ArticleProceedings of the National Academy of Sciences of the United States of America2008
NF-IL6 (C/EBPbeta) induces HIV-1 replication by inhibiting cytidine deaminase APOBEC3G.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 16 citations in OpenAlex.
- Residual immune activation in HIV-Infected individuals expands monocytic-myeloid derived suppressor cells.Cellular immunology · 2021Article
- Monocytic-Myeloid Derived Suppressor Cells of HIV-Infected Individuals With Viral Suppression Exhibit Suppressed Innate Immunity toFrontiers in immunology · 2021Article
- Multiple APOBEC3 restriction factors for HIV-1 and one Vif to rule them all.Journal of molecular biology · 2014Review
- HIV type 1 gp120-induced expansion of myeloid derived suppressor cells is dependent on interleukin 6 and suppresses immunity.The Journal of infectious diseases · 2014Article
- Snapin, positive regulator of stimulation- induced Ca²⁺ release through RyR, is necessary for HIV-1 replication in T cells.PloS one · 2013Article
- COP9 signalosome component JAB1/CSN5 is necessary for T cell signaling through LFA-1 and HIV-1 replication.PloS one · 2012Article
- Regulation of HIV-1 transcription in cells of the monocyte-macrophage lineage.Retrovirology · 2009Review
- CCAAT/enhancer-binding proteins and the pathogenesis of retrovirus infection.Future microbiology · 2009Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
T cell activation is crucial for the productive HIV-1 infection of primary T cells; however, little is known about the host molecules involved in this process. We show that the host transcription factor NF-IL6 (also called C/EBPbeta) renders primary CD4(+) T cells highly permissive for HIV-1 replication. NF-IL6 facilitates reverse transcription of the virus by binding to and inhibiting the antiviral cytidine deaminase APOBEC3G. A mutation in NF-IL6 at Ser-288 weakened its binding to APOBEC3G and strongly inhibited HIV-1 replication. NF-IL6 also induced the replication of a Vif-deficient strain of HIV-1 in nonpermissive HUT78 cells. These data indicate that NF-IL6 is a natural inhibitor of APOBEC3G that facilitates HIV-1 replication. Host factors, such as NF-IL6, that are involved in early HIV-1 replication are potential targets for anti-HIV-1 therapy. Our findings shed light on the activation of HIV-1 replication by T cell host molecules and reveal a unique regulation of DNA deamination by APOBEC3G and NF-IL6.
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