Identification and characterization of a novel enhancer in the HTLV-1 proviral genome

Misaki Matsuo, Takaharu Ueno, Kazuaki Monde, Kenji Sugata, Benjy Jek Yang Tan, Akhinur Rahman, Paola Miyazato, Kyosuke Uchiyama, Saiful Islam, Hiroo Katsuya, Shinsuke Nakajima, Masahito Tokunaga, Kisato Nosaka, Hiroyuki Hata, Atae Utsunomiya, Jun-ichi Fujisawa and Yorifumi Satou ()
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Misaki Matsuo: Joint Research Center for Human Retrovirus Infection, Kumamoto University
Takaharu Ueno: Kansai Medical University
Kazuaki Monde: Faculty of Life Sciences, Kumamoto University
Kenji Sugata: Joint Research Center for Human Retrovirus Infection, Kumamoto University
Benjy Jek Yang Tan: Joint Research Center for Human Retrovirus Infection, Kumamoto University
Akhinur Rahman: Joint Research Center for Human Retrovirus Infection, Kumamoto University
Paola Miyazato: Joint Research Center for Human Retrovirus Infection, Kumamoto University
Kyosuke Uchiyama: Joint Research Center for Human Retrovirus Infection, Kumamoto University
Saiful Islam: Joint Research Center for Human Retrovirus Infection, Kumamoto University
Hiroo Katsuya: Joint Research Center for Human Retrovirus Infection, Kumamoto University
Shinsuke Nakajima: Kansai Medical University
Masahito Tokunaga: Imamura General Hospital
Kisato Nosaka: Rheumatology and Infectious Disease, Kumamoto University Hospital
Hiroyuki Hata: Faculty of Life Sciences, Kumamoto University
Atae Utsunomiya: Imamura General Hospital
Jun-ichi Fujisawa: Kansai Medical University
Yorifumi Satou: Joint Research Center for Human Retrovirus Infection, Kumamoto University

Nature Communications, 2022, vol. 13, issue 1, 1-16

Abstract: Abstract Human T-cell leukemia virus type 1 (HTLV-1) is a retrovirus that causes adult T-cell leukemia/lymphoma (ATL), a cancer of infected CD4+ T-cells. There is both sense and antisense transcription from the integrated provirus. Sense transcription tends to be suppressed, but antisense transcription is constitutively active. Various efforts have been made to elucidate the regulatory mechanism of HTLV-1 provirus for several decades; however, it remains unknown how HTLV-1 antisense transcription is maintained. Here, using proviral DNA-capture sequencing, we found a previously unidentified viral enhancer in the middle of the HTLV-1 provirus. The transcription factors, SRF and ELK-1, play a pivotal role in the activity of this enhancer. Aberrant transcription of genes in the proximity of integration sites was observed in freshly isolated ATL cells. This finding resolves certain long-standing questions concerning HTLV-1 persistence and pathogenesis. We anticipate that the DNA-capture-seq approach can be applied to analyze the regulatory mechanisms of other oncogenic viruses integrated into the host cellular genome.

Date: 2022
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DOI: 10.1038/s41467-022-30029-9

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