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J Leukoc Biol. 2013 Aug;94(2):337-41. doi: 10.1189/jlb.0313158. Epub 2013 Jun 6.

RIG-I activation inhibits HIV replication in macrophages.

Author information

1
Temple University School of Medicine, 843 MERB, 3500 N. Broad St., Philadelphia, PA 19140, USA. wenzheho@temple.edu

Abstract

The RIG-I signaling pathway is critical in the activation of the type I IFN-dependent antiviral innate-immune response. We thus examined whether RIG-I activation can inhibit HIV replication in macrophages. We showed that the stimulation of monocyte-derived macrophages with 5'ppp-dsRNA, a synthetic ligand for RIG-I, induced the expression of RIG-I, IFN-α/β, and several IRFs, key regulators of the IFN signaling pathway. In addition, RIG-I activation induced the expression of multiple intracellular HIV-restriction factors, including ISGs, several members of the APOBEC3 family, tetherin and CC chemokines, the ligands for HIV entry coreceptor (CCR5). The inductions of these factors were associated with the inhibition of HIV replication in macrophages stimulated by 5'ppp-dsRNA. These observations highlight the importance of RIG-I signaling in macrophage innate immunity against HIV, which can be beneficial for the treatment of HIV disease, where intracellular immune defense is compromised by the virus.

KEYWORDS:

APOBEC3; interferon regulatory factors; interferon-stimulated genes; type I interferon

PMID:
23744645
PMCID:
PMC3714567
DOI:
10.1189/jlb.0313158
[Indexed for MEDLINE]
Free PMC Article
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