Epigenetic control and reintegration of extrachromosomal proviral DNA in HL60 cells chronically infected with human T cell leukaemia virus type 1.

Extrachromosomal human T cell leukaemia virus type 1 (HTLV-I) proviruses are persistently maintained in HTLV-I-infected human promyelocytic leukaemia (HL60) cells even 24 months after viral infection. By successive recloning of these HTLV-I-infected clones, and by Southern blot analysis of their HTLV-I proviruses, we concluded the following. The copy number of extrachromosomal proviruses fluctuated, and this fluctuation was probably dependent on the epigenetic conditions in the host cell, HL60. The transient appearance of a high copy number of extrachromosomal proviruses was followed by an increase in the copy number of integrated proviruses. Persistence of extrachromosomal proviruses appeared to be caused by an intracellular rather than an intercellular mechanism.