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. 2018 May 9;9:925. doi: 10.3389/fmicb.2018.00925

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Copyright © 2018 Marino-Merlo, Mastino, Grelli, Hermine, Bazarbachi and Macchi.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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HTLV-1 driven leukomogenesis and possible mechanism of antiviral therapy. (A) Main immortalization/transformation process activated by HTLV-1 regulatory protein Tax and HBZ in newly infected CD4+ cells transmit virus to uninfected CD4+ cells and leading to epigenetic and genetic changes in ATL transformed cells. Cell migration and cell-to-cell virus transmission, presumably involving also dendritic cells, favor the release of inflammatory cytokines and chemokines milieu in the microenvironment and contribute to the maintaining of the infected clones. (B) AZT/IFN with or without arsenic trioxide (AS) could interrupt the maintaining route of ATL.