Specific antibodies reacting to JC polyomavirus capsid protein mimotopes in sera from multiple sclerosis and other neurological diseases‐affected patients

• Published in: Journal of cellular physiology Vol. 235; no. 7-8; pp. 5847 - 5855
• Main Authors: Mazzoni, Elisa, Bononi, Ilaria, Pietrobon, Silvia, Torreggiani, Elena, Rossini, Marika, Pugliatti, Maura, Casetta, Ilaria, Castellazzi, Massimiliano, Granieri, Enrico, Guerra, Giovanni, Martini, Fernanda, Tognon, Mauro
• Format: Journal Article
• Language: English
• Published: United States Wiley Subscription Services, Inc 01.07.2020
• Subjects: Adult; Aged; Antibodies - immunology; antibody; Antibody Specificity - immunology; Antigens; Autoimmune diseases; BK Virus - immunology; BK Virus - pathogenicity; Capsid protein; Capsid Proteins - genetics; Capsid Proteins - immunology; Epitopes; Epitopes - genetics; Epitopes - immunology; Female; Humans; IgG antibody; Immunoglobulin G; Immunoglobulins; JC Virus - immunology; JC Virus - pathogenicity; JCPyV; Male; Middle Aged; Mimicry; Multiple sclerosis; Multiple Sclerosis - genetics; Multiple Sclerosis - immunology; Multiple Sclerosis - virology; Nervous System Diseases - genetics; Nervous System Diseases - immunology; Nervous System Diseases - virology; Neurological diseases; Peptides; prevalence; Proteins; serum; Simian virus 40 - immunology; Simian virus 40 - pathogenicity; Synthetic peptides; titer; Virus Diseases - genetics; Virus Diseases - immunology; Virus Diseases - pathology; Virus Diseases - virology; Viruses; VP1 protein; titer; prevalence; antibody; serum; JCPyV; multiple sclerosis
• ISSN: 0021-9541; 1097-4652; 1097-4652
• DOI: 10.1002/jcp.29533

Published data support the hypothesis that viruses could be trigger agents of multiple sclerosis onset. This link is based on evidence of early exposure to viral agents in patients affected by this neurologic disease. JC (JC polyomavirus [JCPyV]), BK (BKPyV), and simian virus 40 (SV40) neurotropic polyomavirus footprints have been detected in brain tissue specimens and samples from patients affected by different neurological diseases. In this investigation, serum samples from patients affected by multiple sclerosis and other inflammatory and noninflammatory neurologic diseases, as well as healthy subjects representing the control, were investigated for immunoglobulin G (IgG) antibodies against JCPyV. To this end, an immunologic approach was employed, which consists of employing indirect enzyme‐linked immunosorbent assay testing with synthetic peptides mimicking viral capsid protein 1 antigens. A significantly lower prevalence of IgG antibodies against JCPyV VP1 epitopes, with a low titer, was detected in serum samples from patients with multiple sclerosis (MS) and other neurologic diseases than in healthy subjects. Our study indicates that the prevalence of JCPyV antibodies from patients with multiple sclerosis is 50% lower than in healthy subjects, suggesting specific immune impairments. These results indicate that patients affected by neurological diseases, including MS, respond poorly to JCPyV VP1 antigens, suggesting specific immunologic dysfunctions. A significantly lower prevalence of immunoglobulin G (IgG) antibodies against JC polyomavirus (JCPyV) VP1 epitopes, with a low titer, was detected in serum samples from patients with multiple sclerosis (MS) and other neurological diseases than in healthy subjects (HS). Our study indicates that the prevalence of JCPyV antibodies from patients with MS is 50% lower than in HS, suggesting specific immune impairments. These results indicate that patients affected by neurological diseases, including multiple sclerosis, respond poorly to JCPyV VP1 antigens, suggesting specific immunologic dysfunctions. Please enlarge this figure three times otherwise it cannot be see/read