Possible Relations Between Epstein-Barr Virus Past Infection and Classic Multiple Sclerosis in Guilan, Iran

نویسندگان

  • Hamidreza Honarmand
  • Masoumeh Ahmadi Jalali Moghadam
  • Hamidreza Hatamian
  • Ali Roudbary
چکیده

BACKGROUND Multiple sclerosis (MS) is a demyelinating condition affecting the central nervous system. Although the cause of this condition is unknown, patients with MS seem to have genetic vulnerability to certain environmental factors such as infection that could trigger this condition. OBJECTIVES We conducted this study to determine whether MS risk increases following primary infection with Epstein-Barr virus (EBV) and also to investigate any association between MS and seropositivity to anti-EBNA-1 IgG, anti-EBV-CA IgG, and anti-EBV-EA. PATIENTS AND METHODS EBV infection was confirmed using the Enzyme-Linked Immunoassay in the patient (n = 46) and control (n = 46) groups via commercial assays (anti-EBNA-1 IgG, anti-EBV-CA IgG, and anti-EBV-EA kits). The data were analyzed by using three statistical tests (Pearson chi-square, Spearman rho correlation, and odds ratio). RESULTS Seropositivity to anti-EBNA-1 IgG did not show a significant difference between the patient and control groups (92.9% and 88.4%, respectively), and nor was seropositivity to anti-EBV-CA IgG different between the two groups (95.2% and 95.3%, consequently). The anti-EBV-EA-D test was negative in all the patients and in 95.3% of the controls. Seropositivity to both anti-EBNA-1 and anti-EBV-CA indicating past infection did not show significant associations with the later development of MS (Pearson chi-square asymptotic significance [Asymp. Sig.] [2-sided] = 0.317, Spearman's rho correlation test Sig. [2-sided] = 0.689, odds ratio = 1.95). CONCLUSIONS Seropositivity to both EBNA1- IgG and EBV-CA- IgG did not show a causal association with MS. The findings of this study suggest that EBV past infection could not be a causative factor in the development of MS and a protective factor against classic MS.

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عنوان ژورنال:

دوره 8  شماره 

صفحات  -

تاریخ انتشار 2015