Abstract
Although infection by HIV-1 (refs 1 and 2) has been implicated as the primary cause of AIDS and related disorders3,4, cofactorial mechanisms may be involved in the pathogenesis of the disease. For example, several viruses commonly detected in AIDS patients and capable of transactivating the long terminal repeat of HIV-1, such as herpesviruses5–7, papovaviruses7, adenoviruses8 and HTLV-I (ref. 9), have been suggested as potential cofactors. Another candidate is human herpesvirus-6 (HHV-6, originally.designated human B-lymphotropic virus)10–12, which has not only been iden-tified in most patients with AIDS by virus isolation10,13,14, DNA amplification techniques15 and serological analysis16, but is also predominantly tropic and cytopathic in vitro for CD4+ T lym-phocytes17,18. Here we demonstrate that HHV-6 and HIV-1 can productively co-infect individual human CD4+ T lymphocytes, resulting in accelerated HIV-1 expression and cellular death. We also present evidence that HHV-6 transactivates the HIV-1 long terminal repeat (LTR). These observations indicate that HHV-6 might contribute directly or indirectly to the depletion of CD4+ T cells in AIDS.
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Lusso, P., Ensoli, B., Markham, P. et al. Productive dual infection of human CD4+ T lymphocytes by HIV-1 and HHV-6. Nature 337, 370–373 (1989). https://doi.org/10.1038/337370a0
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DOI: https://doi.org/10.1038/337370a0
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