Screening and characterization of myositis‐related autoantibodies in COVID‐19 patients

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Abstract

An efficient host immune response against severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2, COVID‐19) appears to be crucial for controlling and resolving this viral infection. However, many studies have reported autoimmune characteristics in severe COVID‐19 patients. Moreover, clinical observations have revealed that COVID‐19‐associated acute distress respiratory syndrome shares many features in common with inflammatory myopathy including interstitial lung disease (ILD), most particularly rapidly progressive (RP)‐ILD. This study explored this phenomenon by seeking to identify and characterize myositis‐specific and related autoantibodies in 25 COVID‐19 patients with mild or severe symptoms. Line blot analysis with the EUROLINE Myopathies Ag kit identified 9 (36%) patients with COVID‐19 with one or more autoantibodies against several myositis‐related antigens (Jo‐1, Ku, Mi‐2β, PL‐7, PL‐12, PM‐Scl 75, PM‐Scl 100, Ro‐52, and SRP); no anti‐MDA5 antibodies were detected. As the presence of antibodies identified by line blots was unrelated to disease severity, we further characterized the autoantibodies by radioimmunoassay, in which [ ³⁵S]methionine‐labeled K562 cellular antigens were precipitated and visualized by gel electrophoresis. This result was confirmed by an immunoprecipitation assay and immunoblotting; 2 patients exhibited anti‐Ku70 and anti‐Ku80 antibodies. Our data suggest that it is necessary to use more than one method to characterize and evaluate autoantibodies in people recovered from COVID‐19, in order to avoid misinterpreting those autoantibodies as diagnostic markers for autoimmune diseases.

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Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China

Chaolin Huang, Yeming Wang, Xingwang Li … (2020)

Summary Background A recent cluster of pneumonia cases in Wuhan, China, was caused by a novel betacoronavirus, the 2019 novel coronavirus (2019-nCoV). We report the epidemiological, clinical, laboratory, and radiological characteristics and treatment and clinical outcomes of these patients. Methods All patients with suspected 2019-nCoV were admitted to a designated hospital in Wuhan. We prospectively collected and analysed data on patients with laboratory-confirmed 2019-nCoV infection by real-time RT-PCR and next-generation sequencing. Data were obtained with standardised data collection forms shared by WHO and the International Severe Acute Respiratory and Emerging Infection Consortium from electronic medical records. Researchers also directly communicated with patients or their families to ascertain epidemiological and symptom data. Outcomes were also compared between patients who had been admitted to the intensive care unit (ICU) and those who had not. Findings By Jan 2, 2020, 41 admitted hospital patients had been identified as having laboratory-confirmed 2019-nCoV infection. Most of the infected patients were men (30 [73%] of 41); less than half had underlying diseases (13 [32%]), including diabetes (eight [20%]), hypertension (six [15%]), and cardiovascular disease (six [15%]). Median age was 49·0 years (IQR 41·0–58·0). 27 (66%) of 41 patients had been exposed to Huanan seafood market. One family cluster was found. Common symptoms at onset of illness were fever (40 [98%] of 41 patients), cough (31 [76%]), and myalgia or fatigue (18 [44%]); less common symptoms were sputum production (11 [28%] of 39), headache (three [8%] of 38), haemoptysis (two [5%] of 39), and diarrhoea (one [3%] of 38). Dyspnoea developed in 22 (55%) of 40 patients (median time from illness onset to dyspnoea 8·0 days [IQR 5·0–13·0]). 26 (63%) of 41 patients had lymphopenia. All 41 patients had pneumonia with abnormal findings on chest CT. Complications included acute respiratory distress syndrome (12 [29%]), RNAaemia (six [15%]), acute cardiac injury (five [12%]) and secondary infection (four [10%]). 13 (32%) patients were admitted to an ICU and six (15%) died. Compared with non-ICU patients, ICU patients had higher plasma levels of IL2, IL7, IL10, GSCF, IP10, MCP1, MIP1A, and TNFα. Interpretation The 2019-nCoV infection caused clusters of severe respiratory illness similar to severe acute respiratory syndrome coronavirus and was associated with ICU admission and high mortality. Major gaps in our knowledge of the origin, epidemiology, duration of human transmission, and clinical spectrum of disease need fulfilment by future studies. Funding Ministry of Science and Technology, Chinese Academy of Medical Sciences, National Natural Science Foundation of China, and Beijing Municipal Science and Technology Commission.

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COVID-19: consider cytokine storm syndromes and immunosuppression

Puja Mehta, Daniel McAuley, Michael Brown … (2020)

As of March 12, 2020, coronavirus disease 2019 (COVID-19) has been confirmed in 125 048 people worldwide, carrying a mortality of approximately 3·7%, 1 compared with a mortality rate of less than 1% from influenza. There is an urgent need for effective treatment. Current focus has been on the development of novel therapeutics, including antivirals and vaccines. Accumulating evidence suggests that a subgroup of patients with severe COVID-19 might have a cytokine storm syndrome. We recommend identification and treatment of hyperinflammation using existing, approved therapies with proven safety profiles to address the immediate need to reduce the rising mortality. Current management of COVID-19 is supportive, and respiratory failure from acute respiratory distress syndrome (ARDS) is the leading cause of mortality. 2 Secondary haemophagocytic lymphohistiocytosis (sHLH) is an under-recognised, hyperinflammatory syndrome characterised by a fulminant and fatal hypercytokinaemia with multiorgan failure. In adults, sHLH is most commonly triggered by viral infections 3 and occurs in 3·7–4·3% of sepsis cases. 4 Cardinal features of sHLH include unremitting fever, cytopenias, and hyperferritinaemia; pulmonary involvement (including ARDS) occurs in approximately 50% of patients. 5 A cytokine profile resembling sHLH is associated with COVID-19 disease severity, characterised by increased interleukin (IL)-2, IL-7, granulocyte-colony stimulating factor, interferon-γ inducible protein 10, monocyte chemoattractant protein 1, macrophage inflammatory protein 1-α, and tumour necrosis factor-α. 6 Predictors of fatality from a recent retrospective, multicentre study of 150 confirmed COVID-19 cases in Wuhan, China, included elevated ferritin (mean 1297·6 ng/ml in non-survivors vs 614·0 ng/ml in survivors; p 39·4°C 49 Organomegaly None 0 Hepatomegaly or splenomegaly 23 Hepatomegaly and splenomegaly 38 Number of cytopenias * One lineage 0 Two lineages 24 Three lineages 34 Triglycerides (mmol/L) 4·0 mmol/L 64 Fibrinogen (g/L) >2·5 g/L 0 ≤2·5 g/L 30 Ferritin ng/ml 6000 ng/ml 50 Serum aspartate aminotransferase <30 IU/L 0 ≥30 IU/L 19 Haemophagocytosis on bone marrow aspirate No 0 Yes 35 Known immunosuppression † No 0 Yes 18 The Hscore 11 generates a probability for the presence of secondary HLH. HScores greater than 169 are 93% sensitive and 86% specific for HLH. Note that bone marrow haemophagocytosis is not mandatory for a diagnosis of HLH. HScores can be calculated using an online HScore calculator. 11 HLH=haemophagocytic lymphohistiocytosis. * Defined as either haemoglobin concentration of 9·2 g/dL or less (≤5·71 mmol/L), a white blood cell count of 5000 white blood cells per mm3 or less, or platelet count of 110 000 platelets per mm3 or less, or all of these criteria combined. † HIV positive or receiving longterm immunosuppressive therapy (ie, glucocorticoids, cyclosporine, azathioprine).

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Baseline Characteristics and Outcomes of 1591 Patients Infected With SARS-CoV-2 Admitted to ICUs of the Lombardy Region, Italy

Giacomo Grasselli, Alberto Zangrillo, Alberto Zanella … (2020)

In December 2019, a novel coronavirus (severe acute respiratory syndrome coronavirus 2 [SARS-CoV-2]) emerged in China and has spread globally, creating a pandemic. Information about the clinical characteristics of infected patients who require intensive care is limited.

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Author and article information

Contributors

Joung‐Liang Lan: jounglan@me.com

Jye‐Lin Hsu:

ORCID: https://orcid.org/0000-0001-6687-4083

qiqi0910@gmail.com

Journal

Journal ID (nlm-ta): Clin Transl Sci

Journal ID (iso-abbrev): Clin Transl Sci

Journal ID (doi): 10.1111/(ISSN)1752-8062

Journal ID (publisher-id): CTS

Title: Clinical and Translational Science

Publisher: John Wiley and Sons Inc. (Hoboken )

ISSN (Print): 1752-8054

ISSN (Electronic): 1752-8062

Publication date (Electronic): 27 October 2022

Publication date Collection: January 2023

Volume: 16

Issue: 1 ( doiID: 10.1111/cts.v16.1 )

Pages: 140-150

Affiliations

[ ¹ ] Graduate Institute of Biomedical Sciences China Medical University Taichung Taiwan

[ ² ] School of Medicine China Medical University Taichung Taiwan

[ ³ ] Translational Medicine Laboratory China Medical University Hospital Taichung Taiwan

[ ⁴ ] Rheumatology and Immunology Center China Medical University Hospital Taichung Taiwan

[ ⁵ ] Department of Information Management Hsing Wu University New Taipei Taiwan

[ ⁶ ] Rheumatic Diseases Research Center China Medical University Hospital Taichung Taiwan

[ ⁷ ] Departments of Laboratory Medicine and Internal Medicine China Medical University Hospital Taichung Taiwan

[ ⁸ ] Ph.D. Program for Aging, School of Medicine China Medical University Taichung Taiwan

[ ⁹ ] Departments of Laboratory Medicine and Internal Medicine National Taiwan University Hospital, National Taiwan University College of Medicine Taipei Taiwan

[ ¹⁰ ] Drug Development Center China Medical University Taichung Taiwan

Author notes

[*] [* ] Correspondence

Joung‐Liang Lan, Rheumatology and Immunology Center, China Medical University Hospital, No. 2 Yu‐De Road, Taichung, Taiwan.

Email: jounglan@ 123456me.com

Jye‐Lin Hsu, Graduate Institute of Biomedical Sciences, China Medical University, No. 91 Hsueh‐Shih Road, Taichung 40402, Taiwan.

Email: qiqi0910@ 123456gmail.com

Author information

Jye‐Lin Hsu https://orcid.org/0000-0001-6687-4083

Article

Publisher ID: CTS13434 Other ID: CTS-2022-0121

DOI: 10.1111/cts.13434

PMC ID: 9841303

PubMed ID: 36271647

SO-VID: 5efd8e09-6834-496f-8767-c98f95921e7a

License:

This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

History

Date revision received : 06 August 2022

Date received : 27 April 2022

Date accepted : 27 September 2022

Page count

Figures: 2, Tables: 3, Pages: 11, Words: 5195

Funding

Funded by: Taiwan's Ministry of Science and Technology

Award ID: MOST 111‐2628‐B‐039‐001

Funded by: Research and Development Center for Immunology

Funded by: China Medical University , doi 10.13039/501100007300;

Award ID: 1095310A

Funded by: China Medical University Hospital , doi 10.13039/501100004391;

Award ID: DMR‐111‐031

Award ID: DMR‐CELL‐170085

Award ID: DMR‐CELL‐1805

Funded by: China Medical University , doi 10.13039/501100007300;

Award ID: CMU‐111‐MF‐19

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cover-date January 2023

details-of-publishers-convertor Converter:WILEY_ML3GV2_TO_JATSPMC version:6.2.3 mode:remove_FC converted:16.01.2023

Screening and characterization of myositis‐related autoantibodies in COVID‐19 patients

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Novel Coronavirus Disease COVID-19

Most cited references 38

Clinical features of patients infected with 2019 novel coronavirus in Wuhan, China

COVID-19: consider cytokine storm syndromes and immunosuppression

Baseline Characteristics and Outcomes of 1591 Patients Infected With SARS-CoV-2 Admitted to ICUs of the Lombardy Region, Italy

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