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Gene-environment interactions between HLA B7/A2, EBV antibodies are associated with MRI injury in multiple sclerosis.
J Neuroimmunol. 2009 Apr 30; 209(1-2):123-30.JN

Abstract

PURPOSE

To determine the role of gene-environmental interactions between the Class I and Class II HLA alleles and the humoral anti-Epstein-Barr Virus (EBV) responses in the development of brain injury and clinical disability in multiple sclerosis (MS) patients.

METHODS

A total of 93 MS patients (62 females; 31 males) and 122 healthy controls underwent HLA typing and testing for antibodies against EBV. The MS patients underwent brain MRI and quantitative measurements of T1- and T2-lesion volumes (LVs) and brain parenchymal fraction (BPF) were obtained. There were 54 MS cases that underwent MRI and EBV-antibody assessments at the 3-year follow-up. The anti-EBV panel included measurements of the levels of anti-EBV early antigen (EA) IgG, anti-EBV nuclear antigen (EBNA) IgG and anti-EBV viral capsid antigen (VCA) IgM and anti-EBV VCA IgG. The relationships between HLA alleles, anti-EBV antibody levels, MRI and clinical parameters were assessed in regression analysis.

RESULTS

The presence of HLA B7 was associated with increased T1-LV and trends indicating increased anti-EBV VCA IgG levels, higher disability (EDSS) and more destructive MRI parameters (increased T2-LV and decreased BPF). The presence of HLA A2 was associated with lower EDSS and a trend toward decreased anti-EBV VCA IgG levels; the associations with MRI variables were not significant. The HLA B7-A2 haplotype was significantly associated with higher T2-LV and T1-LV and a trend toward lower BPF was observed.

CONCLUSIONS

Our data suggest that gene-environment interactions between specific HLA Class I loci and EBV exposure are associated with MRI markers of lesion injury and brain atrophy in MS patients.

Authors+Show Affiliations

Buffalo Neuroimaging Analysis Center, Department of Neurology, University at Buffalo, State University of New York, Buffalo, NY, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19232441

Citation

Zivadinov, Robert, et al. "Gene-environment Interactions Between HLA B7/A2, EBV Antibodies Are Associated With MRI Injury in Multiple Sclerosis." Journal of Neuroimmunology, vol. 209, no. 1-2, 2009, pp. 123-30.
Zivadinov R, Weinstock-Guttman B, Zorzon M, et al. Gene-environment interactions between HLA B7/A2, EBV antibodies are associated with MRI injury in multiple sclerosis. J Neuroimmunol. 2009;209(1-2):123-30.
Zivadinov, R., Weinstock-Guttman, B., Zorzon, M., Uxa, L., Serafin, M., Bosco, A., Bratina, A., Maggiore, C., Grop, A., Tommasi, M. A., Srinivasaraghavan, B., & Ramanathan, M. (2009). Gene-environment interactions between HLA B7/A2, EBV antibodies are associated with MRI injury in multiple sclerosis. Journal of Neuroimmunology, 209(1-2), 123-30. https://doi.org/10.1016/j.jneuroim.2009.01.023
Zivadinov R, et al. Gene-environment Interactions Between HLA B7/A2, EBV Antibodies Are Associated With MRI Injury in Multiple Sclerosis. J Neuroimmunol. 2009 Apr 30;209(1-2):123-30. PubMed PMID: 19232441.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Gene-environment interactions between HLA B7/A2, EBV antibodies are associated with MRI injury in multiple sclerosis. AU - Zivadinov,Robert, AU - Weinstock-Guttman,Bianca, AU - Zorzon,Marino, AU - Uxa,Laura, AU - Serafin,Maurizia, AU - Bosco,Antonio, AU - Bratina,Alessio, AU - Maggiore,Cosimo, AU - Grop,Attilio, AU - Tommasi,Maria Antonietta, AU - Srinivasaraghavan,Bhooma, AU - Ramanathan,Murali, Y1 - 2009/02/15/ PY - 2008/09/21/received PY - 2009/01/19/revised PY - 2009/01/23/accepted PY - 2009/2/24/entrez PY - 2009/2/24/pubmed PY - 2009/6/23/medline SP - 123 EP - 30 JF - Journal of neuroimmunology JO - J Neuroimmunol VL - 209 IS - 1-2 N2 - PURPOSE: To determine the role of gene-environmental interactions between the Class I and Class II HLA alleles and the humoral anti-Epstein-Barr Virus (EBV) responses in the development of brain injury and clinical disability in multiple sclerosis (MS) patients. METHODS: A total of 93 MS patients (62 females; 31 males) and 122 healthy controls underwent HLA typing and testing for antibodies against EBV. The MS patients underwent brain MRI and quantitative measurements of T1- and T2-lesion volumes (LVs) and brain parenchymal fraction (BPF) were obtained. There were 54 MS cases that underwent MRI and EBV-antibody assessments at the 3-year follow-up. The anti-EBV panel included measurements of the levels of anti-EBV early antigen (EA) IgG, anti-EBV nuclear antigen (EBNA) IgG and anti-EBV viral capsid antigen (VCA) IgM and anti-EBV VCA IgG. The relationships between HLA alleles, anti-EBV antibody levels, MRI and clinical parameters were assessed in regression analysis. RESULTS: The presence of HLA B7 was associated with increased T1-LV and trends indicating increased anti-EBV VCA IgG levels, higher disability (EDSS) and more destructive MRI parameters (increased T2-LV and decreased BPF). The presence of HLA A2 was associated with lower EDSS and a trend toward decreased anti-EBV VCA IgG levels; the associations with MRI variables were not significant. The HLA B7-A2 haplotype was significantly associated with higher T2-LV and T1-LV and a trend toward lower BPF was observed. CONCLUSIONS: Our data suggest that gene-environment interactions between specific HLA Class I loci and EBV exposure are associated with MRI markers of lesion injury and brain atrophy in MS patients. SN - 1872-8421 UR - https://www.unboundmedicine.com/medline/citation/19232441/Gene_environment_interactions_between_HLA_B7/A2_EBV_antibodies_are_associated_with_MRI_injury_in_multiple_sclerosis_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0165-5728(09)00028-9 DB - PRIME DP - Unbound Medicine ER -