Authors
Maciaszek, Joseph WalterParada, Nereida A.
Cruikshank, William W.
Center, David M.
Kornfeld, Hardy
Viglianti, Gregory A.
Student Authors
Joseph Walter MaciaszekAcademic Program
Immunology and VirologyDocument Type
Journal ArticlePublication Date
1997-01-01Keywords
Down-Regulation; Gene Products, tat; HIV Long Terminal Repeat; HIV-1; Humans; Interleukin-16; NF-kappa B; Virus Activation; tat Gene Products, Human Immunodeficiency VirusLife Sciences
Medicine and Health Sciences
Metadata
Show full item recordAbstract
IL-16 is produced by CD8+ lymphocytes and has been reported to inhibit HIV-1 and SIV replication in infected PBMCs. CD4 serves as a receptor for the secreted form of IL-16, and IL-16 binding to CD4 induces signal transduction, which affects the activation state of the cell. We hypothesized, therefore, that the effect of IL-16 on HIV-1 replication might occur at the level of virus expression. In transient transfection studies with HIV-1 LTR-reporter gene constructs we found that pretreatment of CD4+ lymphoid cells with recombinant IL-16 repressed HIV-1 promoter activity up to 60-fold, preventing both PMA and Tat activation. This effect of IL-16 required sequences contained within the core enhancer, but was not simply due to the down-regulation of transcription factors binding to this element.Source
J Immunol. 1997 Jan 1;158(1):5-8.