| Summary: | <p>Abstract</p> <p>Human herpesvirus (HHV)-8 associated oncogenesis, a state of immune impairment, a local inflammatory environment, angiogenesis and HIV infection occurring concurrently are important factors for the development of HIV-associated Kaposi sarcoma (KS).</p> <p>Activation of the interleukin (IL)-6 receptor signalling pathway and constitutive signalling of viral G protein-coupled receptor (vGPCR) play an important role in the activation, proliferation and transformation of HHV-8 infected endothelial cells thus contributing to the initiation and progression of KS. HIV-tat protein, HIV-induced immune suppression and a hyperinflammatory state facilitate the oncogenic activity of HHV-8.</p> <p>In this article we reviewed some aspects of HIV-KS pathogenesis and tried to establish, according to the available information in the literature, whether HIV-KS is a monoclonal neoplasm or a benign angioproliferative disorder.</p> <p>From the data of this review it is evident that most of the HIV-KS lesions are oligoclonal in origin. It remains to be demonstrated whether these multiple monoclonal populations of cells are neoplastic, harbouring specific cytogenetic alterations such as mutations, rearrangements and amplifications, or are, as the current evidence shows, the result of HHV-8 induced intracellular signalling pathways that modulate the expression of cellular genes associated with cell cycle regulation, apoptosis, inflammatory response and angiogenesis, and represent a reactive angioproliferative disorder.</p>
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