No treatments of demonstrated value. HTLV-1 is not thought to have a preferred integration site which might lead to cellular gene activation. No single activated oncogene can be detected in a transformation assay. It is currently assumed that the virus augments T cell proliferation and thus provides an expanded T cell population in which a malignant event can occur. Transactivation of transcription by an HTLV gene product called tax has been observed.
Tax is essential for viral replication.
Viruses which do not contain a functional tax gene are not infectious. They make only trace amounts of RNA suggesting a role in transcriptional activation. Tax can transactivate other host promoters, e.g. an NFkB-like transcription factor characteristic of activated T cells which binds to an upstream element of the TCGF gene, ie an autocrine effect. Mice transgenic for tax develop multiple mesenchymal proliferative disorders. The genes responsible for transformation in these viruses have no cellular homologues.