HSV for tumour lysis

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The role of HHV-8 in Kaposi’s sarcoma

Presented by JC Boshoff and the Cancer Research UK Viral Oncology Group,
Wolfson Institute for Biomedical Research, University College, London, UK.

In the vast majority of infected individuals, Kaposi’s sarcoma herpesvirus (KSHV or HHV-8) persists without harm to its host. When the balance between pathogen and host immunity is disturbed, due to HIV infection or iatrogenic immunosuppression, KSHV reactivation and outgrowth of KSHV-infected cells can occur. Tumours associated with this pathogen include KS, Castleman’s disease and primary effusion lymphoma. Although KSHV encodes for a number of viral products that could induce cell proliferation on their own (e.g. viral cyclin, vFLIP, vGPCR and LANA), evidence that KSHV is transforming in experimental models remains elusive. KS is a tumour of cells differentiating towards lymphatic endothelial cells (LEC). KSHV infects LEC in vitro, and LEC are permissive to infection and morphological transformation by this pathogen. The expression profile of infected LEC reveals that this pathogen induces genes associated with cell attachment, migration and differentiation. KSHV also induces an array of cytokines and their receptors, including PDGF-A, -B and PDGFR-α, endothelin-1 and angiopoietin-2. ELISA confirms significant upregulation of angiopoietin-2 in the supernatant from infected LEC. Individuals with KS have significantly higher plasma levels of angiopoietin-2 and the lymphangiogenic molecule VEGFD, but not the angiogenic molecule VEGFA. Furthermore, plasma VEGFD and angiopoietin-2 levels decrease during KS resolution. These data infer that KS is a tumour of the lymphatic endothelial lineage and lymphangiogenic molecules are involved in its pathogenesis. KSHV-infected LEC provide an experimental model to study Kaposi’s sarcomagenesis, and KS should provide a model to test anti-lymphangiogenic therapeutics.

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