Abstract
The function of the Rex protein of human T-cell leukemia virus type I (HTLV-I) has been demonstrated to be very similar to the Rev protein of human immunodeficiency virus type 1 (HIV-1). Both of these retroviral regulatory proteins rescue unspliced viral RNAs from the nuclei of infected cells. The Rev protein of HIV-1 has been reported to shuttle between the nucleus/nucleolus and the cytoplasm. Here, we have found that Rex also relocated out of the nucleus in the presence of actinomycin D. This effect was demonstrated in dose- and time-course-dependent manners. In comparison with previous reports on HIV-1 Rev, these effects with Rex seemed to be similar, but less distinct, which may reflect precise differences in the subcellular localization and/or shuttling pathways of Rev and Rex. Interestingly, the endogenous truncated form of the Rex protein, p21x, significantly interfered with the intracellular translocation of Rex, when coexpressedin trans.As expression of p21xoccurs in various HTLV-I-infected cells, p21xmay play a role in the life-cycle of HTLV-I, through regulating the dynamic subcellular distribution of the viral trans-activator, Rex.
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