Volume 8 Supplement 1

15th International Conference on Human Retroviruses: HTLV and Related Viruses

Open Access

HTLV-I Tax inhibits innate antiviral signaling via NF-κB-dependent induction of SOCS1

  • Soratree Charoenthongtrakul1Email author,
  • Qinjie Zhou1,
  • Noula Shembade1,
  • Nicole S Harhaj1,
  • Glen N Barber1 and
  • Edward W Harhaj1
Retrovirology20118(Suppl 1):A191

https://doi.org/10.1186/1742-4690-8-S1-A191

Published: 6 June 2011

The human T cell leukemia virus type I (HTLV-I) inhibits host antiviral signaling pathways although the underlying mechanisms are unclear. Here we found that the HTLV-I Tax oncoprotein induced the expression of SOCS1, an inhibitor of interferon signaling. Tax required NF-κB, but not CREB, to induce the expression of SOCS1 in T cells. Furthermore, Tax interacted with SOCS1 in both transfected cells and in HTLV-I transformed cell lines. Although SOCS1 is normally a short-lived protein, in the presence of Tax, the stability of SOCS1 was greatly increased. Accordingly, Tax enhanced the replication of a heterologous virus, vesicular stomatitis virus (VSV), in a SOCS1-dependent manner. Surprisingly, Tax required SOCS1 to inhibit RIG-dependent antiviral signaling, but not the interferon-induced JAK/STAT pathway. Inhibition of SOCS1 by RNA-mediated interference in the HTLV-I transformed cell line MT-2 reduced HTLV-I replication and p19Gag levels. Taken together, our results reveal that Tax inhibits antiviral signaling, in part, by hijacking an interferon regulatory protein.

Authors’ Affiliations

(1)
Department of Microbiology and Immunology, The University of Miami, Miller School of Medicine

Copyright

© Charoenthongtrakul et al; licensee BioMed Central Ltd. 2011

This article is published under license to BioMed Central Ltd. This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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