Shared Pathogenicity Features and Sequences between EBV, SARS-CoV-2, and HLA Class I Molecule-binding Motifs with a Potential Role in Autoimmunity

Adıgüzel, Yekbun; Mahroum, Naim; Muller, Sylviane; Blank, Miri; Halpert, Gilad; Shoenfeld, Yehuda

doi:10.1007/s12016-023-08962-4

Cited by 2 publications

(2 citation statements)

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“…For example, anti-interferon autoantibodies capable of impairing antiviral responses are detected in approximately 10.2% of severe COVID-19 cases ( 4 ). Additionally, SARS-CoV-2 binding to tissue antigens may induce cross-reactivity of immune cells and subsequent autoimmune damage in organs like the Livers and nervous system ( 5 – 7 ). Understanding the autoimmune aspects of COVID-19 is crucial, as they may exacerbate disease severity and cause prolonged symptoms in recovered patients.…”

Section: Introductionmentioning

confidence: 99%

“…Viral infections often provoke autoimmunity via molecular mimicry, wherein viral antigens resemble self-antigens ( 8 ). SARS-CoV-2 proteins may share sequences or structures with host proteins, leading to cross-reactivity of antibodies or T cells ( 5 ). Additionally, the severe inflammation and cytokine storm induced by COVID-19 may cause the breakdown of self-tolerance.…”

Section: Introductionmentioning

confidence: 99%

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Neurological risks of COVID-19 in women: the complex immunology underpinning sex differences

Gu,

Zhang,

Liu

et al. 2023

Front. Immunol.

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The COVID-19 pandemic has uncovered many mysteries about SARS-CoV-2, including its potential to trigger abnormal autoimmune responses. Emerging evidence suggests women may face higher risks from COVID-induced autoimmunity manifesting as persistent neurological symptoms. Elucidating the mechanisms underlying this female susceptibility is now imperative. We synthesize key insights from existing studies on how COVID-19 infection can lead to immune tolerance loss, enabling autoreactive antibodies and lymphocyte production. These antibodies and lymphocytes infiltrate the central nervous system. Female sex hormones like estrogen and X-chromosome mediated effects likely contribute to dysregulated humoral immunity and cytokine profiles among women, increasing their predisposition. COVID-19 may also disrupt the delicate immunological balance of the female microbiome. These perturbations precipitate damage to neural damage through mechanisms like demyelination, neuroinflammation, and neurodegeneration – consistent with the observed neurological sequelae in women. An intentional focus on elucidating sex differences in COVID-19 pathogenesis is now needed to inform prognosis assessments and tailored interventions for female patients. From clinical monitoring to evaluating emerging immunomodulatory therapies, a nuanced women-centered approach considering the hormonal status and immunobiology will be vital to ensure equitable outcomes. Overall, deeper insights into the apparent female specificity of COVID-induced autoimmunity will accelerate the development of solutions mitigating associated neurological harm.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%