Serum IgG against Simian Virus 40 antigens are hampered by high levels of sHLA-G in patients affected by inflammatory neurological diseases, as multiple sclerosis

Roberta Rizzo, Silvia Pietrobon, E. Mazzoni, Daria Bortolotti, Fernanda Martini, Massimiliano Castellazzi, I. Casetta, Enrico Fainardi, Dario Luca, E. Granieri, M. Tognon, Enrico Granieri, Massimiliano Castellazzi, I. Casetta, Maria Rosalia Tola, Franco Dallocchio, Tiziana Bellini, Antonella Rotola, D. Di Luca, Silvia SeraceniCarlo Contini, Silvia Sabbioni, Massimo Negrini, Mauro Tognon, T. Antonelli, Elisabetta Groppo, M. Gentile, Eleonora Baldi, Maria Luisa Caniatti, S. Ceruti, M. R. Manfrinato, Alessandro Trentini, D. Bortolotti, Elena Miotto, Manuela Ferracin, Elisa Mazzoni, S. Pietrobon, I. Masini, John Charles Rotondo, F. Martini, Agostino Baruzzi, R. Roberto D'Alessandro, Roberto Michelucci, Fabrizio Salvi, Sergio Stecchi, Cinzia Scandellari, G. Terzano, Franco Granella, P. Nichelli, Patrizia Sola, Diana Ferraro, F. Vitetta, Anna Maria Simone, R. Bedin, N. Marcello, L. Motti, S. Montepietra, D. Guidetti, Paolo Immovilli, Enrico Montanari, I. Pesci, A. Guareschi, G. Greco, M. Santangelo, A. M. Mauro, Susanna Malagù, Fabrizio Rasi, M. Spadoni, M. Galeotti, L. Fiorani, Walter Neri, A. Ravasio, M. Pasquinelli, S. Gutman, C. Monaldini

Research output: Contribution to journalArticle

Abstract

Background: Many investigators detected the simian polyomavirus SV40 footprints in human brain tumors and neurologic diseases and recently it has been indicated that SV40 seems to be associated with multiple sclerosis (MS) disease. Interestingly, SV40 interacts with human leukocyte antigen (HLA) class I molecules for cell entry. HLA class I antigens, in particular non-classical HLA-G molecules, characterized by an immune-regulatory function, are involved in MS disease, and the levels of these molecules are modified according with the disease status. Objective: We investigated in serum samples, from Italian patients affected by MS, other inflammatory diseases (OIND), non-inflammatory neurological diseases (NIND) and healthy subjects (HS), SV40-antibody and soluble sHLA-G and the association between SV40-prevalence and sHLA-G levels. Methods: ELISA tests were used for SV40-antibodies detection and sHLA-G quantitation in serum samples. Results: The presence of SV40 antibodies was observed in 6 % of patients affected by MS (N = 4/63), 10 % of OIND (N = 8/77) and 15 % of NIND (N = 9/59), which is suggestive of a lower prevalence in respect to HS (22 %, N = 18/83). MS patients are characterized by higher sHLA-G serum levels (13.9 ± 0.9 ng/ml; mean ± St. Error) in comparison with OIND (6.7 ± 0.8 ng/ml), NIND (2.9 ± 0.4 ng/ml) and HS (2.6 ± 0.7 ng/ml) subjects. Interestingly, we observed an inverse correlation between SV40 antibody prevalence and sHLA-G serum levels in MS patients. Conclusion: The data obtained showed a low prevalence of SV40 antibodies in MS patients. These results seems to be due to a generalized status of inability to counteract SV40 infection via antibody production. In particular, we hypothesize that SV40 immune-inhibitory direct effect and the presence of high levels of the immune-inhibitory HLA-G molecules could co-operate in impairing B lymphocyte activation towards SV40 specific peptides.

Original languageEnglish
Article number216
Pages (from-to)1-6
JournalJournal of Translational Medicine
Volume14
Issue number1
DOIs
Publication statusPublished - Jul 22 2016

Fingerprint

Simian virus 40
Viruses
Multiple Sclerosis
Immunoglobulin G
Antigens
Serum
HLA Antigens
Antibodies
Healthy Volunteers
Molecules
Nervous System Neoplasms
Polyomavirus
Histocompatibility Antigens Class I
Brain Diseases
Lymphocytes
Lymphocyte Activation
Nervous System Diseases
Brain Neoplasms
Antibody Formation
B-Lymphocytes

Keywords

  • HLA-G
  • Multiple sclerosis
  • SV40

ASJC Scopus subject areas

  • Medicine(all)
  • Biochemistry, Genetics and Molecular Biology(all)

Cite this

Serum IgG against Simian Virus 40 antigens are hampered by high levels of sHLA-G in patients affected by inflammatory neurological diseases, as multiple sclerosis. / Rizzo, Roberta; Pietrobon, Silvia; Mazzoni, E.; Bortolotti, Daria; Martini, Fernanda; Castellazzi, Massimiliano; Casetta, I.; Fainardi, Enrico; Luca, Dario; Granieri, E.; Tognon, M.; Granieri, Enrico; Castellazzi, Massimiliano; Casetta, I.; Tola, Maria Rosalia; Dallocchio, Franco; Bellini, Tiziana; Rotola, Antonella; Di Luca, D.; Seraceni, Silvia; Contini, Carlo; Sabbioni, Silvia; Negrini, Massimo; Tognon, Mauro; Antonelli, T.; Groppo, Elisabetta; Gentile, M.; Baldi, Eleonora; Caniatti, Maria Luisa; Ceruti, S.; Manfrinato, M. R.; Trentini, Alessandro; Bortolotti, D.; Miotto, Elena; Ferracin, Manuela; Mazzoni, Elisa; Pietrobon, S.; Masini, I.; Rotondo, John Charles; Martini, F.; Baruzzi, Agostino; Roberto D'Alessandro, R.; Michelucci, Roberto; Salvi, Fabrizio; Stecchi, Sergio; Scandellari, Cinzia; Terzano, G.; Granella, Franco; Nichelli, P.; Sola, Patrizia; Ferraro, Diana; Vitetta, F.; Simone, Anna Maria; Bedin, R.; Marcello, N.; Motti, L.; Montepietra, S.; Guidetti, D.; Immovilli, Paolo; Montanari, Enrico; Pesci, I.; Guareschi, A.; Greco, G.; Santangelo, M.; Mauro, A. M.; Malagù, Susanna; Rasi, Fabrizio; Spadoni, M.; Galeotti, M.; Fiorani, L.; Neri, Walter; Ravasio, A.; Pasquinelli, M.; Gutman, S.; Monaldini, C.

In: Journal of Translational Medicine, Vol. 14, No. 1, 216, 22.07.2016, p. 1-6.

Research output: Contribution to journalArticle

Rizzo, R, Pietrobon, S, Mazzoni, E, Bortolotti, D, Martini, F, Castellazzi, M, Casetta, I, Fainardi, E, Luca, D, Granieri, E, Tognon, M, Granieri, E, Castellazzi, M, Casetta, I, Tola, MR, Dallocchio, F, Bellini, T, Rotola, A, Di Luca, D, Seraceni, S, Contini, C, Sabbioni, S, Negrini, M, Tognon, M, Antonelli, T, Groppo, E, Gentile, M, Baldi, E, Caniatti, ML, Ceruti, S, Manfrinato, MR, Trentini, A, Bortolotti, D, Miotto, E, Ferracin, M, Mazzoni, E, Pietrobon, S, Masini, I, Rotondo, JC, Martini, F, Baruzzi, A, Roberto D'Alessandro, R, Michelucci, R, Salvi, F, Stecchi, S, Scandellari, C, Terzano, G, Granella, F, Nichelli, P, Sola, P, Ferraro, D, Vitetta, F, Simone, AM, Bedin, R, Marcello, N, Motti, L, Montepietra, S, Guidetti, D, Immovilli, P, Montanari, E, Pesci, I, Guareschi, A, Greco, G, Santangelo, M, Mauro, AM, Malagù, S, Rasi, F, Spadoni, M, Galeotti, M, Fiorani, L, Neri, W, Ravasio, A, Pasquinelli, M, Gutman, S & Monaldini, C 2016, 'Serum IgG against Simian Virus 40 antigens are hampered by high levels of sHLA-G in patients affected by inflammatory neurological diseases, as multiple sclerosis', Journal of Translational Medicine, vol. 14, no. 1, 216, pp. 1-6. https://doi.org/10.1186/s12967-016-0981-y
Rizzo, Roberta ; Pietrobon, Silvia ; Mazzoni, E. ; Bortolotti, Daria ; Martini, Fernanda ; Castellazzi, Massimiliano ; Casetta, I. ; Fainardi, Enrico ; Luca, Dario ; Granieri, E. ; Tognon, M. ; Granieri, Enrico ; Castellazzi, Massimiliano ; Casetta, I. ; Tola, Maria Rosalia ; Dallocchio, Franco ; Bellini, Tiziana ; Rotola, Antonella ; Di Luca, D. ; Seraceni, Silvia ; Contini, Carlo ; Sabbioni, Silvia ; Negrini, Massimo ; Tognon, Mauro ; Antonelli, T. ; Groppo, Elisabetta ; Gentile, M. ; Baldi, Eleonora ; Caniatti, Maria Luisa ; Ceruti, S. ; Manfrinato, M. R. ; Trentini, Alessandro ; Bortolotti, D. ; Miotto, Elena ; Ferracin, Manuela ; Mazzoni, Elisa ; Pietrobon, S. ; Masini, I. ; Rotondo, John Charles ; Martini, F. ; Baruzzi, Agostino ; Roberto D'Alessandro, R. ; Michelucci, Roberto ; Salvi, Fabrizio ; Stecchi, Sergio ; Scandellari, Cinzia ; Terzano, G. ; Granella, Franco ; Nichelli, P. ; Sola, Patrizia ; Ferraro, Diana ; Vitetta, F. ; Simone, Anna Maria ; Bedin, R. ; Marcello, N. ; Motti, L. ; Montepietra, S. ; Guidetti, D. ; Immovilli, Paolo ; Montanari, Enrico ; Pesci, I. ; Guareschi, A. ; Greco, G. ; Santangelo, M. ; Mauro, A. M. ; Malagù, Susanna ; Rasi, Fabrizio ; Spadoni, M. ; Galeotti, M. ; Fiorani, L. ; Neri, Walter ; Ravasio, A. ; Pasquinelli, M. ; Gutman, S. ; Monaldini, C. / Serum IgG against Simian Virus 40 antigens are hampered by high levels of sHLA-G in patients affected by inflammatory neurological diseases, as multiple sclerosis. In: Journal of Translational Medicine. 2016 ; Vol. 14, No. 1. pp. 1-6.
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abstract = "Background: Many investigators detected the simian polyomavirus SV40 footprints in human brain tumors and neurologic diseases and recently it has been indicated that SV40 seems to be associated with multiple sclerosis (MS) disease. Interestingly, SV40 interacts with human leukocyte antigen (HLA) class I molecules for cell entry. HLA class I antigens, in particular non-classical HLA-G molecules, characterized by an immune-regulatory function, are involved in MS disease, and the levels of these molecules are modified according with the disease status. Objective: We investigated in serum samples, from Italian patients affected by MS, other inflammatory diseases (OIND), non-inflammatory neurological diseases (NIND) and healthy subjects (HS), SV40-antibody and soluble sHLA-G and the association between SV40-prevalence and sHLA-G levels. Methods: ELISA tests were used for SV40-antibodies detection and sHLA-G quantitation in serum samples. Results: The presence of SV40 antibodies was observed in 6 {\%} of patients affected by MS (N = 4/63), 10 {\%} of OIND (N = 8/77) and 15 {\%} of NIND (N = 9/59), which is suggestive of a lower prevalence in respect to HS (22 {\%}, N = 18/83). MS patients are characterized by higher sHLA-G serum levels (13.9 ± 0.9 ng/ml; mean ± St. Error) in comparison with OIND (6.7 ± 0.8 ng/ml), NIND (2.9 ± 0.4 ng/ml) and HS (2.6 ± 0.7 ng/ml) subjects. Interestingly, we observed an inverse correlation between SV40 antibody prevalence and sHLA-G serum levels in MS patients. Conclusion: The data obtained showed a low prevalence of SV40 antibodies in MS patients. These results seems to be due to a generalized status of inability to counteract SV40 infection via antibody production. In particular, we hypothesize that SV40 immune-inhibitory direct effect and the presence of high levels of the immune-inhibitory HLA-G molecules could co-operate in impairing B lymphocyte activation towards SV40 specific peptides.",
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author = "Roberta Rizzo and Silvia Pietrobon and E. Mazzoni and Daria Bortolotti and Fernanda Martini and Massimiliano Castellazzi and I. Casetta and Enrico Fainardi and Dario Luca and E. Granieri and M. Tognon and Enrico Granieri and Massimiliano Castellazzi and I. Casetta and Tola, {Maria Rosalia} and Franco Dallocchio and Tiziana Bellini and Antonella Rotola and {Di Luca}, D. and Silvia Seraceni and Carlo Contini and Silvia Sabbioni and Massimo Negrini and Mauro Tognon and T. Antonelli and Elisabetta Groppo and M. Gentile and Eleonora Baldi and Caniatti, {Maria Luisa} and S. Ceruti and Manfrinato, {M. R.} and Alessandro Trentini and D. Bortolotti and Elena Miotto and Manuela Ferracin and Elisa Mazzoni and S. Pietrobon and I. Masini and Rotondo, {John Charles} and F. Martini and Agostino Baruzzi and {Roberto D'Alessandro}, R. and Roberto Michelucci and Fabrizio Salvi and Sergio Stecchi and Cinzia Scandellari and G. Terzano and Franco Granella and P. Nichelli and Patrizia Sola and Diana Ferraro and F. Vitetta and Simone, {Anna Maria} and R. Bedin and N. Marcello and L. Motti and S. Montepietra and D. Guidetti and Paolo Immovilli and Enrico Montanari and I. Pesci and A. Guareschi and G. Greco and M. Santangelo and Mauro, {A. M.} and Susanna Malag{\`u} and Fabrizio Rasi and M. Spadoni and M. Galeotti and L. Fiorani and Walter Neri and A. Ravasio and M. Pasquinelli and S. Gutman and C. Monaldini",
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TY - JOUR

T1 - Serum IgG against Simian Virus 40 antigens are hampered by high levels of sHLA-G in patients affected by inflammatory neurological diseases, as multiple sclerosis

AU - Rizzo, Roberta

AU - Pietrobon, Silvia

AU - Mazzoni, E.

AU - Bortolotti, Daria

AU - Martini, Fernanda

AU - Castellazzi, Massimiliano

AU - Casetta, I.

AU - Fainardi, Enrico

AU - Luca, Dario

AU - Granieri, E.

AU - Tognon, M.

AU - Granieri, Enrico

AU - Castellazzi, Massimiliano

AU - Casetta, I.

AU - Tola, Maria Rosalia

AU - Dallocchio, Franco

AU - Bellini, Tiziana

AU - Rotola, Antonella

AU - Di Luca, D.

AU - Seraceni, Silvia

AU - Contini, Carlo

AU - Sabbioni, Silvia

AU - Negrini, Massimo

AU - Tognon, Mauro

AU - Antonelli, T.

AU - Groppo, Elisabetta

AU - Gentile, M.

AU - Baldi, Eleonora

AU - Caniatti, Maria Luisa

AU - Ceruti, S.

AU - Manfrinato, M. R.

AU - Trentini, Alessandro

AU - Bortolotti, D.

AU - Miotto, Elena

AU - Ferracin, Manuela

AU - Mazzoni, Elisa

AU - Pietrobon, S.

AU - Masini, I.

AU - Rotondo, John Charles

AU - Martini, F.

AU - Baruzzi, Agostino

AU - Roberto D'Alessandro, R.

AU - Michelucci, Roberto

AU - Salvi, Fabrizio

AU - Stecchi, Sergio

AU - Scandellari, Cinzia

AU - Terzano, G.

AU - Granella, Franco

AU - Nichelli, P.

AU - Sola, Patrizia

AU - Ferraro, Diana

AU - Vitetta, F.

AU - Simone, Anna Maria

AU - Bedin, R.

AU - Marcello, N.

AU - Motti, L.

AU - Montepietra, S.

AU - Guidetti, D.

AU - Immovilli, Paolo

AU - Montanari, Enrico

AU - Pesci, I.

AU - Guareschi, A.

AU - Greco, G.

AU - Santangelo, M.

AU - Mauro, A. M.

AU - Malagù, Susanna

AU - Rasi, Fabrizio

AU - Spadoni, M.

AU - Galeotti, M.

AU - Fiorani, L.

AU - Neri, Walter

AU - Ravasio, A.

AU - Pasquinelli, M.

AU - Gutman, S.

AU - Monaldini, C.

PY - 2016/7/22

Y1 - 2016/7/22

N2 - Background: Many investigators detected the simian polyomavirus SV40 footprints in human brain tumors and neurologic diseases and recently it has been indicated that SV40 seems to be associated with multiple sclerosis (MS) disease. Interestingly, SV40 interacts with human leukocyte antigen (HLA) class I molecules for cell entry. HLA class I antigens, in particular non-classical HLA-G molecules, characterized by an immune-regulatory function, are involved in MS disease, and the levels of these molecules are modified according with the disease status. Objective: We investigated in serum samples, from Italian patients affected by MS, other inflammatory diseases (OIND), non-inflammatory neurological diseases (NIND) and healthy subjects (HS), SV40-antibody and soluble sHLA-G and the association between SV40-prevalence and sHLA-G levels. Methods: ELISA tests were used for SV40-antibodies detection and sHLA-G quantitation in serum samples. Results: The presence of SV40 antibodies was observed in 6 % of patients affected by MS (N = 4/63), 10 % of OIND (N = 8/77) and 15 % of NIND (N = 9/59), which is suggestive of a lower prevalence in respect to HS (22 %, N = 18/83). MS patients are characterized by higher sHLA-G serum levels (13.9 ± 0.9 ng/ml; mean ± St. Error) in comparison with OIND (6.7 ± 0.8 ng/ml), NIND (2.9 ± 0.4 ng/ml) and HS (2.6 ± 0.7 ng/ml) subjects. Interestingly, we observed an inverse correlation between SV40 antibody prevalence and sHLA-G serum levels in MS patients. Conclusion: The data obtained showed a low prevalence of SV40 antibodies in MS patients. These results seems to be due to a generalized status of inability to counteract SV40 infection via antibody production. In particular, we hypothesize that SV40 immune-inhibitory direct effect and the presence of high levels of the immune-inhibitory HLA-G molecules could co-operate in impairing B lymphocyte activation towards SV40 specific peptides.

AB - Background: Many investigators detected the simian polyomavirus SV40 footprints in human brain tumors and neurologic diseases and recently it has been indicated that SV40 seems to be associated with multiple sclerosis (MS) disease. Interestingly, SV40 interacts with human leukocyte antigen (HLA) class I molecules for cell entry. HLA class I antigens, in particular non-classical HLA-G molecules, characterized by an immune-regulatory function, are involved in MS disease, and the levels of these molecules are modified according with the disease status. Objective: We investigated in serum samples, from Italian patients affected by MS, other inflammatory diseases (OIND), non-inflammatory neurological diseases (NIND) and healthy subjects (HS), SV40-antibody and soluble sHLA-G and the association between SV40-prevalence and sHLA-G levels. Methods: ELISA tests were used for SV40-antibodies detection and sHLA-G quantitation in serum samples. Results: The presence of SV40 antibodies was observed in 6 % of patients affected by MS (N = 4/63), 10 % of OIND (N = 8/77) and 15 % of NIND (N = 9/59), which is suggestive of a lower prevalence in respect to HS (22 %, N = 18/83). MS patients are characterized by higher sHLA-G serum levels (13.9 ± 0.9 ng/ml; mean ± St. Error) in comparison with OIND (6.7 ± 0.8 ng/ml), NIND (2.9 ± 0.4 ng/ml) and HS (2.6 ± 0.7 ng/ml) subjects. Interestingly, we observed an inverse correlation between SV40 antibody prevalence and sHLA-G serum levels in MS patients. Conclusion: The data obtained showed a low prevalence of SV40 antibodies in MS patients. These results seems to be due to a generalized status of inability to counteract SV40 infection via antibody production. In particular, we hypothesize that SV40 immune-inhibitory direct effect and the presence of high levels of the immune-inhibitory HLA-G molecules could co-operate in impairing B lymphocyte activation towards SV40 specific peptides.

KW - HLA-G

KW - Multiple sclerosis

KW - SV40

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