Biological Plausibility of a Link Between Arterial Ischemic Stroke and Infection with Varicella-Zoster Virus or Herpes Simplex Virus
There are now 9 human herpesviruses; the increase from 8 to 9 was caused by a recent decision to split human herpesvirus (HHV) strains 6A and 6B into distinct species. The 9 species are subdivided into three subfamilies, called alpha: herpes simplex virus (HSV) types 1 and 2 and varicella-zoster virus (VZV); beta: cytomegalovirus (CMV), HHV6A, HHV6B and HHV7; gamma: Epstein-Barr virus (EBV) and Kaposi's sarcoma-associated herpesvirus (sometimes called HHV8). These same herpesviruses have evolved with humankind around the world since the great migration of modern humans across the Mandeb Strait out of Africa around 60 to 100 thousand years ago1. In the current report in this issue of Circulation, the authors sought to determine whether any of 5 herpesvirus infections—HSV1, HSV2, VZV, CMV or EBV—increased the risk of arterial ischemic stroke (AIS) in children 18 years of age or younger2. They conclude that HSV1 infection and to a lesser extent VZV infection may act as triggers for childhood AIS. This Editorial will examine the biological plausibility of that assertion, based on both a literature review and the known pathogenesis of infection with HSV, VZV and also the live attenuated varicella vaccine virus.
- Received January 19, 2016.
- Accepted January 21, 2016.