Autoantibodies in COVID-19: frequency and function

Gao, Zhaowei; Zhang, Huizhong; Liu, Chong; Dong, Ke

doi:10.1016/j.autrev.2021.102754

Cited by 55 publications

(41 citation statements)

References 19 publications

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“…In a study analysing serum samples from hospitalized COVID-19 patients, antiphospholipid autoantibodies were detected in 52% of samples, which were further associated with neutrophil hyperactivity and more severe clinical outcomes [109]. Other studies have also identified autoantibodies against interferons, neutrophils, connective tissues, cyclic citrullinated peptides, and cell nucleus in 10-50% of patients with COVID-19 [110][111][112]113]. While it is unconfirmed if such autoantibodies are long-lasting in COVID-19, research review has strongly linked these autoantibodies to chronic autoimmune diseases, such as antiphospholipid and Sjogren syndromes, lupus erythematosus, and rheumatoid arthritis [114].…”

Section: Pathological Inflammationmentioning

confidence: 99%

Long COVID or post-COVID-19 syndrome: putative pathophysiology, risk factors, and treatments

Yong

2021

Infectious Diseases

804

609

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Long COVID or post-COVID-19 syndrome first gained widespread recognition among social support groups and later in scientific and medical communities. This illness is poorly understood as it affects COVID-19 survivors at all levels of disease severity, even younger adults, children, and those not hospitalized. While the precise definition of long COVID may be lacking, the most common symptoms reported in many studies are fatigue and dyspnoea that last for months after acute COVID-19. Other persistent symptoms may include cognitive and mental impairments, chest and joint pains, palpitations, myalgia, smell and taste dysfunctions, cough, headache, and gastrointestinal and cardiac issues. Presently, there is limited literature discussing the possible pathophysiology, risk factors, and treatments in long COVID, which the current review aims to address. In brief, long COVID may be driven by long-term tissue damage (e.g. lung, brain, and heart) and pathological inflammation (e.g. from viral persistence, immune dysregulation, and autoimmunity). The associated risk factors may include female sex, more than five early symptoms, early dyspnoea, prior psychiatric disorders, and specific biomarkers (e.g. D-dimer, CRP, and lymphocyte count), although more research is required to substantiate such risk factors. While preliminary evidence suggests that personalized rehabilitation training may help certain long COVID cases, therapeutic drugs repurposed from other similar conditions, such as myalgic encephalomyelitis or chronic fatigue syndrome, postural orthostatic tachycardia syndrome, and mast cell activation syndrome, also hold potential. In sum, this review hopes to provide the current understanding of what is known about long COVID.

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Section: Pathological Inflammationmentioning

confidence: 99%

Long COVID or post-COVID-19 syndrome: putative pathophysiology, risk factors, and treatments

Yong

2021

Infectious Diseases

804

609

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“…However, this autoimmune response can be seen in many COVID-19 patients, including children [257] , [258] , [259] . Likewise, the development of autoantibodies against many host antigens other than Type I interferon has been shown in severe COVID-19 patients and dozens of other diseases associated with such autoimmune responses [260] , [261] , [262] , [263] .…”

Section: Immune System Involvement and Retinoid Signaling Disorder In Covid-19mentioning

confidence: 99%

A novel hypothesis for COVID-19 pathogenesis: Retinol depletion and retinoid signaling disorder

Sarohan¹,

Kızıl

İnkaya

et al. 2021

Cellular Signalling

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The SARS-CoV-2 virus has caused a worldwide COVID-19 pandemic. In less than a year and a half, more than 200 million people have been infected and more than four million have died. Despite some improvement in the treatment strategies, no definitive treatment protocol has been developed. The pathogenesis of the disease has not been clearly elucidated yet. A clear understanding of its pathogenesis will help develop effective vaccines and drugs. The immunopathogenesis of COVID-19 is characteristic with acute respiratory distress syndrome and multiorgan involvement with impaired Type I interferon response and hyperinflammation. The destructive systemic effects of COVID-19 cannot be explained simply by the viral tropism through the ACE2 and TMPRSS2 receptors. In addition, the recently identified mutations cannot fully explain the defect in all cases of Type I interferon synthesis. We hypothesize that retinol depletion and resulting impaired retinoid signaling play a central role in the COVID-19 pathogenesis that is characteristic for dysregulated immune system, defect in Type I interferon synthesis, severe inflammatory process, and destructive systemic multiorgan involvement. Viral RNA recognition mechanism through RIG-I receptors can quickly consume a large amount of the body's retinoid reserve, which causes the retinol levels to fall below the normal serum levels. This causes retinoid insufficiency and impaired retinoid signaling, which leads to interruption in Type I interferon synthesis and an excessive inflammation. Therefore, reconstitution of the retinoid signaling may prove to be a valid strategy for management of COVID-19 as well for some other chronic, degenerative, inflammatory, and autoimmune diseases.

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“…Importantly, this analysis used a non-informative prior; that is, we did not assume any previous knowledge of what the true state of nature is. This is fitting since there little is known on the prevalence of autoimmune phenomena among critically ill patients 5 and, to our knowledge, this is the first report on autoimmunity among severe COVID-19 patients that has a control group of similarly ill, critical patients. We then performed an exploratory analysis assigning speculated, a priori differences between the COVID + and COVID − populations – Bayesian prior probabilities.…”

Section: Resultsmentioning

confidence: 85%

COVID-19 associated autoimmunity is a feature of severe respiratory disease - a Bayesian analysis

Trahtemberg

Rottapel

Santos

et al. 2021

Preprint

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Background: Serological and clinical features with similarities to systemic autoimmunity have been reported in severe COVID-19, but there is a lack of studies that include contemporaneous controls who do not have COVID-19. Methods: Observational cohort study of adult patients admitted to an intensive care unit with acute respiratory failure. Patients were divided into COVID+ and COVID- based on SARS-CoV-2 PCR from nasopharyngeal swabs and/or endotracheal aspirates. No COVID-19 specific interventions were given. The primary clinical outcome was death in the ICU within 3 months; secondary outcomes included in-hospital death and disease severity measures. Measurements including autoantibodies, were done longitudinally. ANOVA and Fisher's exact test were used with alpha=0.05, with a false discovery rate of q=0.05. Bayesian analysis was performed to provide credible estimates of the possible states of nature compatible with our results. Results: 22 COVID+ and 20 COVID- patients were recruited, 69% males, median age 60.5 years. Overall, 64% had anti-nuclear antibodies, 38% had antigen-specific autoantibodies, 31% had myositis related autoantibodies, and 38% had high levels of anti-cytokine autoantibodies. There were no statistically significant differences between COVID+ and COVID- for any of the clinical or autoantibody parameters. A specific pattern of anti-nuclear antibodies was associated with worse clinical severity for both cohorts. Conclusions: Severe COVID+ patients have similar humoral autoimmune features as comparably ill COVID- patients, suggesting that autoantibodies are a feature of critical illness regardless of COVID-19 status. The clinical significance of autoimmune serology and the correlation with severity in critical illness remains to be elucidated.

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Autoantibodies in COVID-19: frequency and function

Cited by 55 publications

References 19 publications

Long COVID or post-COVID-19 syndrome: putative pathophysiology, risk factors, and treatments

Long COVID or post-COVID-19 syndrome: putative pathophysiology, risk factors, and treatments

A novel hypothesis for COVID-19 pathogenesis: Retinol depletion and retinoid signaling disorder

COVID-19 associated autoimmunity is a feature of severe respiratory disease - a Bayesian analysis

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