Induction of human herpesvirus-8 gene expression by recombinant interferon gamma

David J. Blackbourn*, Sue Fujimura, Tim Kutzkey, Jay A. Levy

*Corresponding author for this work

Research output: Contribution to journalLetterpeer-review

27 Citations (Scopus)


The most likely etiological agent of Kaposi's sarcoma (KS) is human herpesvirus (HHV)-8, also referred to as KS-associated herpesvirus (KSHV) [1] Although this virus encodes genes with the potential for cellular transformation, they are not all expressed in the majority of cells in KS lesions, nor in latently infected pleural effusion lymphoma cells. These findings raise the issue of whether the virus plays a direct or an indirect role in cell transformation. Indeed, whether KS is a true malignancy, or rather a hyperplastic condition is still unresolved. Because KS is often associated with immune system dysfunction (i.e. in HIV-infected individuals and in iatrogenic immunosuppressed kidney transplant recipients) hyperplasia could be provoked by a dysregulated immune system that might exacerbate HHV-8 pathogenesis [2] Fiorelli et al. [3] reported that the CD8 T cells infiltrating KS lesions produced high levels of IFN-γ. It is unclear whether this IFN-γ production occurs as a result of the KS lesion, or contributes to its cause, but at least in infected peripheral blood mononuclear cells, this cytokine can maintain HHV-8 infection in vitro[4]
Original languageEnglish
Pages (from-to)98-99
Number of pages2
Issue number1
Publication statusPublished - 2000


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