, ifn-alpha receptors,ig, immunoglobulin,il, interleukin,irf, interferon regulatory factor,isgs, ifn-stimulated genes,itp, immune-thrombocytopenic purpura,jak, janus kinase,ldh, lactate dehydrogenase,m, membrane,mab, monoclonal ab,mda-5, melanoma differentiation-associated protein,mers-cov, middle east respiratory syndrome coronavirus,mis-c, multisystem inflammatory syndrome in children,n, nucleocapsid,net, nuclear extracellular traps,nf-κb, nuclear factor-kappa b,nk, natural killer,nlrp3, nod-like receptor family,pyrin domain containing 3, orf,open reading frame, pacs,post-active covid-19 syndrome, pad-4,peptidylarginine deiminase 4, pamps,pathogen-associated molecular patterns, pdc,plasmacytoid dendritic cells, pmn,polymorphonuclear leukocytes, prrs,pattern recognition receptors, ra,rheumatoid arthritis, rbd,receptor binding domain, rf,rheumatoid factor, rig-i,retinoic acid-inducible gene i, ros,reactive oxygen species, rt-pcr,reverse transcription polymerase chain reaction, s,spike, sad,systemic autoimmune disease, sars-cov2,severe acute respiratory coronavirus 2, sjs,primary sjögren's syndrome, sle,systemic lupus erythematosus, ssc,systemic sclerosis, ssrna,single-stranded ribonucleic acid, stat,signal transducer and activator of transcription, tcr,t cell receptor, tlr,toll-like receptor, tmprss2,transmembrane serine protease 2, tnf,tumor necrosis factor, treg,regulatory t cells, vdj,variable, diversity and joining ig genes
                sars-cov2, infection, rheumatoid arthritis, systemic lupus erythematosus, risk factors, inflammation, ace2, angiotensin converting enzyme 2, acpa, anti-cyclic citrullinated peptide autoab, ana, antinuclear autoab, apl, antiphospholipid, autoab, autoantibodies, baff/blyss, b-cell-activating factor/b lymphocyte stimulator, ccl, chemokine ligand, covid-19, coronavirus disease 2019, dmards, disease-modifying anti-rheumatic drugs, e, envelope, hep-2, human epithelioma cell line 2, ifn-i, interferon type i, ifnar, ifn-alpha receptors, ig, immunoglobulin, il, interleukin, irf, interferon regulatory factor, isgs, ifn-stimulated genes, itp, immune-thrombocytopenic purpura, jak, janus kinase, ldh, lactate dehydrogenase, m, membrane, mab, monoclonal ab, mda-5, melanoma differentiation-associated protein, mers-cov, middle east respiratory syndrome coronavirus, mis-c, multisystem inflammatory syndrome in children, n, nucleocapsid, net, nuclear extracellular traps, nf-κb, nuclear factor-kappa b, nk, natural killer, nlrp3, nod-like receptor family, pyrin domain containing 3, orf, open reading frame, pacs, post-active covid-19 syndrome, pad-4, peptidylarginine deiminase 4, pamps, pathogen-associated molecular patterns, pdc, plasmacytoid dendritic cells, pmn, polymorphonuclear leukocytes, prrs, pattern recognition receptors, ra, rheumatoid arthritis, rbd, receptor binding domain, rf, rheumatoid factor, rig-i, retinoic acid-inducible gene i, ros, reactive oxygen species, rt-pcr, reverse transcription polymerase chain reaction, s, spike, sad, systemic autoimmune disease, sars-cov2, severe acute respiratory coronavirus 2, sjs, primary sjögren's syndrome, sle, systemic lupus erythematosus, ssc, systemic sclerosis, ssrna, single-stranded ribonucleic acid, stat, signal transducer and activator of transcription, tcr, t cell receptor, tlr, toll-like receptor, tmprss2, transmembrane serine protease 2, tnf, tumor necrosis factor, treg, regulatory t cells, vdj, variable, diversity and joining ig genes

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