Impairment of the type I interferon response by HIV-1: Potential targets for HIV eradication. (October 2017)

• Record Type: Journal Article
• Authors: Sandstrom, Teslin S.; Ranganath, Nischal; Angel, Jonathan B.
• Is Part Of: Cytokine & growth factor reviews. Volume 37(2017)
• Page Start: 1
• Page End: 16
• Publication Date: 2017-10
• Subjects: βTrCP beta transducin repeat-containing protein -- ADAR1 adenosine deaminase acting on RNA 1 -- AGM African green monkey -- APOBEC3 apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like 3 -- ART antiretroviral therapy -- BDCA-2 blood dendritic cell antigen 2 -- BST-2 bone marrow stromal cell antigen 2 -- CDK2 cyclin-dependent kinase 2 -- cGAS cyclic guanosine monophosphate-adenosine monophosphate synthase -- CLR C-type lectin receptor -- DC dendritic cell -- dNTP deoxynucleotide triphosphate -- dsRNA double-stranded RNA -- EIF2α eukaryotic initiation factor 2 -- HIV-1 human immunodeficiency virus 1 -- HLA human leukocyte antigen -- IFI16 IFN-γ-inducible protein 16 -- IFI27 IFN-α-inducible protein 27 -- IFI44 interferon-induced protein 44 -- IFI44L interferon-induced protein 44-like -- IFIT interferon induced protein with tetratricopeptide repeats -- IFN interferon -- IFN1 type I interferon -- IFNAR IFNα/β receptor -- IFNAR1 IFNα/β receptor subunit 1 -- IFNAR2 IFNα/β receptor subunit 2 -- IPS-1 interferon-β promoter stimulator 1 -- IRAK interleukin-1 receptor associated kinase -- IRF interferon regulatory factor -- IRFBS interferon regulatory factor binding site -- ISG IFN-stimulated gene -- ISG15 interferon-stimulated gene 15 -- ISGF3 interferon-stimulated gene factor 3 -- ISRE interferon-stimulated response element -- JAK1 janus kinase 1 -- LGP2 laboratory of genetics and physiology 2 -- LRA latency reversal agent -- MDM monocyte derived macrophage -- MDDC monocyte derived dendritic cell -- MDA5 melanoma differentiation-associated gene 5 -- MHC I major histocompatibility complex I -- MxB human myxovirus-resistance protein B -- NFκB nuclear factor kappa-light-chain-enhancer of activated B cells -- NHP non-human primate -- NK Cell natural killer cell -- NLR nucleotide-binding oligomerization domain-like receptor -- OAS 2′5′ oligoadenylate synthetase -- PACT protein kinase R activator -- PAMP pathogen associated molecular pattern -- PBMC peripheral blood mononuclear cells -- pDC plasmacytoid dendritic cell -- PKR protein kinase R -- PRR pattern recognition receptor -- RIG-I retinoic acid inducible gene I -- RLR RIG-I-like receptor -- RM rhesus macaque -- SAMHD1 sterile alpha motif domain and HD domain-containing protein 1 -- SIV simian immunodeficiency virus -- SHIV SIV/HIV chimeric virus -- SOCS suppressor of cytokine signalling -- ssRNA single-stranded RNA -- STAT signal transducer and activator of transcription -- STING stimulator of interferon genes -- TAR trans-activation response -- TBK1 TANK-binding kinase -- TLR toll-like receptor -- TRAF6 TNF receptor associated factor 6 -- TRBP trans-activation response RNA binding protein -- TREX1 three-prime repair exonuclease 1 -- TYK2 tyrosine kinase 2; HIV-1 -- Type I IFN -- Immune evasion -- Pattern recognition receptor -- IFN-stimulated gene; Cytokines -- Periodicals; 571.84
• DOI: 10.1016/j.cytogfr.2017.04.004
• Languages: English
• ISSNs: 1359-6101

Abstract

Graphical abstract: Highlights: This review summarizes current knowledge of defects in the type I IFN response in primary cell models of HIV-1 infection. Type I IFN expression is upregulated during HIV-1 infection, but does not result in viral clearance. HIV-1 can interfere with the type I IFN response by impairing the function of antiviral, interferon stimulated genes. Despite these defects, therapeutic activation of type I IFN signalling may facilitate the clearance of the HIV-1 reservoir. Abstract: By interfering with the type I interferon (IFN1) response, human immunodeficiency virus 1 (HIV-1) can circumvent host antiviral signalling and establish persistent viral reservoirs. HIV-1-mediated defects in the IFN pathway are numerous, and include the impairment of protein receptors involved in pathogen detection, downstream signalling cascades required for IFN1 upregulation, and expression or function of key IFN1-inducible, antiviral proteins. Despite this, the activation of IFN1-inducible, antiviral proteins has been shown to facilitate the killing of latently HIV-infected cells in vitro . Understanding how IFN1 signalling is blocked in physiologically-relevant models of HIV-1 infection, and whether these defects can be reversed, is therefore of great importance for the development of novel therapeutic strategies aimed at eradicating the HIV-1 reservoir.