Figure 3.

Expansion of HTLV-1 integration site clones in vivo. The abundance of HTLV-1 integration site clonal populations during chronic infection may be influenced by (A) alteration of host gene expression by viral LTRs and (B) features of the genomic environment that alter proviral expression of Tax and HBZ, which can both drive cell proliferation and expose the cell to the cytotoxic lymphocyte (CTL) response. Clone-specific factors not associated with genomic integration site but which may influence clone abundance include the specificity of the T cell antigen receptor.