Figure 1.

The various complex interactions between HHV-8 and HIV that lead to the formation of KS lesions. These include the production of inflammatory cytokines and growth factors by HHV-8. The lesion in turn produces FGF-2. The involvement of LANA leads to the inhibition of p53 and activation of signaling pathways. HIV in combination with HHV-8 causes bcl-2-mediated inhibition of p53. HIV Tat-1-1 protein acts a transcription factor to promote angiogenesis, growth and inhibition of apoptosis in addition to promoting viral replication.