Vitamin D serum levels and viral load of human herpesvirus 6 and Epstein-Barr virus in patients with multiple sclerosis after one year of follow-up
ECTRIMS Online Library. Alvarez-Lafuente R. 10/27/17; 200662; P1007
Roberto Alvarez-Lafuente
Roberto Alvarez-Lafuente
Contributions
Abstract

Abstract: P1007

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - 17 Environmental factors

Background: Low levels of 25-hydroxyvitamin D (25-(OH)D2) have been described as one of the possible environmental factors involved in multiple sclerosis (MS) etiopathogenesis. In addition, Epstein-Barr virus (EBV) and human herpesvirus 6 (HHV-6) infection have also been proposed as MS triggers. A possible effect of vitamin D levels on viral status have been suggested.
Objectives: To analyse the replication/reactivation of EBV and HHV-6 in MS patients regarding the serum levels of 25-(OH)D2, in order to investigate the possible relationship between vitamin D levels and viral status.
Methods: 200 MS patients were included in this retrospective longitudinal study of one year follow-up. For each one of the patients, two peripheral blood and serum samples were collected, in such a way that data were obtained from both semesters of the year. DNA was extracted from blood in order to analyse EBV and HHV-6 viral load in peripheral blood cells by quantitative real-time PCR. 25-(OH)D2 was determined using a delayed one step chemiluminiscent microparticle immunoassay (Abbott) from serum samples.
Results: The median value for 25-(OH)D2 in the first semester of the year among the MS patients included in the study was 17.5 ng/ml (ranging between 15.5 ng/ml in March and 19.3 ng/ml in June); the median value for 25-(OH)D2 in the second semester of the year was 24.6 ng/ml (ranging between 19.6 ng/ml in December and 28.4 ng/ml in September). In the first semester of the year, 22% of MS patients were positive by qPCR for EBV when 25-(OH)D2< 11 ng/ml, and only just 4% were positive when 25-(OH)D2>20 ng/ml (p=0.03). In addition, EBV viral load was higher in those MS patients with lower 25-(OH)D2 levels, compared to those with levels above 20 ng/ml (p=0.04). For HHV-6, there were no differences between MS patients with high and low 25-(OH)D2 levels. Moreover, no differences were found in the second semester of the year, neither for EBV nor HHV-6, when 25-(OH)D2 levels were higher and only 28.4% of the samples had levels < 20 ng/ml in comparison with the 64.3% in the first semester of the year.
Conclusions: Vitamin D levels could be involved in the regulation of the replication/reactivation of EBV in peripheral blood cells of MS patients; moreover, viral load seems to be higher when 25-(OH)D2 levels in serum are low. Further studies, also in healthy controls, are required.
Disclosure:
M.I. Dominguez-Mozo: nothing to disclose.
S. Perez-Perez: nothing to disclose.
M.A. Garcia-Martinez: nothing to disclose.
I. Ortega-Madueño: nothing to disclose.
M.J. Torrejón: nothing to disclose.
R. Arroyo: received honoraria for speaking and participating as investigators in clinical trials and non-financial support from Merck-Serono, Teva, Sanofi-Aventis, Genzyme, Novartis, Biogen Idec, Roche and Bayer-Schering.
R. Alvarez-Lafuente: Reports grants and personal fees from Merck Serono, personal fees and non-financial support from Biogen IDEC, grants, personal fees and non-financial support from Novartis Pharmaceuticals S.A., grants and personal fees from Genzyme, non-financial support from TEVA Pharma, S.L., non-financial support from Roche.

Abstract: P1007

Type: Poster

Abstract Category: Pathology and pathogenesis of MS - 17 Environmental factors

Background: Low levels of 25-hydroxyvitamin D (25-(OH)D2) have been described as one of the possible environmental factors involved in multiple sclerosis (MS) etiopathogenesis. In addition, Epstein-Barr virus (EBV) and human herpesvirus 6 (HHV-6) infection have also been proposed as MS triggers. A possible effect of vitamin D levels on viral status have been suggested.
Objectives: To analyse the replication/reactivation of EBV and HHV-6 in MS patients regarding the serum levels of 25-(OH)D2, in order to investigate the possible relationship between vitamin D levels and viral status.
Methods: 200 MS patients were included in this retrospective longitudinal study of one year follow-up. For each one of the patients, two peripheral blood and serum samples were collected, in such a way that data were obtained from both semesters of the year. DNA was extracted from blood in order to analyse EBV and HHV-6 viral load in peripheral blood cells by quantitative real-time PCR. 25-(OH)D2 was determined using a delayed one step chemiluminiscent microparticle immunoassay (Abbott) from serum samples.
Results: The median value for 25-(OH)D2 in the first semester of the year among the MS patients included in the study was 17.5 ng/ml (ranging between 15.5 ng/ml in March and 19.3 ng/ml in June); the median value for 25-(OH)D2 in the second semester of the year was 24.6 ng/ml (ranging between 19.6 ng/ml in December and 28.4 ng/ml in September). In the first semester of the year, 22% of MS patients were positive by qPCR for EBV when 25-(OH)D2< 11 ng/ml, and only just 4% were positive when 25-(OH)D2>20 ng/ml (p=0.03). In addition, EBV viral load was higher in those MS patients with lower 25-(OH)D2 levels, compared to those with levels above 20 ng/ml (p=0.04). For HHV-6, there were no differences between MS patients with high and low 25-(OH)D2 levels. Moreover, no differences were found in the second semester of the year, neither for EBV nor HHV-6, when 25-(OH)D2 levels were higher and only 28.4% of the samples had levels < 20 ng/ml in comparison with the 64.3% in the first semester of the year.
Conclusions: Vitamin D levels could be involved in the regulation of the replication/reactivation of EBV in peripheral blood cells of MS patients; moreover, viral load seems to be higher when 25-(OH)D2 levels in serum are low. Further studies, also in healthy controls, are required.
Disclosure:
M.I. Dominguez-Mozo: nothing to disclose.
S. Perez-Perez: nothing to disclose.
M.A. Garcia-Martinez: nothing to disclose.
I. Ortega-Madueño: nothing to disclose.
M.J. Torrejón: nothing to disclose.
R. Arroyo: received honoraria for speaking and participating as investigators in clinical trials and non-financial support from Merck-Serono, Teva, Sanofi-Aventis, Genzyme, Novartis, Biogen Idec, Roche and Bayer-Schering.
R. Alvarez-Lafuente: Reports grants and personal fees from Merck Serono, personal fees and non-financial support from Biogen IDEC, grants, personal fees and non-financial support from Novartis Pharmaceuticals S.A., grants and personal fees from Genzyme, non-financial support from TEVA Pharma, S.L., non-financial support from Roche.

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