Cis-perturbation of cancer drivers by the HTLV-1/BLV proviruses is an early determinant of leukemogenesis

Nicolas Rosewick, Keith Durkin, Maria Artesi, Ambroise Marçais, Vincent Hahaut, Philip Griebel, Natasa Arsic, Véronique Avettand-Fenoel, Arsène Burny, Carole Charlier, Olivier Hermine, Michel Georges and Anne Van den Broeke ()
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Nicolas Rosewick: Unit of Animal Genomics, GIGA-R, Université de Liège (ULg)
Keith Durkin: Unit of Animal Genomics, GIGA-R, Université de Liège (ULg)
Maria Artesi: Unit of Animal Genomics, GIGA-R, Université de Liège (ULg)
Ambroise Marçais: Service d’hématologie, Hôpital Universitaire Necker, Université René Descartes, Assistance publique hôpitaux de Paris
Vincent Hahaut: Unit of Animal Genomics, GIGA-R, Université de Liège (ULg)
Philip Griebel: Vaccine and Infectious Disease Organization, VIDO-Intervac, University of Saskatchewan
Natasa Arsic: Vaccine and Infectious Disease Organization, VIDO-Intervac, University of Saskatchewan
Véronique Avettand-Fenoel: Laboratoire de Virologie, AP-HP, Hôpital Necker-Enfants Malades, Université Paris Descartes
Arsène Burny: Laboratory of Experimental Hematology, Institut Jules Bordet, Université Libre de Bruxelles (ULB)
Carole Charlier: Unit of Animal Genomics, GIGA-R, Université de Liège (ULg)
Olivier Hermine: Service d’hématologie, Hôpital Universitaire Necker, Université René Descartes, Assistance publique hôpitaux de Paris
Michel Georges: Unit of Animal Genomics, GIGA-R, Université de Liège (ULg)
Anne Van den Broeke: Unit of Animal Genomics, GIGA-R, Université de Liège (ULg)

Nature Communications, 2017, vol. 8, issue 1, 1-15

Abstract: Abstract Human T-cell leukaemia virus type-1 (HTLV-1) and bovine leukaemia virus (BLV) infect T- and B-lymphocytes, respectively, provoking a polyclonal expansion that will evolve into an aggressive monoclonal leukaemia in ∼5% of individuals following a protracted latency period. It is generally assumed that early oncogenic changes are largely dependent on virus-encoded products, especially TAX and HBZ, while progression to acute leukaemia/lymphoma involves somatic mutations, yet that both are independent of proviral integration site that has been found to be very variable between tumours. Here, we show that HTLV-1/BLV proviruses are integrated near cancer drivers which they affect either by provirus-dependent transcription termination or as a result of viral antisense RNA-dependent cis-perturbation. The same pattern is observed at polyclonal non-malignant stages, indicating that provirus-dependent host gene perturbation contributes to the initial selection of the multiple clones characterizing the asymptomatic stage, requiring additional alterations in the clone that will evolve into full-blown leukaemia/lymphoma.

Date: 2017
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DOI: 10.1038/ncomms15264

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