Molecular Mimicry between Meningococcal B Factor H-Binding Protein and Human Proteins

Abstract

This study calls attention on molecular mimicry and the consequent autoimmune cross reactivity as the molecular mechanism that can cause adverse events following meningococcal B vaccination and warns against active immunizations based on entire antigen.

Keywords

molecular mimicry / Trumenba vaccine / factor H-binding protein / human proteome / adverse events

References

[1] Hollingshead S, Tang CM. An overview of Neisseria meningitidis . Methods Mol Biol 2019; 1969: 1-16

[2] Biolchi A, Tomei S, Brunelli B. et al. 4CMenB immunization induces serum bactericidal antibodies against non-serogroup B meningococcal strains in adolescents. Infect Dis Ther 2021; 10(01) 307-316

[3] Seib KL, Scarselli M, Comanducci M, Toneatto D, Masignani V. Neisseria meningitidis factor H-binding protein fHbp: a key virulence factor and vaccine antigen. Expert Rev Vaccines 2015; 14(06) 841-859

[4] FDA. Accessed October 30, 2023 at: https://www.fda.gov/media/89936/download

[5] Kanduc D. Molecular mimicry between respiratory syncytial virus F antigen and the human proteome. Glob Med Genet 2023; 10(01) 19-21

[6] Kanduc D. Exposure to SARS-CoV-2 and infantile diseases. Glob Med Genet 2023; 10(02) 72-78

[7] Kanduc D. Homology, similarity, and identity in peptide epitope immunodefinition. J Pept Sci 2012; 18(08) 487-494

[8] Kanduc D. Pentapeptides as minimal functional units in cell biology and immunology. Curr Protein Pept Sci 2013; 14(02) 111-120

[9] Kanduc D. Hydrophobicity and the physico-chemical basis of immunotolerance. Pathobiology 2020; 87(04) 268-276

[10] Kanduc D. The role of proteomics in defining autoimmunity. Expert Rev Proteomics 2021; 18(03) 177-184

[11] UniProt Consortium. UniProt: a worldwide hub of protein knowledge. Nucleic Acids Res 2019; 47(D1): D506-D515

[12] Izumikawa T, Saigoh K, Shimizu J, Tsuji S, Kusunoki S, Kitagawa H. A chondroitin synthase-1 (ChSy-1) missense mutation in a patient with neuropathy impairs the elongation of chondroitin sulfate chains initiated by chondroitin N-acetylgalactosaminyltransferase-1. Biochim Biophys Acta 2013; 1830(10) 4806-4812

[13] Bronstein JM, Tiwari-Woodruff S, Buznikov AG, Stevens DB. Involvement of OSP/claudin-11 in oligodendrocyte membrane interactions: role in biology and disease. J Neurosci Res 2000; 59(06) 706-711

[14] Wu L, Peng J, Ma Y. et al. Leukodystrophy associated with mitochondrial complex I deficiency due to a novel mutation in the NDUFAF1 gene. Mitochondrial DNA A DNA Mapp Seq Anal 2016; 27(02) 1034-1037

[15] Vallat JM, Nizon M, Magee A. et al. Contactin-associated protein 1 (CNTNAP1) mutations induce characteristic lesions of the paranodal region. J Neuropathol Exp Neurol 2016; 75(12) 1155-1159

[16] Coutelier M, Goizet C, Durr A. et al. Alteration of ornithine metabolism leads to dominant and recessive hereditary spastic paraplegia. Brain 2015; 138(Pt 8): 2191-2205

[17] Bao X, Wu Y, Wong LJ. et al. Alpers syndrome with prominent white matter changes. Brain Dev 2008; 30(04) 295-300

[18] Synofzik M, Haack TB, Kopajtich R. et al. Absence of BiP co-chaperone DNAJC3 causes diabetes mellitus and multisystemic neurodegeneration. Am J Hum Genet 2014; 95(06) 689-697

[19] Edvardson S, Cinnamon Y, Jalas C. et al. Hereditary sensory autonomic neuropathy caused by a mutation in dystonin. Ann Neurol 2012; 71(04) 569-572

[20] Guernsey DL, Jiang H, Bedard K. et al. Mutation in the gene encoding ubiquitin ligase LRSAM1 in patients with Charcot-Marie-Tooth disease. PLoS Genet 2010; 6(08) e1001081

[21] Stendel C, Roos A, Deconinck T. et al. Peripheral nerve demyelination caused by a mutant Rho GTPase guanine nucleotide exchange factor, Frabin/FGD4. Am J Hum Genet 2007; 81(01) 158-164

[22] Meretoja J. Genetic aspects of familial amyloidosis with corneal lattice dystrophy and cranial neuropathy. Clin Genet 1973; 4(03) 173-185

[23] Soong BW, Huang YH, Tsai PC. et al. Exome sequencing identifies GNB4 mutations as a cause of dominant intermediate Charcot-Marie-Tooth disease. Am J Hum Genet 2013; 92(03) 422-430

[24] Patton BL. Laminins of the neuromuscular system. Microsc Res Tech 2000; 51(03) 247-261

[25] Tingaud-Sequeira A, Raldúa D, Lavie J. et al. Functional validation of ABHD12 mutations in the neurodegenerative disease PHARC. Neurobiol Dis 2017; 98: 36-51

[26] Ruskamo S, Nieminen T, Kristiansen CK. et al. Molecular mechanisms of Charcot-Marie-Tooth neuropathy linked to mutations in human myelin protein P2. Sci Rep 2017; 7(01) 6510

[27] Moldovan M, Alvarez S, Pinchenko V. et al. Na(v)1.8 channelopathy in mutant mice deficient for myelin protein zero is detrimental to motor axons. Brain 2011; 134(Pt 2): 585-601

[28] Rosenbaum T, Kim HA, Boissy YL, Ling B, Ratner N. Neurofibromin, the neurofibromatosis type 1 Ras-GAP, is required for appropriate P0 expression and myelination. Ann N Y Acad Sci 1999; 883: 203-214

[29] McFerrin J, Patton BL, Sunderhaus ER, Kretzschmar D. NTE/PNPLA6 is expressed in mature Schwann cells and is required for glial ensheathment of Remak fibers. Glia 2017; 65(05) 804-816

[30] Duarri A, Jezierska J, Fokkens M. et al. Mutations in potassium channel kcnd3 cause spinocerebellar ataxia type 19. Ann Neurol 2012; 72(06) 870-880

[31] Raffaele Di Barletta M, Ricci E, Galluzzi G. et al. Different mutations in the LMNA gene cause autosomal dominant and autosomal recessive Emery-Dreifuss muscular dystrophy. Am J Hum Genet 2000; 66(04) 1407-1412

[32] Chen YZ, Hashemi SH, Anderson SK. et al. Senataxin, the yeast Sen1p orthologue: characterization of a unique protein in which recessive mutations cause ataxia and dominant mutations cause motor neuron disease. Neurobiol Dis 2006; 23(01) 97-108

[33] Huck JH, Verhoeven NM, Struys EA, Salomons GS, Jakobs C, van der Knaap MS. Ribose-5-phosphate isomerase deficiency: new inborn error in the pentose phosphate pathway associated with a slowly progressive leukoencephalopathy. Am J Hum Genet 2004; 74(04) 745-751

[34] Varon R, Gooding R, Steglich C. et al. Partial deficiency of the C-terminal-domain phosphatase of RNA polymerase II is associated with congenital cataracts facial dysmorphism neuropathy syndrome. Nat Genet 2003; 35(02) 185-189

[35] Breckpot J, Takiyama Y, Thienpont B. et al. A novel genomic disorder: a deletion of the SACS gene leading to spastic ataxia of Charlevoix-Saguenay. Eur J Hum Genet 2008; 16(09) 1050-1054

[36] Dijkmans TF, van Hooijdonk LW, Fitzsimons CP, Vreugdenhil E. The doublecortin gene family and disorders of neuronal structure. Cent Nerv Syst Agents Med Chem 2010; 10(01) 32-46

[37] Boonsimma P, Michael Gasser M, Netbaramee W. et al. Mutational and phenotypic expansion of ATP1A3-related disorders: report of nine cases. Gene 2020; 749: 144709

[38] Howard HC, Mount DB, Rochefort D. et al. The K-Cl cotransporter KCC3 is mutant in a severe peripheral neuropathy associated with agenesis of the corpus callosum. Nat Genet 2002; 32(03) 384-392

[39] Abrams AJ, Hufnagel RB, Rebelo A. et al. Mutations in SLC25A46, encoding a UGO1-like protein, cause an optic atrophy spectrum disorder. Nat Genet 2015; 47(08) 926-932

[40] Holzerova E, Danhauser K, Haack TB. et al. Human thioredoxin 2 deficiency impairs mitochondrial redox homeostasis and causes early-onset neurodegeneration. Brain 2016; 139(Pt 2): 346-354

[41] Nishino I, Spinazzola A, Hirano M. Thymidine phosphorylase gene mutations in MNGIE, a human mitochondrial disorder. Science 1999; 283(5402): 689-692

[42] Ibdah JA, Tein I, Dionisi-Vici C. et al. Mild trifunctional protein deficiency is associated with progressive neuropathy and myopathy and suggests a novel genotype-phenotype correlation. J Clin Invest 1998; 102(06) 1193-1199

[43] Strom TM, Hörtnagel K, Hofmann S. et al. Diabetes insipidus, diabetes mellitus, optic atrophy and deafness (DIDMOAD) caused by mutations in a novel gene (wolframin) coding for a predicted transmembrane protein. Hum Mol Genet 1998; 7(13) 2021-2028

[44] Palmer EE, Kumar R, Gordon CT. et al; DDD Study. A recurrent de novo nonsense variant in ZSWIM6 results in severe intellectual disability without frontonasal or limb malformations. Am J Hum Genet 2017; 101(06) 995-1005

[45] Sheikh KA, Sun J, Liu Y. et al. Mice lacking complex gangliosides develop Wallerian degeneration and myelination defects. Proc Natl Acad Sci U S A 1999; 96(13) 7532-7537

RIGHTS & PERMISSIONS

2023 Global Medical Genetics