Inhibition of HIV-1 productive infection in hepatoblastoma HepG2 cells by recombinant tumor necrosis factor-α

Ranjit Banerjee, Kirk Sperber, Teresa Pizzella, Lloyd Mayer

Research output: Contribution to journalArticlepeer-review

21 Scopus citations


Objective: To evaluate the role of liver cells in and the effect of tumor necrosis factor-α (TNF-α) on HIV-1 replication. Methods: Human hepatoblastoma HepC2 cells were infected with various strains of HIV-1 and the effect of TNF-α treatment, either before or after infection, was monitored by p24 antigen assays. Northern blot analysis and gel retardation assays were performed to determine the expression of CD4 and HIV-1 trans-acting region (TAR)-binding proteins in these cells, respectively. Results: HepG2 cells are CD4+ and support active HIV-1 replication, producing infectious virions, as measured by both p24 production and ability to infect T-cell lines with the virus produced by HepC2 cells. In contrast to the stimulatory effect of TNF-α on HIV-1 replication in T-cells and monocytes, up to 200U/ml TNF-α treatment, at various times, either before or after HIV-1 infection, substantially inhibited p24 antigen production in HepC2 cells without causing any remarkable cytotoxicity. Gel-retardation assay revealed enhancement of a DNA-binding protein in TNF-α-treated HepG2 cells that binds to a specific sequence of the HIV-1 TAR, compared with the untreated control. Conclusions: These results indicate the importance of cellular factor(s) in HIV-1 infection and suggest that cytokines in different tissues can induce opposite effects. TAR-binding protein may act as an inhibitory factor for HIV-1 replication in the HepG2 cell line.

Original languageEnglish
Pages (from-to)1127-1131
Number of pages5
Issue number10
StatePublished - Oct 1992


  • HIV-1 inhibition
  • HepG2 cells
  • Tumor necrosis factor-α


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