Human herpesvirus 6(HHV-6) is a human pathogen of emerging clinical significance. HHV-6 was first isolated from patients with lymphoproliferative disorders in 1986 (Salahuddin et al., 1986). HHV-6 isolates are classified into two groups as variants A(HHV-6A) and variant B(HHV-6B) (Schirmer et al., 1991. The two variants are closely related but show consistent differences in biological, immunological, epidemiological, and molecular properties. HHV-6B is the major causative agent of exanthem subitum (ES) (Yamanishi et al., 1988), but no clear disease has yet been associated with HHV-6A.
Human herpesvirus 7 (HHV-7) was isolated in 1990 from a healthy individual whose cells were stimulated with antibody against CD3 and then incubated with interleukin-2 (Frenkel et al., 1990). This virus is one of the causative agents of ES (Tanaka et al., 1994). Therefore, HHV-6 and HHV-7 are also called Roseolovirus. HHV-6 and HHV-7 are ubiquitous, and more than 90% of adults have antibody to both viruses. These viruses have extensive homology and belong to the β-herpesvirus subfamily.
The genome of HHV-6A is 159 321 bp in size, has a base composition of 43% G + C, and contains 119 open reading frames. The overall structure is 143 kb bounded by 8 kb of direct repeats, DRL (left) and DRR (right), containing 0.35 kb of terminal and junctional arrays of human telomere-like simple repeats (Gompels et al., 1995). A total of 115 potential open reading frames (ORFs) were identified within the 161 573-bp contiguous sequence of the entire HHV-6B genome (HST) (Isegawa et al., 1999).