ABSTRACT
Subsequent restriction enzyme analysis of DNA obtained from patients has demonstrated that all the HHV-6 strains known to date can be separated into two main variants [12], classi ed as A (HHV-6A) and B (HHV-6B). Both variants are closest in homology to HHV-7 and cytomegalovirus (CMV) [152]. ese two variants di er in biological, immunological, and molecular characteristics in that they exhibit di erences in cell tropism, transcription regulation, and splicing patterns; although current serologic tests cannot easily distinguish between them. Variant B is known to be the etiological agent of exanthem subitum, whereas variant A has not as yet been found to cause any speci c disease process [5]. With DNA analysis of peripheral blood lymphocytes in healthy donors, variant B has been demonstrated to be three times more common than variant A [13]. Variant A appears to be more common in samples of uninvolved skin [5], in Kaposi’s sarcoma [14], and in human immunode ciency virus-1 (HIV-1)- infected individuals (both symptomatic and asymptomatic) [15,16].
