Reference : Host-pathogen interactome mapping for HTLV-1 and -2 retroviruses.
Scientific journals : Article
Life sciences : Biochemistry, biophysics & molecular biology
Host-pathogen interactome mapping for HTLV-1 and -2 retroviruses.
Simonis, Nicolas [> >]
Rual, Jean-Francois [> >]
Lemmens, Irma [> >]
Boxus, Mathieu [> >]
Hirozane-Kishikawa, Tomoko [> >]
GATOT, Jean-Stéphane mailto [> >]
Dricot, Amelie [> >]
Hao, Tong [> >]
Vertommen, Didier [> >]
Legros, Sebastien [> >]
Daakour, Sarah [> >]
Klitgord, Niels [> >]
Martin, Maud mailto [Université de Liège - ULiège > Chimie et bio-industries > Biologie cell. et moléc. >]
Willaert, Jean-Francois [> >]
Dequiedt, Franck mailto [Université de Liège - ULiège > > GIGA-Research >]
Navratil, Vincent [> >]
Cusick, Michael E. [> >]
Burny, Arsene [> >]
Van Lint, Carine [> >]
Hill, David E. [> >]
Tavernier, Jan [> >]
Kettmann, Richard mailto [Université de Liège - ULiège > Chimie et bio-industries > Biologie cell. et moléc. >]
Vidal, Marc [> >]
Twizere, Jean-Claude mailto [Université de Liège - ULiège > Chimie et bio-industries > Biologie cell. et moléc. >]
Yes (verified by ORBi)
United Kingdom
[en] Host-Pathogen Interactions ; Human T-lymphotropic virus 1/immunology/pathogenicity ; Human T-lymphotropic virus 2/immunology/pathogenicity ; Humans ; Systems Biology/methods ; T-Lymphocytes/immunology/virology ; Two-Hybrid System Techniques
[en] BACKGROUND: 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. RESULTS: We employ a scalable methodology for the systematic mapping and comparison of pathogen-host protein interactions that includes stringent yeast two-hybrid screening and systematic retest, as well as two independent validations through an additional protein interaction detection method and a functional transactivation assay. The final data set contained 166 interactions between 10 viral proteins and 122 human proteins. Among the 166 interactions identified, 87 and 79 involved HTLV-1 and HTLV-2 -encoded proteins, respectively. Targets for HTLV-1 and HTLV-2 proteins implicate a diverse set of cellular processes including the ubiquitin-proteasome system, the apoptosis, different cancer pathways and the Notch signaling pathway. CONCLUSIONS: This study constitutes a first pass, with homogeneous data, at comparative analysis of host targets for HTLV-1 and -2 retroviruses, complements currently existing data for formulation of systems biology models of retroviral induced diseases and presents new insights on biological pathways involved in retroviral infection.
Researchers ; Professionals

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