Enhanced Human T-Cell Lymphotropic Virus Type I Expression Following Induction of the Cellular Stress Response

Janice M. Andrews, Michael J. Oglesbee, Alex V. Trevino, Deborah J. Guyot, Garret C. Newbound, Michael Dale Lairmore

Research output: Contribution to journalArticle

30 Scopus citations

Abstract

Human T-cell lymphotropic virus type I (HTLV-I) infection is typically associated with long incubation periods between virus exposure and disease manifestation. Although viral protein expression is considered to play an important role in the pathogenesis of HTLV-I-associated diseases, limited information is known regarding host cell mechanisms that control viral gene expression. This study was designed to evaluate modulation of HTLV-I gene expression following induction of the cellular stress response in HTLV-I-infected lymphocytes. The cellular stress response was elicited by treatment with either Na arsenite or thermal stress and was monitored by demonstrating increased expression of the 72-kDa heat shock protein. Induction of the cellular stress response in HTLV-I-infected lymphocytes resulted in significantly increased HTLV-I-mediated syncytia formation due to enhanced HTLV-I envelope (gp46) expression. Intracellular viral proteins and released pg4 capsid protein were increased in stressed infected lymphocytes as compared to nonstressed infected lymphocytes. Furthermore, HTLV-I-LTR reporter gene constructs had increased activity (three- to sixfold) in a transiently transfected, uninfected lymphocyte cell line following induction of the cellular stress response. Quantitation of HTLV-I RNA expression by slot blot analysis of infected lymphocytes suggested variable increases in RNA accumulation. Northern blot analysis demonstrated no qualitative changes in expression of RNA species. These data suggest a relationship between modulation of viral replication and a basic cellular response to stress and have important implications for understanding host cell control mechanisms of HTLV-I expression.

Original languageEnglish (US)
Pages (from-to)816-820
Number of pages5
JournalVirology
Volume208
Issue number2
DOIs
StatePublished - Apr 20 1995
Externally publishedYes

ASJC Scopus subject areas

  • Virology
  • Infectious Diseases

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