3-5% of individuals with chronic HTLV-1 retroviral infection develop an intractable T-cell neoplasm known as adult T-cell leukemia/lymphoma (ATL). The viral regulatory protein Tax is implicated in this oncogenic process.
A UAS construct of the viral HTLV-1\Tax gene has been introduced into flies. Multiple aspects of Tax-related oncogenesis have been investigated using this system, including the role of the NF-κB pathway and the impact of posttranslational modifications of the Tax protein. Expression of HTLV-1\Tax in the developing eye induces ommatidial perturbation and a rough eye phenotype; expression in plasmatocytes results in increased plasmatocyte proliferation. The rough eye phenotype has been used in a screen for interacting genes.
[updated May 2019 by FlyBase; FBrf0222196]
Human T-cell leukemia virus type 1 (HTLV-1) was the first human retrovirus to be discovered. Since it is usually asymptomatic in the beginning of the infection and disease typically manifests later in life, silent transmission occurs, which is associated with sexual relations, breastfeeding, and blood transfusions. It causes serious diseases in humans, including adult T-cell leukemia/lymphoma (ATL) and an incapacitating neurological disease (HTLV-associated myelopathy/tropical spastic paraparesis [HAM/TSP]) (Goncalves et al., 2010; pubmed:20610824).
HTLV-1 is a complex human delta retrovirus that currently infects 10-20 million people worldwide. While HTLV-1 infection is generally asymptomatic, 3%-5% of infected individuals develop a highly malignant and intractable T-cell neoplasm known as adult T-cell leukemia/lymphoma (ATL) decades after infection (Giam and Semmes, 2016; pubmed:27322308).
How HTLV-1 infection progresses to ATL is not well understood. Two viral regulatory proteins, Tax and HTLV-1 basic zipper protein (HBZ), encoded by the sense and antisense viral transcripts, respectively, are thought to play indispensable roles in the oncogenic process of ATL (Giam and Semmes, 2016; pubmed:27322308).
