Fifth International Congress Drug Therapy in HIV Infection 22-26 October, 2000 Glasgow, UK

KAPOSI’S SARCOMA HERPESVIRUS: FROM CELL BIOLOGY TO PATHOGENESIS

C. Boshoff
GlaxoWellcome Fellow, Wolfson Institute, Cruciform Building, University College London, London, UK

Int Cong Drug Therapy HIV 2000 Oct 22-26;5:Abstract No. PL5.3
AIDS 2000, Oct 22-26;14(Suppl. 4);S5

Kaposi’s sarcoma-associated herpesvirus (KSHV or HHV-8) is implicated in the etiopathogenesis of Kaposi’s sarcoma (KS), primary effusion lymphoma and a subtype of Castleman’s disease. Serological surveys indicate that the seroprevalence of KSHV, in general, correlates with the incidence of KS in different populations.

In multicentric Castleman’s disease, KSHV is present in a population of plasmablasts in the mantle zone. In KS, KSHV is present in the spindle cells, which do express markers associated with lymphatic, rather than vascular, endothelium.

In all three neoplasia associated with KSHV, the virus is latently present in the vast majority of tumour cells, suggesting that KSHV latent proteins directly induce the proliferation of these cells. Among the latently expressed proteins are cellular cyclin and FLIP (FLICE inhibitory) homologues, and latent nuclear (LNA-1) and membrane (K15) proteins. The potential role of these proteins in cell proliferation and transformation will be discussed.

Kaposi’s sarcoma lesions can resolve with partial restoration of the immune system, i.e. post-transplantation KS resolves when immunosuppression is stopped and AIDS-KS often improves with HAART. This suggests that cytotoxic T cell (CTL) responses against KSHV might be important in the pathogenesis of KS. The identification of CTLs against this virus will be discussed.

Presenting author: C. Boshoff

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2000-10-22
PL5-3

Originally published in AIDS Volume 14, Supplement 4 and hosted with permission of the publisher Lippincott Williams & Wilkins, 250 Waterloo Road, London, SE1 8RD, UK. Tel: +44 (0)20 7981 0700 Fax: +44 (0) 7981 0701

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