Molecular mimicry and autoimmunity in the time of COVID-19

Rojas, Manuel; Herrán, María; Ramírez-Santana, Carolina; Leung, Patrick S.C.; Anaya, Juan-Manuel; Ridgway, William M.; Gershwin, M. Eric

doi:10.1016/j.jaut.2023.103070

Cited by 18 publications

(20 citation statements)

References 263 publications

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“…Pathologic mechanisms include molecular mimicry, bystander activation of T lymphocytes, transient immunosuppression, and inflammation ( 15 ). Molecular mimicry is the primary suspect implicated in the pathophysiology of autoimmunity during COVID-19 infection ( 16 ). Furthermore, COVID-19 may result in autoimmune encephalitis (AE), which may manifest as limbic encephalitis, anti-NMDA receptor encephalitis, steroid-responsive encephalitis, AE presenting as new-onset refractory status epilepticus (NORSE), and unknown type of AE ( 17 ).…”

Section: Discussionmentioning

confidence: 99%

Case report: A case of anti-glycine receptor encephalomyelitis triggered by post-transplant or COVID-19 infection?

Zhang,

Dai

et al. 2024

Front. Neurol.

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Even though long-term immunosuppressant drugs (ISD) are employed to inhibit immune system activity, enhancing graft functionality and patient survival in solid organ transplantation (SOT), these transplants often lead to immune complications, with post-transplant autoimmune diseases of the central nervous system (CNS) being uncommon. Here, we detail the case of a 66-year-old woman who underwent a renal transplantation 8 months prior, who was admitted with subacute onset of encephalomyelitis, accompanied by headaches, paraplegia, weakness, vomiting, and abdominal pain, with a positive COVID-19 nasopharyngeal swab test 1 month before admission. MRI scans of the brain revealed multiple lesions in the white matter of the bilateral deep frontal lobe, the left temporal lobe and insula lobe. Additionally, there were multiple short segment lesions in the spinal cord and subdural hematoma at T1, T6-T7 posterior. The serum revealed a positive result for GlyR-IgG. Following the administration of corticosteroid and intravenous immunoglobulin, there was a significant improvement in the patient’s symptoms within 2 weeks, and her brain MRI showed a reduction in the lesion. Despite its rarity, we believe this to be the inaugural documentation of anti-GlyR encephalomyelitis occurring during renal transplantation. A full panel of antibodies for autoimmune encephalomyelitis is the key leading to the diagnosis.

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Section: Discussionmentioning

confidence: 99%

Case report: A case of anti-glycine receptor encephalomyelitis triggered by post-transplant or COVID-19 infection?

Zhang,

Dai

et al. 2024

Front. Neurol.

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“…The mechanisms by which vaccinations may potentially induce de novo CNS inflammatory disorders include molecular mimicry, epitope spreading, or demasking/release of epitopes ( 17 , 36 ). It is possible that similarities between foreign epitopes (provided by vaccine exposure) and self-antigen leads to aberrant activation of autoreactive T or B cell clones (molecular mimicry) ( 37 ). Alternatively, an initial antigenic stimulus may induce spreading of the specificity of the immune response, which includes self-epitopes other than the one which initiated inflammation (epitope-spreading) ( 38 ).…”

Section: Discussionmentioning

confidence: 99%

Central nervous system immune-related disorders after SARS-CoV-2 vaccination: a multicenter study

Vogrig,

Tartaglia,

Dentoni

et al. 2024

Front. Immunol.

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BackgroundCOVID-19 vaccines have been approved due to their excellent safety and efficacy data and their use has also permitted to reduce neurological complications of SARS-CoV-2. However, clinical trials were underpowered to detect rare adverse events. Herein, the aim was to characterize the clinical spectrum and immunological features of central nervous system (CNS) immune-related events following SARS-CoV-2 vaccination.MethodsMulticenter, retrospective, cohort study (December 1, 2020-April 30, 2022). Inclusion criteria were (1) de novo CNS disorders developing after SARS-CoV-2 vaccination (probable causal relationship as per 2021 Butler criteria) (2); evidence for an immune-mediated etiology, as per (i) 2016 Graus criteria for autoimmune encephalitis (AE); (ii) 2015 Wingerchuk criteria for neuromyelitis optica spectrum disorders; (iii) criteria for myelitis.ResultsNineteen patients were included from 7 tertiary referral hospitals across Italy and France (one of them being a national referral center for AE), over almost 1 year and half of vaccination campaign. Vaccines administered were mRNA-based (63%) and adenovirus-vectored (37%). The median time between vaccination and symptoms onset was 14 days (range: 2-41 days). CSF was inflammatory in 74%; autoantibodies were detected in 5%. CSF cytokine analysis (n=3) revealed increased CXCL-10 (IP-10), suggesting robust T-cell activation. The patients had AE (58%), myelitis (21%), acute disseminated encephalomyelitis (ADEM) (16%), and brainstem encephalitis (5%). All patients but 2 received immunomodulatory treatment. At last follow-up (median 130 days; range: 32-540), only one patient (5%) had a mRS>2.ConclusionCNS adverse events of COVID-19 vaccination appear to be very rare even at reference centers and consist mostly of antibody-negative AE, myelitis, and ADEM developing approximately 2 weeks after vaccination. Most patients improve following immunomodulatory treatment.

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“…The authors suggest that “molecular mimicry between a self and a microbial peptide antigen cannot be assumed as a basis for autoimmune pathologies.” Also, a linear amino acid sequence does not necessarily comport with the three‐dimensional (3D) nature of a protein molecule 189 . Peptide modeling (i.e., 3D structure), molecular docking analyses, and affinity estimation for human leukocyte antigens are emerging as critical strategies when studying the links of molecular mimicry in the development of autoimmunity 190 …”

Section: Discussionmentioning

confidence: 99%

“…189 Peptide modeling (i.e., 3D structure), molecular docking analyses, and affinity estimation for human leukocyte antigens are emerging as critical strategies when studying the links of molecular mimicry in the development of autoimmunity. 190 The IOM in its report on the Adverse Effects of Vaccines notes that sequence similarity is not sufficient to demonstrate causality, noting that "linear amino acid sequence homology or even similar conformational structure between an exogenous agent and a self-antigen alone are not sufficient to prove that molecular mimicry is the pathogenic mechanism for a disease. Many such homologies exist, and the vast majority of these are not associated with biologically relevant autoimmune phenomenon or actual human disease."…”

Section: Molecular Mimicrymentioning

confidence: 99%

Do vaccines cause epilepsy? Review of cases in the National Vaccine Injury Compensation Program

Scott,

Moshé,

Holmes

2023

Epilepsia

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ObjectiveThe National Childhood Vaccine Injury Act of 1986 created the National Vaccine Injury Compensation Program (VICP), a no‐fault alternative to the traditional tort system. Since 1988, the total compensation paid exceeds $5 billion. While epilepsy is one of the leading reasons for filing a claim, there has been no review of the process and validity of the legal outcomes given current medical information. The objectives were to review the evolution of the VICP program in regard to vaccine‐related epilepsy and assess the rationale behind decisions made by the court.MethodsPublicly available cases involving epilepsy claims in the VICP were searched through Westlaw and the United States Court of Federal Claims websites. All published reports were reviewed for petitioner's theories supporting vaccine‐induced epilepsy, respondent's counterarguments, the final decision regarding compensation and the rationale underlying these decisions. The primary goal was to determine which factors went into decisions regarding whether vaccines caused epilepsy.ResultsSince the first epilepsy case in 1989, there have been many changes in the program including the removal of residual seizure disorder as a vaccine‐related injury, publication of the Althen prongs, release of the acellular form of pertussis, and recognition that in genetic conditions the underlying genetic abnormality rather than the immunization causes epilepsy. We identified 532 unique cases with epilepsy: 105 with infantile spasms and 427 with epilepsy without infantile spasms. The petitioners’ experts often espoused outdated, erroneous causation theories that lacked an acceptable medical or scientific foundation and were frequently criticized by the court.SignificanceDespite the lack of epidemiological or mechanistic evidence indicating that childhood vaccines covered by the VICP result in or aggravate epilepsy, these cases continue to be adjudicated. After 35 years of intense litigation, it is time to reconsider whether epilepsy should continue to be a compensable vaccine‐induced injury.

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Molecular mimicry and autoimmunity in the time of COVID-19

Cited by 18 publications

References 263 publications

Case report: A case of anti-glycine receptor encephalomyelitis triggered by post-transplant or COVID-19 infection?

Case report: A case of anti-glycine receptor encephalomyelitis triggered by post-transplant or COVID-19 infection?

Central nervous system immune-related disorders after SARS-CoV-2 vaccination: a multicenter study

Do vaccines cause epilepsy? Review of cases in the National Vaccine Injury Compensation Program

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