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In Reply: The concept of an interaction between EBV and human endogenous retroviruses, including an MSRV, is interesting, particularly given that herpesviruses such as EBV and human herpesvirus 6 (HHV-6) may trigger retroviral activation.¹ The human endogenous retrovirus type H (HERV-H) has also been associated with MS.² Combinations of the HERV-H and herpesvirus antigens result in highly increased cellular immune responses, as measured by blast transformation assays based on peripheral blood mononuclear cells among both MS patients and healthy controls.³ However, it is not clear how these viral interactions would explain the apparent protective effect of younger infant siblings found in our study.

Drs Ruprecht and Perron state that our study suggests that late EBV infection increases MS risk. However, our findings are also consistent with several other possible mechanisms. Where our work extends previous observations on the link between EBV infection and MS is in indicating an early-life protective . . . [Full Text of this Article]

Terence Dwyer, MD, FAFPHM; Anne-Louise Ponsonby, PhD, FAFPHM
anne-louise.ponsonby@anu.edu.au
Murdoch Childrens Research Institute
Melbourne, Australia

Ingrid van der Mei, PhD; Leigh Blizzard, PhD
Menzies Research Institute
University of Tasmania
Hobart, Australia

Bruce Taylor, MD, FRACP
University of Otago
Christchurch, New Zealand

Andrew Kemp, PhD, FRACP
University of Sydney
Sydney, Australia

Trevor Kilpatrick, PhD, FRACP
University of Melbourne
Melbourne, Australia

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