The effect of the cellular stress response on human T-lymphotropic virus type I envelope protein expression.
In this report the influence of the cellular stress response in mediating changes in human T-lymphotropic virus type I (HTLV-I) viral envelope (Env) protein metabolism is determined. Previously, we reported that induction of the cellular stress response enhanced HTLV-I-mediated syncytia formation following induction of the cellular stress response in persistently infected lymphocytes. In this study, we show that the increase in HTLV-I-mediated syncytia formation following stress response induction is a result of increased cell surface expression of viral Env protein (gp46). Cellular stress in MT 2.6 cells did not alter the turnover of intracellular Env protein (gp68) as no changes in viral protein half-life were demonstrated as compared to non-stressed cells. However, Env expression in stressed cells treated with a protein synthesis inhibitor (cycloheximide) indicates the effect is mediated through increased translation of viral Env protein.
Andrews
J M
JM
Center for Retrovirus Research and Department of Veterinary Biosciences, The Ohio State University, Columbus 43210, USA. jan_andrews@ncsu.edu
Oglesbee
M
M
Lairmore
M D
MD
D002461:Cell Line, Transformed; D015870:Gene Expression; D015686:Gene Products, env / Q000096:biosynthesis*; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins / Q000096:biosynthesis; D018869:Heat-Shock Response; D015368:Human T-lymphotropic virus 1 / Q000378:metabolism* / Q000502:physiology; D006801:Humans; D011498:Protein Precursors / Q000096:biosynthesis; D015682:Retroviridae Proteins, Oncogenic / Q000096:biosynthesis*
D015686:Gene Products, env; D050884:HSP72 Heat-Shock Proteins; D006360:Heat-Shock Proteins; D011498:Protein Precursors; D015682:Retroviridae Proteins, Oncogenic; C055266:gp46 protein, Human T-cell leukemia virus type I