Heat shock enhances the expression of the human T cell leukemia virus type-I (HTLV-I) trans-activator (Tax) antigen in human HTLV-I infected primary and cultured T cells

Marie Kunihiro, Hideki Fujii, Takuya Miyagi, Yoshiaki Takahashi, Reiko Tanaka, Takuya Fukushima, Aftab A. Ansari, Yuetsu Tanaka

Research output: Contribution to journalArticlepeer-review

4 Citations (Scopus)

Abstract

The environmental factors that lead to the reactivation of human T cell leukemia virus type-1 (HTLV-I) in latently infected T cells in vivo remain unknown. It has been previously shown that heat shock (HS) is a potent inducer of HTLV-I viral protein expression in long-term cultured cell lines. However, the precise HTLV-I protein(s) and mechanisms by which HS induces its effect remain ill-defined. We initiated these studies by first monitoring the levels of the trans-activator (Tax) protein induced by exposure of the HTLV-I infected cell line to HS. HS treatment at 43 °C for 30 min for 24 h led to marked increases in the level of Tax antigen expression in all HTLV-I-infected T cell lines tested including a number of HTLV-I-naturally infected T cell lines. HS also increased the expression of functional HTLV-I envelope gp46 antigen, as shown by increased syncytium formation activity. Interestingly, the enhancing effect of HS was partially inhibited by the addition of the heat shock protein 70 (HSP70)-inhibitor pifithlin-µ (PFT). In contrast, the HSP 70-inducer zerumbone (ZER) enhanced Tax expression in the absence of HS. These data suggest that HSP 70 is at least partially involved in HS-mediated stimulation of Tax expression. As expected, HS resulted in enhanced expression of the Tax-inducible host antigens, such as CD83 and OX40. Finally, we confirmed that HS enhanced the levels of Tax and gp46 antigen expression in primary human CD4+ T cells isolated from HTLV-I-infected humanized NOD/SCID/γc null (NOG) mice and HTLV-I carriers. In summary, the data presented herein indicate that HS is one of the environmental factors involved in the reactivation of HTLV-I in vivo via enhanced Tax expression, which may favor HTLV-I expansion in vivo.

Original languageEnglish
Article number191
JournalViruses
Volume8
Issue number7
DOIs
Publication statusPublished - 2016 Jul 11
Externally publishedYes

Keywords

  • Adult T cell leukemia (ATL)
  • Heat shock
  • HTLV-I
  • Tax

ASJC Scopus subject areas

  • Infectious Diseases
  • Virology

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