IL‐13 and TNF‐α inhibit dual‐tropic HIV‐1 in primary macrophages by reduction of surface expression of CD4, chemokine receptors CCR5, CXCR4 and post‐entry viral gene expression

摘要: We show that IL-13 in the presence of TNF-alpha effected an equal or greater antiviral activity against a dual-tropic HIV-1 (R5X4) macrophages. A temporary continued exposure macrophages to both cytokines significantly decreased infection and replication R5X4 HIV-1(89.6) (median, 128-fold, n = 9, p 0.024) as compared untreated controls when analyzed over six decreasing multiplicities infection. quantitative flow cytometric assay revealed induced significant (approximately 50 %) reduction number CD4 CC chemokine receptor 5 (CCR5) antibody binding sites while completely abrogating surface expression CXC 4 (CXCR4). In TNF-alpha, CCR5 was abrogated CXCR4 remained reduced controls. coreceptors associated with decrease reverse-transcribed viral DNA at 24 h post-infection. Quantification gene using amphotropic MLV Env pseudotyped luciferase reporter viruses suggested inhibited within by up 90 % absence TNF-alpha. conclusion, our data suggest is powerful counter-regulatory agent TNF-alpha-induced also acting inhibiting de novo