An increase in p50/p65 NF-kB Binding to the HIV-1 LTR Is Not Sufficient to Increase Viral Expression in the Primary Human Astrocyte

Katherine Conant, Walter J. Atwood, Renee Traub, Carlo Tornatore, Eugene O. Major

Research output: Contribution to journalArticle

Abstract

Human astrocytes can be infected with HIV-1 both in vivo and in vitro. The amount of HIV-1 p24 structural protein production is low in comparison to that of the macrophage. Several weeks following infection or transfection, however, cocultivation with uninfected lymphocytes or stimulation with the cytokines TNF-α and IL1-β will increase viral production from this cell type. In the present study we demonstrate that phorbol 12-myristate 13-acetate (PMA) also increases HIV-1 p24 production from the primary human astrocyte. Using electrophoretic mobility shift assay (EMSA) in combination with supershift studies using specific antibodies, we demonstrate that PMA, Pike TNF-α, increases the p50/p65 form of NF-kB. Furthermore we demonstrate that the protein kinase inhibitor H7 inhibits PMA- and TNF-α-associated increases in HIV-1 expression at a time when it has little to no inhibitory effect on the associated increases in p50/p65 NF-kB. Thus, unless p50/p65 NF-kB or its binding is affected by H7 in a manner that cannot be resolved by EMSA, an increase in this form of NF-kB is not always sufficient to increase HIV-1 expression from the astrocyte.

Original languageEnglish (US)
Article number71685
Pages (from-to)586-590
Number of pages5
JournalVirology
Volume205
Issue number2
DOIs
StatePublished - Dec 1994

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ASJC Scopus subject areas

  • Virology

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