Content area
Full text
About the Authors:
Emily C. Leibovitch
Affiliations Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America, Institute for Biomedical Sciences, School of Medicine and Health Sciences of The George Washington University, Washington, DC, United States of America
Giovanna S. Brunetto
Affiliation: Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Breanna Caruso
Affiliation: Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Kaylan Fenton
Affiliation: Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Joan Ohayon
Affiliation: Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Daniel S. Reich
Affiliation: Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Steven Jacobson
* E-mail: [email protected]
Affiliation: Neuroimmunology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland, United States of America
Introduction
Human herpesvirus 6 (HHV-6) comprises two ubiquitous human beta-herpesviruses: HHV-6A and HHV-6B. HHV-6A and HHV-6B share about 95% nucleotide identity, but some regions have up to 25% divergence [1], [2], which likely underlies the differences in tropism [3], drug susceptibilities [4] and disease associations between these two viruses. These differences have led to their recent reclassification as separate viral species [5].
Primary infection with HHV-6 occurs around the age of two, and as with other herpesviruses, latency persists for the life of the host. HHV-6B is the etiologic agent of roseola [6], a self-limiting febrile illness of early childhood. Primary infections with HHV-6 vary geographically; HHV-6B predominates in childhood infections in the US [6] and Japan [7], while a recent report suggests that HHV-6A may predominate in asymptomatic childhood infections in Zambia [8].
HHV-6A and HHV-6B have each been associated with diseases of the central nervous system (CNS) (reviewed in [9]) including multiple sclerosis (MS) [10], [11], encephalitis [12] and epilepsy (reviewed in [13]). These viruses are also known to reactivate following bone marrow [14], [15] and solid organ [16] transplant, causing complications that range from febrile illness [17] to...