Lusso P, Ensoli B, Markham P D, Ablashi D V, Salahuddin S Z, Tschachler E, Wong-Staal F, Gallo R C
Laboratory of Tumor Cell Biology, National Cancer Institute, Bethesda, Maryland 20892.
Nature. 1989 Jan 26;337(6205):370-3. doi: 10.1038/337370a0.
Although infection by HIV-1 has been implicated as the primary cause of AIDS and related disorders, 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 herpesviruses, papovaviruses, adenoviruses and HTLV-I have been suggested as potential cofactors. Another candidate is human herpesvirus-6 (HHV-6, originally designated human B-lymphotropic virus), which has not only been identified in most patients with AIDS by virus isolation, DNA amplification techniques and serological analysis, but is also predominantly tropic and cytopathic in vitro for CD4+ T lymphocytes. 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.
虽然HIV-1感染被认为是艾滋病及相关病症的主要病因，但疾病发病机制可能涉及多种辅助因素。例如，在艾滋病患者中常见的几种病毒，如疱疹病毒、乳头多瘤空泡病毒、腺病毒和HTLV-I，它们能够反式激活HIV-1的长末端重复序列，被认为是潜在的辅助因素。另一个候选因素是人类疱疹病毒6型（HHV-6，最初被命名为人类B淋巴细胞嗜性病毒），它不仅通过病毒分离、DNA扩增技术和血清学分析在大多数艾滋病患者中被检测到，而且在体外对CD4+ T淋巴细胞具有主要嗜性和细胞病变作用。在此我们证明，HHV-6和HIV-1能够有效共同感染单个人类CD4+ T淋巴细胞，导致HIV-1表达加速和细胞死亡。我们还提供证据表明，HHV-6可反式激活HIV-1长末端重复序列（LTR）。这些观察结果表明，HHV-6可能直接或间接导致艾滋病患者CD4+ T细胞的耗竭。
