Several clinical observations also suggest a significant role of HHV-6 in AIDS progression. For example, HHV-6 has been frequently isolated from HIV-infected patients (Salahuddin 1986; Levy 1990; Agut 1988) and widespread HHV-6 infection is documented in patients with AIDS at post-mortem examination (Corbellino 1993; Knox and Carrigan 1994). Additionally, sustained HHV-6 replication has been observed in the lymph nodes of HIV-infected patients associated with increased HIV-1 load (Knox and Carrigan 1996; Emery 1999), HHV-6 is frequently reactivated in early symptomatic HIV-1 infected patients (Secchiero 1995), and the disease progression is accelerated in infants with early acquisition of HHV-6 infection (Kositanont 1999). Interestingly, HHV-6 reactivation/re-infection seems to occur before the time when other opportunistic infections usually appear. It is also remarkable that treatment with the potent HHV-6 inhibitor, foscarnet, significantly prolonged the survival of a group of AIDS patients (Studies of Ocular Complications of AIDS Research Group, 1992). Ensoli and colleagues (Ensoli 1989) showed that HHV-6 is a potent transactivator of the Long Terminal Repeat (LTR) of HIV, SIV, and HIV-2. While HHV-6 by itself causes significant immunologic damage and dysregulation, the combination of active HIV and HHV-6 leads to more severe immunosuppression in AIDS patients, thereby enhancing the progression of the disease.