Ontology highlight
ABSTRACT: 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.
SUBMITTER: Simonis N
PROVIDER: S-EPMC3351729 | biostudies-literature | 2012 Mar
REPOSITORIES: biostudies-literature
Simonis Nicolas N Rual Jean-François JF Lemmens Irma I Boxus Mathieu M Hirozane-Kishikawa Tomoko T Gatot Jean-Stéphane JS Dricot Amélie A Hao Tong T Vertommen Didier D Legros Sébastien S Daakour Sarah S Klitgord Niels N Martin Maud M Willaert Jean-François JF Dequiedt Franck F Navratil Vincent V Cusick Michael E ME Burny Arsène A Van Lint Carine C Hill David E DE Tavernier Jan J Kettmann Richard R Vidal Marc M Twizere Jean-Claude JC
Retrovirology 20120329
<h4>Background</h4>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 ...[more]