TY - JOUR
T1 - Induction of human herpesvirus-8 gene expression by recombinant interferon gamma
AU - Blackbourn, David J.
AU - Fujimura, Sue
AU - Kutzkey, Tim
AU - Levy, Jay A.
PY - 2000
Y1 - 2000
N2 - 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]
AB - 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]
UR - http://www.scopus.com/inward/record.url?scp=0033969044&partnerID=8YFLogxK
U2 - 10.1097/00002030-200001070-00017
DO - 10.1097/00002030-200001070-00017
M3 - Letter
C2 - 10714578
AN - SCOPUS:0033969044
SN - 0269-9370
VL - 14
SP - 98
EP - 99
JO - AIDS
JF - AIDS
IS - 1
ER -