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, Elisa Mazzoni, Daria Bortolotti, Fernanda Martini, Massimiliano Castellazzi, Ilaria Casetta, Enrico Fainardi, Dario Luca, Enrico Granieri, Mauro Tognon, E. Granieri, M. Castellazzi, I. Casetta, M. R. Tola, E. Fainardi, F. Dallocchio, T. Bellini, R. Rizzo, A. RotolaD. Di Luca, S. Seraceni, C. Contini, S. Sabbioni, M. Negrini, M. Tognon, T. Antonelli, E. Groppo, M. Gentile, E. Baldi, M. L. Caniatti, S. Ceruti, M. R. Manfrinato, A. Trentini, D. Bortolotti, E. Miotto, M. Ferracin, E. Mazzoni, S. Pietrobon, I. Masini, J. C. Rotondo, F. Martini, A. Baruzzi, R. Roberto D'Alessandro, R. Michelucci, F. Salvi, S. Stecchi, C. Scandellari, G. Terzano, F. Granella, P. Nichelli, P. Sola, D. Ferraro, F. Vitetta, A. M. Simone, R. Bedin, N. Marcello, L. Motti, S. Montepietra, D. Guidetti, P. Immovilli, E. Montanari, I. Pesci, A. Guareschi, G. Greco, M. Santangelo, A. M. Mauro, S. Malagù, F. Rasi, M. Spadoni, M. Galeotti, L. Fiorani, W. Neri, A. Ravasio, M. Pasquinelli, S. Gutman, C. Monaldini

Research output: Contribution to journalArticle

4 Citations (Scopus)

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
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, Elisa; Bortolotti, Daria; Martini, Fernanda; Castellazzi, Massimiliano; Casetta, Ilaria; Fainardi, Enrico; Luca, Dario; Granieri, Enrico; Tognon, Mauro; Granieri, E.; Castellazzi, M.; Casetta, I.; Tola, M. R.; Fainardi, E.; Dallocchio, F.; Bellini, T.; Rizzo, R.; Rotola, A.; Di Luca, D.; Seraceni, S.; Contini, C.; Sabbioni, S.; Negrini, M.; Tognon, M.; Antonelli, T.; Groppo, E.; Gentile, M.; Baldi, E.; Caniatti, M. L.; Ceruti, S.; Manfrinato, M. R.; Trentini, A.; Bortolotti, D.; Miotto, E.; Ferracin, M.; Mazzoni, E.; Pietrobon, S.; Masini, I.; Rotondo, J. C.; 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, A. M.; Bedin, R.; Marcello, N.; Motti, L.; Montepietra, S.; Guidetti, D.; Immovilli, P.; Montanari, E.; Pesci, I.; Guareschi, A.; Greco, G.; Santangelo, M.; Mauro, A. M.; Malagù, S.; Rasi, F.; Spadoni, M.; Galeotti, M.; Fiorani, L.; Neri, W.; Ravasio, A.; Pasquinelli, M.; Gutman, S.; Monaldini, C.

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

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, Fainardi, E, Dallocchio, F, Bellini, T, Rizzo, R, 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. https://doi.org/10.1186/s12967-016-0981-y
Rizzo, Roberta ; Pietrobon, Silvia ; Mazzoni, Elisa ; Bortolotti, Daria ; Martini, Fernanda ; Castellazzi, Massimiliano ; Casetta, Ilaria ; Fainardi, Enrico ; Luca, Dario ; Granieri, Enrico ; Tognon, Mauro ; Granieri, E. ; Castellazzi, M. ; Casetta, I. ; Tola, M. R. ; Fainardi, E. ; Dallocchio, F. ; Bellini, T. ; Rizzo, R. ; Rotola, A. ; Di Luca, D. ; Seraceni, S. ; Contini, C. ; Sabbioni, S. ; Negrini, M. ; Tognon, M. ; Antonelli, T. ; Groppo, E. ; Gentile, M. ; Baldi, E. ; Caniatti, M. L. ; Ceruti, S. ; Manfrinato, M. R. ; Trentini, A. ; Bortolotti, D. ; Miotto, E. ; Ferracin, M. ; Mazzoni, E. ; Pietrobon, S. ; Masini, I. ; Rotondo, J. C. ; 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, A. M. ; Bedin, R. ; Marcello, N. ; Motti, L. ; Montepietra, S. ; Guidetti, D. ; Immovilli, P. ; Montanari, E. ; Pesci, I. ; Guareschi, A. ; Greco, G. ; Santangelo, M. ; Mauro, A. M. ; Malagù, S. ; Rasi, F. ; Spadoni, M. ; Galeotti, M. ; Fiorani, L. ; Neri, W. ; 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.
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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 Elisa Mazzoni and Daria Bortolotti and Fernanda Martini and Massimiliano Castellazzi and Ilaria Casetta and Enrico Fainardi and Dario Luca and Enrico Granieri and Mauro Tognon and E. Granieri and M. Castellazzi and I. Casetta and Tola, {M. R.} and E. Fainardi and F. Dallocchio and T. Bellini and R. Rizzo and A. Rotola and {Di Luca}, D. and S. Seraceni and C. Contini and S. Sabbioni and M. Negrini and M. Tognon and T. Antonelli and E. Groppo and M. Gentile and E. Baldi and Caniatti, {M. L.} and S. Ceruti and Manfrinato, {M. R.} and A. Trentini and D. Bortolotti and E. Miotto and M. Ferracin and E. Mazzoni and S. Pietrobon and I. Masini and Rotondo, {J. C.} and F. Martini and A. Baruzzi and {Roberto D'Alessandro}, R. and R. Michelucci and F. Salvi and S. Stecchi and C. Scandellari and G. Terzano and F. Granella and P. Nichelli and P. Sola and D. Ferraro and F. Vitetta and Simone, {A. M.} and R. Bedin and N. Marcello and L. Motti and S. Montepietra and D. Guidetti and P. Immovilli and E. Montanari and I. Pesci and A. Guareschi and G. Greco and M. Santangelo and Mauro, {A. M.} and S. Malag{\`u} and F. Rasi and M. Spadoni and M. Galeotti and L. Fiorani and W. 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, Elisa

AU - Bortolotti, Daria

AU - Martini, Fernanda

AU - Castellazzi, Massimiliano

AU - Casetta, Ilaria

AU - Fainardi, Enrico

AU - Luca, Dario

AU - Granieri, Enrico

AU - Tognon, Mauro

AU - Granieri, E.

AU - Castellazzi, M.

AU - Casetta, I.

AU - Tola, M. R.

AU - Fainardi, E.

AU - Dallocchio, F.

AU - Bellini, T.

AU - Rizzo, R.

AU - Rotola, A.

AU - Di Luca, D.

AU - Seraceni, S.

AU - Contini, C.

AU - Sabbioni, S.

AU - Negrini, M.

AU - Tognon, M.

AU - Antonelli, T.

AU - Groppo, E.

AU - Gentile, M.

AU - Baldi, E.

AU - Caniatti, M. L.

AU - Ceruti, S.

AU - Manfrinato, M. R.

AU - Trentini, A.

AU - Bortolotti, D.

AU - Miotto, E.

AU - Ferracin, M.

AU - Mazzoni, E.

AU - Pietrobon, S.

AU - Masini, I.

AU - Rotondo, J. C.

AU - Martini, F.

AU - Baruzzi, A.

AU - Roberto D'Alessandro, R.

AU - Michelucci, R.

AU - Salvi, F.

AU - Stecchi, S.

AU - Scandellari, C.

AU - Terzano, G.

AU - Granella, F.

AU - Nichelli, P.

AU - Sola, P.

AU - Ferraro, D.

AU - Vitetta, F.

AU - Simone, A. M.

AU - Bedin, R.

AU - Marcello, N.

AU - Motti, L.

AU - Montepietra, S.

AU - Guidetti, D.

AU - Immovilli, P.

AU - Montanari, E.

AU - Pesci, I.

AU - Guareschi, A.

AU - Greco, G.

AU - Santangelo, M.

AU - Mauro, A. M.

AU - Malagù, S.

AU - Rasi, F.

AU - Spadoni, M.

AU - Galeotti, M.

AU - Fiorani, L.

AU - Neri, W.

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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