Abstract
Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus associated with human diseases, such as adult T-cell leukemia (ATL) and HTLV-1-associated myelopathy/Tropic spastic paraparesis (HAM/TSP). As a retrovirus, its life cycle includes a step where HTLV-1 is integrated into the host genomic DNA and forms proviral DNA. In the chronic phase of the infection, HTLV‑1 is known to proliferate as a provirus via the mitotic division of the infected host cells. There are generally tens of thousands of infected clones within an infected individual. They exist not only in peripheral blood, but also in various lymphoid organs. Viral proteins encoded in HTLV-1 genome play a role in the proliferation and survival of the infected cells. As is the case with other chronic viral infections, HTLV-1 gene expression induces the activation of the host immunity against the virus. Thus, the transcription from HTLV-1 provirus needs to be controlled in order to evade the host immune surveillance. There should be a dynamic and complex regulation in vivo, where an equilibrium between viral antigen expression and host immune surveillance is achieved. The mechanisms regulating viral gene expression from the provirus are a key to understanding the persistent/latent infection with HTLV-1 and its pathogenesis. In this article, we would like to review our current understanding on this topic.
Highlights
It has been estimated that Human T-cell leukemia virus type 1 (HTLV-1) has been infecting humans for several thousand years [1]
There is sense- and antisense-transcription from HTLV-1 provirus, driven by sequences contained in the long terminal repeats (LTRs) that serve as promoters
Most viral antigens are encoded in the sense transcripts from the 51 -LTR, so infected cells with high expression of viral antigens would be eliminated by the host immune surveillance
Summary
It has been estimated that Human T-cell leukemia virus type 1 (HTLV-1) has been infecting humans for several thousand years [1]. HTLV‐1 is required to keep a latent state in the chronic phase of infection, but it to to reactivate viral gene expression for de novo infection. To understand regulatory mechanisms on HTLV‐1 provirus integrated within the host genomic DNA is a key to elucidate the virological and pathophysiological genomic DNA is a key to elucidate the virological and pathophysiological aspect of HTLV-1 infection, including the mechanisms leading to transformation of the infected cells or the establishment of chronic inflammatory diseases. The most intensively characterized viral protein, is a strong transactivator of HTLV-1 51 -LTR Rex is another positive regulator for the expression of viral antigens, which controls the nuclear export of viral mRNAs. There are several accessory proteins encoded in the sense orientation in the pX region, including p13, p30, p12, p27, p21Rex and p8 [14,15,16,17,18]. The regulatory and accessory viral proteins coordinately control viral antigen expression, contributing to achieve a persistent infection with HTLV-1
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