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. 2021 Aug;205(2):99-105.
doi: 10.1111/cei.13623. Epub 2021 Jun 13.

Establishing the prevalence of common tissue-specific autoantibodies following severe acute respiratory syndrome coronavirus 2 infection

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Establishing the prevalence of common tissue-specific autoantibodies following severe acute respiratory syndrome coronavirus 2 infection

Alex G Richter et al. Clin Exp Immunol. 2021 Aug.

Abstract

Coronavirus 19 (COVID-19) has been associated with both transient and persistent systemic symptoms that do not appear to be a direct consequence of viral infection. The generation of autoantibodies has been proposed as a mechanism to explain these symptoms. To understand the prevalence of autoantibodies associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection, we investigated the frequency and specificity of clinically relevant autoantibodies in 84 individuals previously infected with SARS-CoV-2, suffering from COVID-19 of varying severity in both the acute and convalescent setting. These were compared with results from 32 individuals who were on the intensive therapy unit (ITU) for non-COVID reasons. We demonstrate a higher frequency of autoantibodies in the COVID-19 ITU group compared with non-COVID-19 ITU disease control patients and that autoantibodies were also found in the serum 3-5 months post-COVID-19 infection. Non-COVID patients displayed a diverse pattern of autoantibodies; in contrast, the COVID-19 groups had a more restricted panel of autoantibodies including skin, skeletal muscle and cardiac antibodies. Our results demonstrate that respiratory viral infection with SARS-CoV-2 is associated with the detection of a limited profile of tissue-specific autoantibodies, detectable using routine clinical immunology assays. Further studies are required to determine whether these autoantibodies are specific to SARS-CoV-2 or a phenomenon arising from severe viral infections and to determine the clinical significance of these autoantibodies.

Keywords: COVID-19; SARS-CoV-2; autoantibodies; autoimmunity; long COVID.

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Conflict of interest statement

Mark T. Drayson reports personal fees from Abingdon Health, outside the submitted work. All other authors declare no competing interests.

Figures

FIGURE 1
FIGURE 1
Frequency and quantity of autoantibodies in each cohort
FIGURE 2
FIGURE 2
Tissue‐specific staining patterns following coronavirus 19 (COVID‐19). (a) Intracellular cement staining pattern, weak positive (P24), (b) smooth muscle staining pattern, 1/100 titre (P85), (c) skeletal muscle staining pattern, weak positive (P106), (d) cardiac muscle staining pattern demonstrating striations (P87)

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