par Simonis, Nicolas 
;Rual, Jean-François;Lemmens, Irma;Boxus, Mathieu;Hirozane-Kishikawa, Tomoko;Gatot, Jean-Stéphane ;Dricot, Amélie;Hao, Tong;Vertommen, Didier;Legros, Sébastien;Daakour, Sarah;Klitgord, Niels;Martin, Maud ;Willaert, Jean-François;Dequiedt, Franck;Navratil, Vincent;Cusick, Michael E;Burny, Arsène ;Van Lint, Carine ;Hill, David E;Tavernier, Jan;Kettmann, Richard ;Vidal, Marc;Twizere, Jean-Claude
Référence Retrovirology, 9, page (26)
Publication Publié, 2012
;Rual, Jean-François;Lemmens, Irma;Boxus, Mathieu;Hirozane-Kishikawa, Tomoko;Gatot, Jean-Stéphane ;Dricot, Amélie;Hao, Tong;Vertommen, Didier;Legros, Sébastien;Daakour, Sarah;Klitgord, Niels;Martin, Maud ;Willaert, Jean-François;Dequiedt, Franck;Navratil, Vincent;Cusick, Michael E;Burny, Arsène ;Van Lint, Carine ;Hill, David E;Tavernier, Jan;Kettmann, Richard ;Vidal, Marc;Twizere, Jean-ClaudeRéférence Retrovirology, 9, page (26)
Publication Publié, 2012
Article révisé par les pairs
| Résumé : | Human T-cell leukemia virus type 1 (HTLV-1) and type 2 both target T lymphocytes, yet induce radically different phenotypic outcomes. HTLV-1 is a causative agent of Adult T-cell leukemia (ATL), whereas HTLV-2, highly similar to HTLV-1, causes no known overt disease. HTLV gene products are engaged in a dynamic struggle of activating and antagonistic interactions with host cells. Investigations focused on one or a few genes have identified several human factors interacting with HTLV viral proteins. Most of the available interaction data concern the highly investigated HTLV-1 Tax protein. Identifying shared and distinct host-pathogen protein interaction profiles for these two viruses would enlighten how they exploit distinctive or common strategies to subvert cellular pathways toward disease progression. |
