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      Complement as a target in COVID-19?

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          Abstract

          There is an urgent need to develop effective therapies for COVID-19. Here, we urge immunologists and clinicians to consider the potential of targeting the complement system in these patients.

          Abstract

          This Comment article from Lambris and colleagues considers the therapeutic potential of targeting the complement system in patients with COVID-19.

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          Coronavirus infections and immune responses

          Geng Li, Yaohua Fan, Yanni Lai … (2020)
          Abstract Coronaviruses (CoVs) are by far the largest group of known positive‐sense RNA viruses having an extensive range of natural hosts. In the past few decades, newly evolved Coronaviruses have posed a global threat to public health. The immune response is essential to control and eliminate CoV infections, however, maladjusted immune responses may result in immunopathology and impaired pulmonary gas exchange. Gaining a deeper understanding of the interaction between Coronaviruses and the innate immune systems of the hosts may shed light on the development and persistence of inflammation in the lungs and hopefully can reduce the risk of lung inflammation caused by CoVs. In this review, we provide an update on CoV infections and relevant diseases, particularly the host defense against CoV‐induced inflammation of lung tissue, as well as the role of the innate immune system in the pathogenesis and clinical treatment.
          Article 0 comments Cited 860 times – based on 0 reviews     Review now
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            Highly pathogenic coronavirus N protein aggravates lung injury by MASP-2-mediated complement over-activation

            Ting Gao, Mingdong Hu, Xiaopeng Zhang … (2020)
            An excessive immune response contributes to SARS-CoV, MERS-CoV and SARS-CoV-2 pathogenesis and lethality, but the mechanism remains unclear. In this study, the N proteins of SARS-CoV, MERS-CoV and SARS-CoV-2 were found to bind to MASP-2, the key serine protease in the lectin pathway of complement activation, resulting in aberrant complement activation and aggravated inflammatory lung injury. Either blocking the N protein:MASP-2 interaction or suppressing complement activation can significantly alleviate N protein-induced complement hyper-activation and lung injury in vitro and in vivo . Complement hyper-activation was also observed in COVID-19 patients, and a promising suppressive effect was observed when the deteriorating patients were treated with anti-C5a monoclonal antibody. Complement suppression may represent a common therapeutic approach for pneumonia induced by these highly pathogenic coronaviruses.
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              Generation of anaphylatoxin C3a in plasma and bronchoalveolar lavage fluid in trauma patients at risk for the adult respiratory distress syndrome.

              G Zilow, M Kirschfink, U. Rother … (1992)
              To determine the generation of anaphylatoxin C3a in plasma and bronchoalveolar lavage fluid in trauma patients at risk for the adult respiratory distress syndrome (ARDS).
              Article 0 comments Cited 23 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Fabio Ciceri: ciceri.fabio@hsr.it
                John D. Lambris:
                ORCID: http://orcid.org/0000-0002-9370-5776
                lambris@pennmedicine.upenn.edu
                Journal
                Journal ID (nlm-ta): Nat Rev Immunol
                Journal ID (iso-abbrev): Nat. Rev. Immunol
                Title: Nature Reviews. Immunology
                Publisher: Nature Publishing Group UK (London )
                ISSN (Print): 1474-1733
                ISSN (Electronic): 1474-1741
                Publication date (Electronic): 23 April 2020
                Pages: 1-2
                Affiliations
                [1 ]ISNI 0000 0001 0790 385X, GRID grid.4691.a, Department of Clinical Medicine and Surgery, , Federico II University of Naples, ; Naples, Italy
                [2 ]ISNI 0000 0004 0635 6999, GRID grid.6083.d, National Center for Scientific Research ‘Demokritos’, Aghia Paraskevi, ; Athens, Greece
                [3 ]GRID grid.410712.1, Institute of Experimental Trauma-Immunology, , University Hospital of Ulm, ; Ulm, Germany
                [4 ]Amyndas Pharmaceuticals, Glyfada, Greece
                [5 ]ISNI 0000 0004 1756 8807, GRID grid.417728.f, Humanitas Clinical and Research Center, ; Milan, Italy
                [6 ]GRID grid.452490.e, Humanitas University, ; Milan, Italy
                [7 ]GRID grid.15496.3f, IRCCS Ospedale San Raffaele, , University Vita-Salute San Raffaele, ; Milan, Italy
                [8 ]ISNI 0000 0004 1936 8972, GRID grid.25879.31, Department of Pathology and Laboratory Medicine, Perelman School of Medicine, , University of Pennsylvania, ; Philadelphia, PA USA
                Author information
                http://orcid.org/0000-0002-6634-3271
                http://orcid.org/0000-0002-9370-5776
                Article
                Publisher ID: 320
                DOI: 10.1038/s41577-020-0320-7
                PMC ID: 7187144
                PubMed ID: 32327719
                SO-VID: e43bd13a-159a-401e-8bc8-b934caf12dd2
                Copyright © © Springer Nature Limited 2020
                License:

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

                History
                Date accepted : 15 April 2020
                Categories
                Subject: Comment

                Keywords: sars-cov-2
                Data availability:
                Keywords: sars-cov-2

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