Severe COVID-19 is associated with elevated serum IgA and antiphospholipid IgA-antibodies.
- Hasan Ali O Department of Medical Genetics, Life Sciences Institute, University of British Columbia, Vancouver, Canada.
- Bomze D Institute of Immunobiology, Kantonsspital St. Gallen, St. Gallen, Switzerland.
- Risch L Labormedizinisches Zentrum Dr. Risch, Vaduz, Liechtenstein.
- Brugger SD Department of Infectious Diseases and Hospital Hygiene, University Hospital Zurich, Zurich, Switzerland.
- Paprotny M Department of General Internal Medicine, Landesspital Liechtenstein, Vaduz, Liechtenstein.
- Weber M Department of General Internal Medicine, Landesspital Liechtenstein, Vaduz, Liechtenstein.
- Thiel S Department of General Internal Medicine, Landesspital Liechtenstein, Vaduz, Liechtenstein.
- Kern L Department of Pulmonology, Kantonsspital St. Gallen, St. Gallen, Switzerland.
- Albrich WC Division of Infectious Diseases and Hospital Epidemiology, Kantonsspital St. Gallen, St. Gallen, Switzerland.
- Kohler P Division of Infectious Diseases and Hospital Epidemiology, Kantonsspital St. Gallen, St. Gallen, Switzerland.
- Kahlert CR Division of Infectious Diseases and Hospital Epidemiology, Kantonsspital St. Gallen, St. Gallen, Switzerland.
- Vernazza P Division of Infectious Diseases and Hospital Epidemiology, Kantonsspital St. Gallen, St. Gallen, Switzerland.
- Bühler PK Institute of Intensive Care Medicine, University Hospital Zurich, Zurich, Switzerland.
- Schüpbach RA Institute of Intensive Care Medicine, University Hospital Zurich, Zurich, Switzerland.
- Gómez-Mejia A Department of Infectious Diseases and Hospital Hygiene, University Hospital Zurich, Zurich, Switzerland.
- Popa AM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
- Bergthaler A Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria.
- Penninger JM Department of Medical Genetics, Life Sciences Institute, University of British Columbia, Vancouver, Canada.
- Flatz L Department of Dermatology, University Hospital Zurich, Zurich, Switzerland.
- 2020-09-30
Published in:
- Clinical infectious diseases : an official publication of the Infectious Diseases Society of America. - 2020
English
BACKGROUND
Severe coronavirus disease 2019 (COVID-19) frequently entails complications that bear similarities to autoimmune diseases. To date, there is little data on possible IgA-mediated autoimmune responses. Here, we aim to determine whether COVID-19 is associated with a vigorous total IgA response and if IgA antibodies are associated with complications of severe illness. Since thrombotic events are frequent in severe COVID-19 and resemble hypercoagulation of antiphospholipid syndrome (APS), our approach focused on antiphospholipid antibodies (aPL).
METHODS
In this retrospective cohort study clinical data and aPL from 64 patients with COVID-19 were compared from three independent tertiary hospitals (one in Liechtenstein, two in Switzerland). Samples were collected from April 9 th to May 1 st, 2020.
RESULTS
Clinical records of 64 patients with COVID-19 were reviewed and divided into a cohort with mild illness (mCOVID) (41%), a discovery cohort with severe illness (sdCOVID) (22%) and a confirmation cohort with severe illness (scCOVID) (38%). Total IgA, IgG and aPL were measured with clinical diagnostic kits. Severe illness was significantly associated with increased total IgA (sdCOVID, P=0.01; scCOVID, p-value<0.001), but not total IgG. Among aPL, both cohorts with severe illness significantly correlated with elevated anti-Cardiolipin IgA (sdCOVID and scCOVID, p-value<0.001), anti-Cardiolipin IgM (sdCOVID, P=0.003; scCOVID, P<0.001), and anti-Beta2 Glycoprotein-1 IgA (sdCOVID and scCOVID, P<0.001). Systemic lupus erythematosus was excluded from all patients as a potential confounder.
CONCLUSIONS
Higher total IgA and IgA-aPL were consistently associated with severe illness. These novel data strongly suggest that a vigorous antiviral IgA-response, possibly triggered in the bronchial mucosa, induces systemic autoimmunity.
Severe coronavirus disease 2019 (COVID-19) frequently entails complications that bear similarities to autoimmune diseases. To date, there is little data on possible IgA-mediated autoimmune responses. Here, we aim to determine whether COVID-19 is associated with a vigorous total IgA response and if IgA antibodies are associated with complications of severe illness. Since thrombotic events are frequent in severe COVID-19 and resemble hypercoagulation of antiphospholipid syndrome (APS), our approach focused on antiphospholipid antibodies (aPL).
METHODS
In this retrospective cohort study clinical data and aPL from 64 patients with COVID-19 were compared from three independent tertiary hospitals (one in Liechtenstein, two in Switzerland). Samples were collected from April 9 th to May 1 st, 2020.
RESULTS
Clinical records of 64 patients with COVID-19 were reviewed and divided into a cohort with mild illness (mCOVID) (41%), a discovery cohort with severe illness (sdCOVID) (22%) and a confirmation cohort with severe illness (scCOVID) (38%). Total IgA, IgG and aPL were measured with clinical diagnostic kits. Severe illness was significantly associated with increased total IgA (sdCOVID, P=0.01; scCOVID, p-value<0.001), but not total IgG. Among aPL, both cohorts with severe illness significantly correlated with elevated anti-Cardiolipin IgA (sdCOVID and scCOVID, p-value<0.001), anti-Cardiolipin IgM (sdCOVID, P=0.003; scCOVID, P<0.001), and anti-Beta2 Glycoprotein-1 IgA (sdCOVID and scCOVID, P<0.001). Systemic lupus erythematosus was excluded from all patients as a potential confounder.
CONCLUSIONS
Higher total IgA and IgA-aPL were consistently associated with severe illness. These novel data strongly suggest that a vigorous antiviral IgA-response, possibly triggered in the bronchial mucosa, induces systemic autoimmunity.
- Language
-
- English
- Open access status
- bronze
- Identifiers
-
- DOI 10.1093/cid/ciaa1496
- PMID 32997739
- Persistent URL
- https://sonar.ch/global/documents/177
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