- Author
- Nicolas Simonis, Jean-François Rual, Irma Lemmens (UGent) , Mathieu Boxus, Tomoko Hirozane-Kishikawa, Jean-Stéphane Gatot, Amélie Dricot, Tong Hao, Didier Vertommen, Sébastien Legros, Sarah Daakour, Niels Klitgord, Maud Martin, Jean-François Willaert, Franck Dequiedt, Vincent Navratil, Michael E Cusick, Arsène Burny, Carine Van Lint, David E Hill, Jan Tavernier (UGent) , Richard Kettmann, Marc Vidal and Jean-Claude Twizere
- Organization
- 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.
- Keywords
- TRANSCRIPTION FACTORS, INTERACTION DATABASE, PROTEIN-INTERACTION NETWORK, ANAPHASE-PROMOTING COMPLEX, VIRUS TYPE-1 TAX, T-CELL LEUKEMIA, HBZ, Tax, ORFeome, Retrovirus, HTLV, Interactome, NUCLEOTIDE-SEQUENCE, GENE-EXPRESSION, FANCONI-ANEMIA, RNA-BINDING
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Citation
Please use this url to cite or link to this publication: http://hdl.handle.net/1854/LU-2916971
- MLA
- Simonis, Nicolas, et al. “Host-Pathogen Interactome Mapping for HTLV-1 and -2 Retroviruses.” RETROVIROLOGY, vol. 9, 2012, doi:10.1186/1742-4690-9-26.
- APA
- Simonis, N., Rual, J.-F., Lemmens, I., Boxus, M., Hirozane-Kishikawa, T., Gatot, J.-S., … Twizere, J.-C. (2012). Host-pathogen interactome mapping for HTLV-1 and -2 retroviruses. RETROVIROLOGY, 9. https://doi.org/10.1186/1742-4690-9-26
- Chicago author-date
- Simonis, Nicolas, Jean-François Rual, Irma Lemmens, Mathieu Boxus, Tomoko Hirozane-Kishikawa, Jean-Stéphane Gatot, Amélie Dricot, et al. 2012. “Host-Pathogen Interactome Mapping for HTLV-1 and -2 Retroviruses.” RETROVIROLOGY 9. https://doi.org/10.1186/1742-4690-9-26.
- Chicago author-date (all authors)
- Simonis, Nicolas, Jean-François Rual, Irma Lemmens, Mathieu Boxus, Tomoko Hirozane-Kishikawa, Jean-Stéphane Gatot, Amélie Dricot, Tong Hao, Didier Vertommen, Sébastien Legros, Sarah Daakour, Niels Klitgord, Maud Martin, Jean-François Willaert, Franck Dequiedt, Vincent Navratil, Michael E Cusick, Arsène Burny, Carine Van Lint, David E Hill, Jan Tavernier, Richard Kettmann, Marc Vidal, and Jean-Claude Twizere. 2012. “Host-Pathogen Interactome Mapping for HTLV-1 and -2 Retroviruses.” RETROVIROLOGY 9. doi:10.1186/1742-4690-9-26.
- Vancouver
- 1.Simonis N, Rual J-F, Lemmens I, Boxus M, Hirozane-Kishikawa T, Gatot J-S, et al. Host-pathogen interactome mapping for HTLV-1 and -2 retroviruses. RETROVIROLOGY. 2012;9.
- IEEE
- [1]N. Simonis et al., “Host-pathogen interactome mapping for HTLV-1 and -2 retroviruses,” RETROVIROLOGY, vol. 9, 2012.
@article{2916971, 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.}}, articleno = {{26}}, author = {{Simonis, Nicolas and Rual, Jean-François and Lemmens, Irma and Boxus, Mathieu and Hirozane-Kishikawa, Tomoko and Gatot, Jean-Stéphane and Dricot, Amélie and Hao, Tong and Vertommen, Didier and Legros, Sébastien and Daakour, Sarah and Klitgord, Niels and Martin, Maud and Willaert, Jean-François and Dequiedt, Franck and Navratil, Vincent and Cusick, Michael E and Burny, Arsène and Van Lint, Carine and Hill, David E and Tavernier, Jan and Kettmann, Richard and Vidal, Marc and Twizere, Jean-Claude}}, issn = {{1742-4690}}, journal = {{RETROVIROLOGY}}, keywords = {{TRANSCRIPTION FACTORS,INTERACTION DATABASE,PROTEIN-INTERACTION NETWORK,ANAPHASE-PROMOTING COMPLEX,VIRUS TYPE-1 TAX,T-CELL LEUKEMIA,HBZ,Tax,ORFeome,Retrovirus,HTLV,Interactome,NUCLEOTIDE-SEQUENCE,GENE-EXPRESSION,FANCONI-ANEMIA,RNA-BINDING}}, language = {{eng}}, pages = {{20}}, title = {{Host-pathogen interactome mapping for HTLV-1 and -2 retroviruses}}, url = {{http://dx.doi.org/10.1186/1742-4690-9-26}}, volume = {{9}}, year = {{2012}}, }
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