Human T-cell lymphotropic virus type I (HTLV-I) is characterized by a remarkable genetic stability and high proviral loads in the absence of malignant disease. This results from the effect of tax on cell cycling. The virus replicates essentially in concert with the cell that is, via mitosis, which can be shown by polymerase chain reaction amplification of the HTLV-I integration sites. This is true of all stages of HTLV-I infection and accompanies adult T-cell leukemia/lymphoma. The very low viremia results from its genetic organization.