Advanced search
1 file | 1.42 MB Add to list
Author
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

Downloads

  • 1742-4690-9-26.pdf
    • full text
    • |
    • open access
    • |
    • PDF
    • |
    • 1.42 MB

Citation

Please use this url to cite or link to this publication:

MLA
Simonis, Nicolas et al. “Host-pathogen Interactome Mapping for HTLV-1 and -2 Retroviruses.” RETROVIROLOGY 9 (2012): n. pag. Print.
APA
Simonis, N., Rual, J.-F., Lemmens, I., Boxus, M., Hirozane-Kishikawa, T., Gatot, J.-S., Dricot, A., et al. (2012). Host-pathogen interactome mapping for HTLV-1 and -2 retroviruses. RETROVIROLOGY, 9.
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.
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.
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}},
}

Altmetric
View in Altmetric
Web of Science
Times cited: