Shared pathogenicity features and sequences between EBV, SARS-CoV-2, and HLA class I molecule-binding motifs with a potential role in autoimmunity

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dc.authorid0000-0002-7919-1326
dc.contributor.authorAdıgüzel, Yekbun
dc.contributor.authorMahroum, Naim
dc.contributor.authorMuller, Sylviane
dc.contributor.authorBlank, Miri
dc.contributor.authorHalpert, Gilad
dc.contributor.authorShoenfeld, Yehuda
dc.date.accessioned2023-10-23T09:26:48Z
dc.date.available2023-10-23T09:26:48Z
dc.date.issued2023
dc.departmentİstanbul Medipol Üniversitesi, Uluslararası Tıp Fakültesi, Dahili Tıp Bilimleri Bölümü, İç Hastalıkları Ana Bilim Dalı
dc.description.abstractEpstein-Barr virus (EBV) and severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) are extraordinary in their ability to activate autoimmunity as well as to induce diverse autoimmune diseases. Here we reviewed the current knowledge on their relation. Further, we suggested that molecular mimicry could be a possible common mechanism of autoimmunity induction in the susceptible individuals infected with SARS-CoV-2. Molecular mimicry between SARS-CoV-2 and human proteins, and EBV and human proteins, are present. Besides, relation of the pathogenicity associated with both coronavirus diseases and EBV supports the notion. As a proof-of-the-concept, we investigated 8mer sequences with shared 5mers of SARS-CoV-2, EBV, and human proteins, which were predicted as epitopes binding to the same human leukocyte antigen (HLA) supertype representatives. We identified significant number of human peptide sequences with predicted-affinities to the HLA-A*02:01 allele. Rest of the peptide sequences had predicted-affinities to the HLA-A*02:01, HLA-B*40:01, HLA-B*27:05, HLA-A*01:01, and HLA-B*39:01 alleles. Carriers of these serotypes can be under a higher risk of autoimmune response induction upon getting infected, through molecular mimicry-based mechanisms common to SARS-CoV-2 and EBV infections. We additionally reviewed established associations of the identified proteins with the EBV-related pathogenicity and with the autoimmune diseases.
dc.identifier.citationAdıgüzel, Y., Mahroum, N., Muller, S., Blank, M., Halpert, G. ve Shoenfeld, Y. (2023). Shared pathogenicity features and sequences between EBV, SARS-CoV-2, and HLA class I molecule-binding motifs with a potential role in autoimmunity. Clinical Reviews in Allergy and Immunology, 65(2), 206-230. https://doi.org/10.1007/s12016-023-08962-4
dc.identifier.doi10.1007/s12016-023-08962-4
dc.identifier.endpage230
dc.identifier.issn1080-0549
dc.identifier.issn1559-0267
dc.identifier.issue2
dc.identifier.pmid37505416
dc.identifier.scopus2-s2.0-85173238253
dc.identifier.scopusqualityQ1
dc.identifier.startpage206
dc.identifier.urihttps://doi.org/10.1007/s12016-023-08962-4
dc.identifier.urihttps://hdl.handle.net/20.500.12511/11624
dc.identifier.volume65
dc.identifier.wos001037533500001en_US
dc.identifier.wosqualityQ1
dc.indekslendigikaynakWeb of Science
dc.indekslendigikaynakScopus
dc.indekslendigikaynakPubMed
dc.institutionauthorMahroum, Naim
dc.language.isoen
dc.publisherSpringer
dc.relation.ispartofClinical Reviews in Allergy and Immunologyen_US
dc.relation.publicationcategoryDiğer
dc.rightsinfo:eu-repo/semantics/embargoedAccess
dc.subjectCOVID-19
dc.subjectPost-COVID
dc.subjectAutoimmune Disease
dc.subjectMHC
dc.subjectInfectious Molecular Mimicry
dc.titleShared pathogenicity features and sequences between EBV, SARS-CoV-2, and HLA class I molecule-binding motifs with a potential role in autoimmunity
dc.typeReview Article

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