The human β-herpesvirus subfamily consists of human cytomegalovirus (HCMV), human herpesvirus 6 (HHV-6), and human herpesvirus 7 (HHV-7). HHV-6 and HHV-7 belong to the Roseolovirus genus of the β-herpesviruses, and the HHV-6 species are divided into two variants: HHV-6A and HHV-6B. These viruses establish a lifelong infection of their host, reactivate frequently, and reactivated viruses are shed into the saliva (Jordan, 1983; Krueger et al., 1990). Some evidence suggests that the molecular mechanisms of viral latency and reactivation are shared among these viruses. HHV-6B is reactivated from latency after coinfection with HHV-7 (Katsafanas et al., 1996), and HCMV disease is frequently associated with concurrent HHV-6 and HHV-7 reactivation in transplant patients (Lautenschlager et al., 2000; Mendez et al., 2001)
The sites of these viruses during latency are not completely defined. For HHV-6B, viral DNA is detected predominantly in the peripheral blood monocytes/macrophages of seropositive healthy adults (Kondo et al., 1991). Furthermore, primary cultured macrophages support latent HHV-6B infection, and viral reactivation is induced in them by treatment with 12-0-tetradecanoylphorbol-13-acetate (TPA) (Kondo et al., 1991). HHV-6B also establishes latency in myeloid cell lines (Yasukawa et al., 1999), and that HHV-6B is detectable in CD34 (+) peripheral blood progenitor cells (Luppi et al., 1999). Therefore, HHV-6B appears to establish latency in hematopoietic progenitor cells.
HHV-6A is detectable in the peripheral blood of seropositive adults (Drobyski et al., 1993); however, a cell population that might harbor latent HHV-6A has not been identified.