from Part III - Pathogenesis, clinical disease, host response, and epidemiology: HHV- 6A, 6B, and 7
Published online by Cambridge University Press: 24 December 2009
Introduction
The discoveries of Human herpesvirus 6 variant A (HHV-6A), Human herpesvirus 6 variant B (HHV-6B) and Human herpesvirus 7 (HHV-7) followed the development of methods for activation and long-term culture of peripheral blood T lymphocytes. Based on their shared biological properties and nucleotide sequences, HHV-6A, HHV-6B, and HHV-7 are classified as members of the roseolovirus genus of the betaherpesvirus subfamily. HHV-6A and HHV-6B are very closely related, with most of their encoded proteins sharing greater than 90% amino acid sequence identity; most HHV-7 protein sequences share 30% to 60% amino acid sequence identity with their HHV-6 counterparts (for review, see Yamanishi et al., 2007 and elsewhere in this volume). Roseoloviruses share many genetic and biologic properties with the more distantly related cytomegaloviruses. All of the roseoloviruses infect T lymphocytes in vivo and in vitro, cause similar damage to infected cells, and have overlapping but distinct disease spectra.
Primary infection with HHV-6B is the major cause of roseola infantum (also known as roseola, exanthem subitum, 3-day-fever, or sixth disease), a febrile rash illness common in early childhood (for review, see Braun et al., 1997; Yamanishi et al., 2007 and elsewhere in this volume); primary HHV-7 infections can also cause roseola, albeit less frequently. Roseoloviruses can affect the central nervous system; patients with HHV-6 primary infection sometimes develop seizures or convulsions.
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