Abstract
The transactivation induced by human herpesvirus 6 (HHV-6) on the HIV-1 promoter was studied both in the presence and in the absence of the retroviral transactivator protein (Tat) constitutively expressed in Jurkat cells. Jurkat-tat cells were infected with HHV-6, transfected with a plasmid containing HIV-1 long terminal repeat (LTR)/chloramphenicol acetyltransferase (CAT), and CAT assays were performed. HHV-6 infection in the presence of Tat resulted in significantly higher LTR activation than that observed by Tat or HHV-6 alone, indicating that HHV-6 and Tat interact synergically. Furthermore, it was demonstrated that expression of HIV-1 tat inhibits HHV-6 replication, as shown by a 3.6-15.4-fold reduction in infectious yield. We suggest that HHV-6 could trigger HIV reactivation in HIV-seropositive patients which, in turn, could inhibit HHV-6 production.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Cell Line, Transformed
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Chloramphenicol O-Acetyltransferase / genetics
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Gene Products, tat / genetics*
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Gene Products, tat / physiology
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HIV Infections / microbiology
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HIV Long Terminal Repeat / genetics*
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HIV Long Terminal Repeat / physiology
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HIV Seropositivity
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HIV-1 / genetics*
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HIV-1 / physiology
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Herpesvirus 6, Human / genetics*
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Herpesvirus 6, Human / physiology
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Humans
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In Vitro Techniques
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Plasmids / genetics
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Promoter Regions, Genetic / genetics
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Promoter Regions, Genetic / physiology
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Transcriptional Activation / genetics*
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Transcriptional Activation / physiology
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Transformation, Genetic / genetics
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Virus Activation / genetics
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Virus Activation / physiology
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Virus Replication / genetics
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Virus Replication / physiology
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tat Gene Products, Human Immunodeficiency Virus
Substances
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Gene Products, tat
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tat Gene Products, Human Immunodeficiency Virus
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Chloramphenicol O-Acetyltransferase