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National Academy of Sciences, Proceedings of the National Academy of Sciences, 11(113), p. 3054-3059, 2016

DOI: 10.1073/pnas.1423199113

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The retrovirus HTLV-1 inserts an ectopic CTCF-binding site into the human genome

This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Significance The retrovirus human T-lymphotropic virus type 1 (HTLV-1) causes inflammatory and malignant diseases in humans. To maintain latency and avoid immune detection in vivo, HTLV-1 minimizes expression of genes on the plus-strand of the integrated provirus but allows constitutive expression of the minus-strand gene, which maintains clonal persistence. It is not understood how this gene expression is regulated. We show that CTCF, a master regulator of chromatin structure and gene expression, binds to HTLV-1, forms loops between the provirus and host genome, and alters expression of proviral and host genes. Because a typical HTLV-1–infected host carries >10 4 infected T-cell clones, each containing a provirus integrated in a different genomic site, CTCF binding gives HTLV-1 the potential to cause widespread abnormalities in the human genome.