Tumor necrosis factor-α drives HIV-1 replication in U937 cell clones and upregulates CXCR4

Priscilla Biswas, Barbara Mantelli, Fanny Delfanti, Manuela Cota, Giuliana Vallanti, Camilla De Filippi, Manuela Mengozzi, E. Vicenzi, A. Lazzarin, Guido Poli

Research output: Contribution to journalArticlepeer-review


U937 cell clones in which efficient (plus) vs poor (minus) replication of HIV-1 occurs have been described. We evaluated the role of host factors in their differential ability to support HIV-1 replication. Plus clones constitutively produced TNF-α and viral replication was inhibited by neutralization of endogenous TNF-α. However, HIV-1 replication was strongly upregulated in minus clones by exogenous TNF-α, which also further accelerated the kinetics of infection in plus clones. We observed an increased accumulation of proviral DNA within one round of HIV-1 replication following TNF-a treatment of plus cells. This effect was associated with increased surface density of CXCR4 in both plus and minus clones. Our results identify TNF-α as one correlate that contributes to the higher ability of U937-plus clones to sustain HIV-1 replication. Furthermore, we suggest that TNF-α may affect steps of the viral life cycle that occur earlier than transcription and also enhance HIV-1 replication by increasing the surface density of CXCR4.

Original languageEnglish
Pages (from-to)55-59
Number of pages5
Issue number1
Publication statusPublished - Jan 7 2001


  • CXCR4
  • HIV-1
  • TNF-α
  • U937

ASJC Scopus subject areas

  • Endocrinology
  • Molecular Biology
  • Immunology
  • Immunology and Allergy


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