HIV-1 gp120 induces NFAT nuclear translocation in resting CD4+ T-cells

Claudia Cicala*, James Arthos, Nina Censoplano, Catherine Cruz, Eva Chung, Elena Martinelli, Richard A. Lempicki, Ven Natarajan, Donald VanRyk, Marybeth Daucher, Anthony S. Fauci

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

35 Scopus citations


The replication of human immunodeficiency virus (HIV) in CD4+ T-cells is strongly dependent upon the state of activation of infected cells. Infection of sub-optimally activated cells is believed to play a critical role in both the transmission of virus and the persistence of CD4+ T-cell reservoirs. There is accumulating evidence that HIV can modulate signal-transduction pathways in a manner that may facilitate replication in such cells. We previously demonstrated that HIV gp120 induces virus replication in resting CD4+ T cells isolated from HIV-infected individuals. Here, we show that in resting CD4+ T-cells, gp120 activates NFATs and induces their translocation into the nucleus. The HIV LTR encodes NFAT recognition sites, and NFATs may play a critical role in promoting viral replication in sub-optimally activated cells. These observations provide insight into a potential mechanism by which HIV is able to establish infection in resting cells, which may have implications for both transmission of HIV and the persistence of viral reservoirs.

Original languageEnglish (US)
Pages (from-to)105-114
Number of pages10
Issue number1
StatePublished - Feb 5 2006
Externally publishedYes


  • HIV
  • LTR
  • NFAT
  • Transcription factor
  • Viral replication
  • Viral reservoir
  • Viral transmission
  • gp120

ASJC Scopus subject areas

  • Virology

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