Molecular mimicry, hyperactive immune system, and SARS-COV-2 are three prerequisites of the autoimmune disease triangle following COVID-19 infection

Vahabi, Maedeh; Ghazanfari, T; Sepehrnia, Saeed

doi:10.1016/j.intimp.2022.109183

Cited by 34 publications

(34 citation statements)

References 135 publications

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“…Finally, we consider bioinformatics analysis to be an essential step in the preliminary evaluation of the risks and autoimmunity spectrum in COVID-19 complications, including the post-COVID-19 syndrome. Similar point of view recently was emphasized by other researchers [44] Additionally, it may be useful in epitope selection for elaboration of the safest anti-COVID-19 vaccines. S [45].…”

Section: Discussionsupporting

confidence: 70%

Post-COVID Endocrine Disorders: Putative Role of Molecular Mimicry and Some Pathomorphological Correlates

Normatov¹,

Карев²,

Kolobov³

et al. 2022

Preprint

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The article is devoted to the problem of autoimmune diseases provocation by coronavirus infection and the role of molecular mimicry in this phenomenon. SARS-CoV-2 can disguise its proteins as human ones in order to avoid immune attack. A bioinformatics analysis of the probable pentapeptide sharing between human autoantigens of endocrinocytes and SARS-CoV-2 spike protein, membrane protein and nucleocapsid protein was performed. Antigen mimicry between S-proteins of all other known human Coronaviruses and typical target autoantigens of endocrinocytes was also explored. Six human-identical regions were found in the SARS-CoV-2 membrane and nucleocapsid proteins, all of them in their immunodominant epitopes. All shared epitopes belong to antigens of endocrine cells commonly targeted during autoimmune endocrinopathies. Moreover, samples of the pituitary, adrenal and thyroid from patients who died from coronovirus infection (COVID-19) were studied morphologically using histochemical methods. A high frequency of SARS-CoV-2 caused inflammation of the studied endocrine organs was found in patients who died from severe COVID-19. At the same time, the abundant expression of virus antigens by the cells of the adenohypophysis was combined with the complete absence of its expression by the cells of the neurohypophysis. SARS-CoV-2 infected cells apparently perished by non-apoptotic pathway. The foci of lesions in endocrine organs contained abundant lymphocytic infiltrates which may witness for the impact of autoimmune processes. The facts revealed emphasize the need of endocrinological diagnostic alertness of a physician while observing patients with post-vaccination and post-COVID-19 health disorders. [3 figures, 6 tables, bibliography: 45 references].

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Section: Discussionsupporting

confidence: 70%

Post-COVID Endocrine Disorders: Putative Role of Molecular Mimicry and Some Pathomorphological Correlates

Normatov¹,

Карев²,

Kolobov³

et al. 2022

Preprint

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“…As already described for other viruses, SARS-CoV-2 may elicit autoimmune conditions through an hyperactivation of both the innate and adaptive immune response ( 27 ). Specifically, SARS-CoV-2 may directly trigger thyroid autoimmunity infecting thyroid follicular cells, where ACE-2 receptor is abundantly expressed ( 28 ); viral presence has indeed been retrieved in thyroid specimens ( 29 , 30 ) and reactivity between TPO antigen and SARS-CoV-2 has been demonstrated in vitro , favoring the hypothesis of molecular mimicry ( 31 ).…”

Section: Discussionmentioning

confidence: 72%

Increased prevalence of autoimmune thyroid disease after COVID-19: A single-center, prospective study

Rossini

Cassibba²,

Perticone³

et al. 2023

Front. Endocrinol.

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IntroductionThyroid dysfunctions associated with SARS-CoV-2 acute infection have been extensively described since the beginning of COVID-19 pandemics. Conversely, few data are available on the occurrence of thyroid autoimmunity after COVID-19 resolution. We assessed the prevalence of autoimmune thyroid disease (ATD) and thyroid dysfunctions in COVID-19 survivors three months after hospital admission.Design and methodsSingle-center, prospective, observational, cohort study performed at ASST Papa Giovanni XXIII Hospital, Bergamo, Italy. 599 COVID-19 survivors were prospectively evaluated for thyroid function and autoimmunity thyroperoxidase antibodies (TPOAb), thyroglobulin antibodies (TgAb). When a positive antibody concentration was detected, thyroid ultrasound was performed. Multiple logistic regression model was used to estimate the association between autoimmunity and demographic characteristics, respiratory support, and comorbidities. Autoimmunity results were compared to a cohort of 498 controls referred to our Institution for non-thyroid diseases before the pandemic onset. A sensitivity analysis comparing 330 COVID-19 patients with 330 age and sex-matched controls was performed.ResultsUnivariate and multivariate analysis found that female sex was positively associated (OR 2.01, SE 0.48, p = 0.003), and type 2 diabetes (T2DM) was negatively associated (OR 0.36, SE 0.16, p = 0.025) with thyroid autoimmunity; hospitalization, ICU admission, respiratory support, or COVID-19 treatment were not associated with thyroid autoimmunity (p > 0.05). TPOAb prevalence was greater in COVID-19 survivors than in controls: 15.7% vs 7.7%, p = 0.002. Ultrasonographic features of thyroiditis were present in 94.9% of the evaluated patients with positive antibodies. TSH was within the normal range in 95% of patients.ConclusionsAutoimmune thyroid disease prevalence in COVID-19 survivors was doubled as compared to age and sex-matched controls, suggesting a role of SARS-CoV-2 in eliciting thyroid autoimmunity.

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“…SARS-CoV-2 infections trigger systemic autoimmune and inflammatory responses which may be regulated through the release of TSLP. Several clinical manifestations of SARS-CoV-2-induced autoimmunity [ 21 , 22 ] and relapse, and/or the exacerbation of other chronic inflammatory diseases have been reported [ 23 , 24 , 25 ]. TSLP expression contributes to B cell lymphopoiesis and causes an expansion of nearly all immature and mature B cell populations in mice [ 26 ], which may lead to the clonal expansion of autoantibody-producing B cells.…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2-Induced TSLP Is Associated with Duration of Hospital Stay in COVID-19 Patients

Gerla

Moitra

Pink

et al. 2023

Viruses

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Thymic stromal lymphopoietin (TSLP) is an epithelium-derived pro-inflammatory cytokine involved in lung inflammatory responses. Previous studies show conflicting observations in blood TSLP in COVID-19, while none report SARS-CoV-2 inducing TSLP expression in bronchial epithelial cells. Our objective in this study was to determine whether TSLP levels increase in COVID-19 patients and if SARS-CoV-2 induces TSLP expression in bronchial epithelial cells. Plasma cytokine levels were measured in patients hospitalized with confirmed COVID-19 and age- and sex-matched healthy controls. Demographic and clinical information from COVID-19 patients was collected. We determined associations between plasma TSLP and clinical parameters using Poisson regression. Cultured human nasal (HNEpC) and bronchial epithelial cells (NHBEs), Caco-2 cells, and patient-derived bronchial epithelial cells (HBECs) obtained from elective bronchoscopy were infected in vitro with SARS-CoV-2, and secretion as well as intracellular expression of TSLP was detected by immunofluorescence. Increased TSLP levels were detected in the plasma of hospitalized COVID-19 patients (603.4 ± 75.4 vs 997.6 ± 241.4 fg/mL, mean ± SEM), the levels of which correlated with duration of stay in hospital (β: 0.11; 95% confidence interval (CI): 0.01–0.21). In cultured NHBE and HBECs but not HNEpCs or Caco-2 cells, TSLP levels were significantly elevated after 24 h post-infection with SARS-CoV-2 (p < 0.001) in a dose-dependent manner. Plasma TSLP in COVID-19 patients significantly correlated with duration of hospitalization, while SARS-CoV-2 induced TSLP secretion from bronchial epithelial cells in vitro. Based on our findings, TSLP may be considered an important therapeutic target for COVID-19 treatment.

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Molecular mimicry, hyperactive immune system, and SARS-COV-2 are three prerequisites of the autoimmune disease triangle following COVID-19 infection

Cited by 34 publications

References 135 publications

Post-COVID Endocrine Disorders: Putative Role of Molecular Mimicry and Some Pathomorphological Correlates

Post-COVID Endocrine Disorders: Putative Role of Molecular Mimicry and Some Pathomorphological Correlates

Increased prevalence of autoimmune thyroid disease after COVID-19: A single-center, prospective study

SARS-CoV-2-Induced TSLP Is Associated with Duration of Hospital Stay in COVID-19 Patients

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