Figure 1.

In HTLV-1 infection, the viral protein Tax interferes at several steps of both canonical and noncanonical NF-κB pathway in order to activate it, inducing cell survival and proliferation, and eventually resulting in oncogenesis. By interaction with IKKγ/NEMO, Tax recruits and activates IKK complex (IKKγ/NEMO, IKKα, IKKβ) in lipid raft domains (LRD) on the Golgi. After IKK activation, Tax recruits the autophagy proteins BECN1, Bif-1 and the PI3KC3 complex through its direct interaction with BECN1, which in turn binds also with IKKα, IKKβ. Then, Tax deregulates the autophagy pathway fostering autophagosomes biogenesis but, at the same time, blocking the autophagosome-lysosome fusion. Autophagosomes accumulation enhances HTLV-1 replication. Moreover, recent data suggest a crosstalk between autophagic and extracellular vesicles (EVs) biogenesis pathways. EVs from HTLV-1 infected cells bearing the viral proteins Tax and HBZ among some host proteins, and transcriptional mRNA of Tax, HBZ and 5’LTR has been reported.