1
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Autoantibodies in hospitalised patients with COVID‐19

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Objectives

          CD209L and its homologous protein CD209 act as alternative entry receptors for the SARS‐CoV‐2 virus and are highly expressed in the virally targeted tissues. We tested for the presence and clinical features of autoantibodies targeting these receptors and compared these with autoantibodies known to be associated with COVID‐19.

          Methods

          Using banked samples ( n = 118) from Johns Hopkins patients hospitalised with COVID‐19, we defined autoantibodies against CD209 and CD209L by enzyme‐linked immunosorbent assay (ELISA). Clinical associations of these antibodies were compared with those of patients with anti‐interferon (IFN) and anti‐angiotensin‐converting enzyme‐2 (ACE2) autoantibodies.

          Results

          Amongst patients hospitalised with COVID‐19, 19.5% (23/118) had IgM autoantibodies against CD209L and were more likely to have coronary artery disease (44% vs 19%, P = 0.03). Antibodies against CD209 were present in 5.9% (7/118); interestingly, all 7 were male ( P = 0.02). In our study, the presence of either antibody was positively associated with disease severity [OR 95% confidence interval (95% CI): 1.80 (0.69–5.03)], but the association did not reach statistical significance. In contrast, 10/118 (8.5%) had IgG autoantibodies against IFNα, and 21 (17.8%) had IgM antibodies against ACE2. These patients had significantly worse prognosis (intubation or death) and prolonged hospital stays. However, when adjusting for patient characteristics on admission, only the presence of anti‐ACE2 IgM remained significant [pooled common OR (95% CI), 4.14 (1.37, 12.54)].

          Conclusion

          We describe IgM autoantibodies against CD209 and CD209L amongst patients hospitalised with COVID‐19. These were not associated with disease severity. Conversely, patients with either anti‐ACE2 IgM or anti‐IFNα IgG antibodies had worse outcomes. Due to the small size of the study cohort, conclusions drawn should be considered cautiously.

          Abstract

          Amongst patients hospitalised with COVID‐19 infection, we describe IgM autoantibodies against CD209 and CD209L receptors, which are alternative entry receptors for the SARS‐CoV‐2 virus. When comparing these autoantibodies with others known to be associated with COVID‐19 infection, they were not associated with disease severity. Conversely, patients with either anti‐ACE2 IgM or anti‐IFNα IgG antibodies had worse outcomes.

          Related collections

          Most cited references54

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          A pneumonia outbreak associated with a new coronavirus of probable bat origin

          Since the outbreak of severe acute respiratory syndrome (SARS) 18 years ago, a large number of SARS-related coronaviruses (SARSr-CoVs) have been discovered in their natural reservoir host, bats 1–4 . Previous studies have shown that some bat SARSr-CoVs have the potential to infect humans 5–7 . Here we report the identification and characterization of a new coronavirus (2019-nCoV), which caused an epidemic of acute respiratory syndrome in humans in Wuhan, China. The epidemic, which started on 12 December 2019, had caused 2,794 laboratory-confirmed infections including 80 deaths by 26 January 2020. Full-length genome sequences were obtained from five patients at an early stage of the outbreak. The sequences are almost identical and share 79.6% sequence identity to SARS-CoV. Furthermore, we show that 2019-nCoV is 96% identical at the whole-genome level to a bat coronavirus. Pairwise protein sequence analysis of seven conserved non-structural proteins domains show that this virus belongs to the species of SARSr-CoV. In addition, 2019-nCoV virus isolated from the bronchoalveolar lavage fluid of a critically ill patient could be neutralized by sera from several patients. Notably, we confirmed that 2019-nCoV uses the same cell entry receptor—angiotensin converting enzyme II (ACE2)—as SARS-CoV.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: found

            Presenting Characteristics, Comorbidities, and Outcomes Among 5700 Patients Hospitalized With COVID-19 in the New York City Area

            There is limited information describing the presenting characteristics and outcomes of US patients requiring hospitalization for coronavirus disease 2019 (COVID-19).
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              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.
                Bookmark

                Author and article information

                Contributors
                arosen@jhmi.edu
                Journal
                Clin Transl Immunology
                Clin Transl Immunology
                10.1002/(ISSN)2050-0068
                CTI2
                Clinical & Translational Immunology
                John Wiley and Sons Inc. (Hoboken )
                2050-0068
                26 December 2024
                2024
                : 13
                : 12 ( doiID: 10.1002/cti2.v13.12 )
                : e70019
                Affiliations
                [ 1 ] Division of Rheumatology, Department of Medicine Johns Hopkins University School of Medicine Baltimore MD USA
                [ 2 ] Division of Infectious Diseases, Department of Medicine Johns Hopkins University School of Medicine Baltimore MD USA
                [ 3 ] Division of Pulmonary and Critical Care, Department of Medicine Johns Hopkins University School of Medicine Baltimore MD USA
                [ 4 ] Division of Allergy and Immunology, Department of Medicine Johns Hopkins University, School of Medicine Baltimore MD USA
                [ 5 ] Department of Biostatistics Bloomberg School of Public Health Baltimore MD USA
                Author notes
                [*] [* ] Correspondence

                Eleni Tiniakou and Antony Rosen, Division of Rheumatology, Department of Medicine, Johns Hopkins University School of Medicine, 5200 Eastern Avenue MFL Building, Center Tower, Suite 5200, Baltimore, MD 21224, USA.

                E‐mail: arosen@ 123456jhmi.edu

                Author information
                https://orcid.org/0000-0003-4749-870X
                Article
                CTI270019 CTI-24-OA-0091.R2
                10.1002/cti2.70019
                11671454
                534e89cb-8a8a-45a8-afd3-5cfb25729075
                © 2024 The Author(s). Clinical & Translational Immunology published by John Wiley & Sons Australia, Ltd on behalf of Australian and New Zealand Society for Immunology, Inc.

                This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

                History
                : 07 October 2024
                : 13 November 2024
                : 25 March 2024
                : 13 November 2024
                Page count
                Figures: 5, Tables: 1, Pages: 9, Words: 10315
                Funding
                Funded by: Bill and Melinda Gates Foundation , doi 10.13039/100000865;
                Funded by: Sherrilyn and Ken Fisher Center for Environmental Infectious Diseases Discovery Program
                Funded by: Donald B. and Dorothy L. Stabler Foundation , doi 10.13039/100029250;
                Funded by: National Institutes of Health , doi 10.13039/100000002;
                Award ID: K08 AI143391
                Award ID: R21HL145216
                Award ID: U5411090366
                Award ID: U54EB007958‐12
                Award ID: U54HL143541‐02S2
                Award ID: UM1AI068613
                Funded by: Jerome L. Greene Foundation , doi 10.13039/100015629;
                Funded by: Gates Philanthropy Partners
                Funded by: Henry M. Jackson Foundation , doi 10.13039/100003896;
                Award ID: 1007957
                Funded by: National Institute of Arthritis and Musculoskeletal and Skin Diseases , doi 10.13039/100000069;
                Award ID: K08 AR077732
                Award ID: P30‐AR070254
                Award ID: R01 AR073208
                Categories
                Original Article
                Original Article
                Custom metadata
                2.0
                2024
                Converter:WILEY_ML3GV2_TO_JATSPMC version:6.5.1 mode:remove_FC converted:27.12.2024

                anti‐ace2 igm,anti‐cd209 igm,anti‐cd209l igm,autoantibodies,covid‐19

                Comments

                Comment on this article