Like other herpesviruses, HHV-6 establishes latent infection in vivo and thereby can persist in the host indefinitely after primary infection. The best-characterized in vitro model of latent infection is represented by long-term (30 days) cultured macrophages, which after exposure to HHV-6 survive a transient period of low-level productive infection (Kondo et al., 1991). Latency-associated HHV-6 transcripts from the IE1/IE2 locus have been identified in latently infected macrophages both in vitro and in vivo (Kondo et al., 2002b). A second in vitro model of HHV-6 latency was described in papillomavirus-immortalized cervical epithelial cells, in which high numbers of viral genome copies were shown to persist in an episomal form for prolonged periods of time in the absence of any sign of productive infection (Chen et al., 1994). Latent HHV-6 infection was also reported in an EBV-negative Burkitt's lymphoma cell line (Bandobashi et al., 1997).
Although circulating monocytes and epithelial cells of the bronchial and salivary glands have been suggested as possible in vivo reservoirs (Krueger et al., 1990; Kondo et al., 1991), there is still uncertainty regarding the exact sites of viral persistence and latency. Long-lived resting memory CD4+ T cells may also be a primary reservoir among peripheral blood cells. In rare cases, chromosomally integrated HHV-6 has been documented in peripheral blood mononuclear cells from patients with different clinical conditions as well as from normal subjects (Luppi et al., 1993, 1994b, 1998; Torelli et al., 1995; Daibata et al., 1999). The pathological consequences of this phenomenon are still at present unclear.
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