These data are consistent with downregulation of CD3 and CD7 being relevant to HTLV-I infection, although cells without HTLV-I infection may also contribute to this change to some extent, as a substantial subpopulation of T cells has been reported to be CD7-deficient under physiological [23], [24] and certain pathological conditions, including autoimmune disorders and viral infection [25]–[29]. The gene discussed is CD7; the disease is viral infectious disease.