Key result
HTLV-1 ORF-I encoded proteins, such as p12 and p8, induce dysregulation of intracellular signaling to escape immune response and increase infected T-cell proliferation.
This review highlights the molecular mechanisms of HTLV-1 ORF-I encoded proteins in immune evasion and T-cell proliferation.
May inform HTLV-1 therapeutic targets; leaves open clinical translation pending prospective validation.
The human T-cell lymphotropic virus type 1 (HTLV-1) is a retrovirus associated with both proliferative and inflammatory disorders. This virus causes a persistent infection, mainly in CD4+ T lymphocyte. The ability to persist in the host is associated with the virus capacity to evade the immune response and to induce infected T-cell proliferation, once the HTLV-1 maintains the infection mainly by clonal expansion of infected cells. There are several evidences that ORF-I encoded proteins, such as p12 and p8, play an important role in this context. The present study will review the molecular mechanisms that HTLV-1 ORF-I encoded proteins have to induce dysregulation of intracellular signaling, in order to escape from immune response and to increase the infected T-cell proliferation rate. The work will also address the impact of ORF-I mutations on the human host and perspectives in this study field.
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Rosadas et al. (2015) conducted a review in HTLV-1 infection. HTLV-1 ORF-I encoded proteins (p12 and p8) was evaluated. HTLV-1 ORF-I encoded proteins, such as p12 and p8, induce dysregulation of intracellular signaling to escape immune response and increase infected T-cell proliferation.
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