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. 1999 Feb;52(1):32-6.
doi: 10.1136/mp.52.1.32.

CD40 upregulation is independent of HHV-8 in the pathogenesis of Kaposi's sarcoma

M M Kennedy  1 , S Biddolph, S B Lucas, D D Howells, S Picton, J O McGee, J J O'Leary
Affiliations

CD40 upregulation is independent of HHV-8 in the pathogenesis of Kaposi's sarcoma

M M Kennedy et al. Mol Pathol. 1999 Feb.

Abstract

Aims: Human herpesvirus 8 (HHV-8) is now acknowledged as the infective cofactor in the pathogenesis of Kaposi's sarcoma. The mode by which HHV-8 causes Kaposi's sarcoma is unresolved and it is probable that it acts in conjunction with other factors including cytokines, anti-apoptosis proteins, and cell surface receptors. CD40, a cell membrane receptor belonging to the tumour necrosis factor receptor super family, promotes B cell survival and is expressed constitutively on endothelial cells. It is upregulated on cytokine treatment and has been documented recently in Kaposi's sarcoma. Because the HHV-8 genome contains cytokine homologues, this study investigated whether CD40 expression in Kaposi's sarcoma correlated with HHV-8 status, using a unique set of HHV-8 positive and negative specimens.

Methods: Twenty one paraffin wax embedded samples of Kaposi's sarcoma were selected, of which 18 were screened for the presence of HHV-8 using both conventional solution phase and TaqMan polymerase chain reaction (PCR). CD40 immunohistochemistry was assessed using a biotinylated amplification system. Staining was scored semiquantitatively.

Results: The results indicated that the expression of CD40 is independent of viral status, being present in both HHV-8 positive and negative specimens.

Conclusions: This suggests that HHV-8 promotes Kaposi's sarcoma cell survival following infection by mechanisms other than those involving CD40.

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