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To the Editor: Dr Levin and colleagues¹ reported an association between EBV antibody and risk of MS. There are many possible explanations for this association, including a nonspecific increased antibody response to EBV and a direct pathogenic role of EBV via T cells or antibody that cross-reacts with autoantigens.

One potential target of cross-reacting antibody is interleukin 10 (IL-10). This cytokine decreases T_H1 lymphocyte function² and may be important in MS pathogenesis because increased T_H1 activity has been related to MS disease activity.³ Furthermore, the EBV BCRF-1 gene product, termed viral IL-10 (vIL-10), shares structural and functional similarity with human IL-10 (hIL-10), and antibody to vIL-10 cross reacts with hIL-10.⁴ It is possible that antibody to EBV vIL-10 cross reacts with hIL-10 and decreases hIL-10 activity, thereby resulting in increased T_H1 function and pathogenesis of MS. In addition to measuring antibody to the "standard" EBV antigens (viral . . . [Full Text of this Article]

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