About: The Inhibition of HIV-1 Entry Imposed by Interferon Inducible Transmembrane Proteins Is Independent of Co-Receptor Usage

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About: The Inhibition of HIV-1 Entry Imposed by Interferon Inducible Transmembrane Proteins Is Independent of Co-Receptor Usage Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : covidontheweb.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	The Inhibition of HIV-1 Entry Imposed by Interferon Inducible Transmembrane Proteins Is Independent of Co-Receptor Usage
Creator	Liu, Shan-Lu Yu, Jingyou
Source	Medline; PMC
abstract	Interferon inducible transmembrane proteins (IFITMs) are one of several IFN-stimulated genes (ISGs) that restrict entry of enveloped viruses, including flaviviruses, filoviruses and retroviruses. It has been recently reported that in U87 glioblastoma cells IFITM proteins inhibit HIV-1 entry in a co-receptor-dependent manner, that is, IFITM1 is more inhibitory on CCR5 tropic HIV-1 whereas IFITM2/3 confers a greater suppression of CXCR4 counterparts. However, how entry of HIV-1 with distinct co-receptor usage is modulated by different IFITM orthologs in physiologically relevant CD4(+) T cells and monocytes/macrophages has not been investigated in detail. Here, we report that overexpression of IFITM1, 2 and 3 in human CD4(+) HuT78 cells, SupT1 cells, monocytic THP-1 cells and U87 cells expressing CD4 and co-receptor CCR5 or CXCR4, suppressed entry of CXCR4 tropic viruses NL4.3 and HXB2, CCR5 tropic viruses AD8 and JRFL, dual tropic 89.6 virus, as well as a panel of 32 transmitted founder (T/F) viruses, with a consistent order of potency, that is, IFITM3 > IFITM2 > IFITM1. Consistent with previous reports, we found that some CCR5-using HIV-1 isolates, such as AD8 and JRFL, were relatively resistant to inhibition by IFITM2 and IFITM3, although the effect can be cell-type dependent. However, in no case have we observed that IFITM1 had a stronger inhibition on entry of any HIV-1 strains tested, including those of CCR5-using T/Fs. We knocked down the endogenous IFITMs in peripheral blood mononuclear cells (PBMCs) and purified CD4(+) T cells and observed that, while this treatment did greatly enhance the multiple-round of HIV-1 replication but had modest effect to rescue the single-round HIV-1 infection, reinforcing our previous conclusion that the predominant effect of IFITMs on HIV-1 infection is in viral producer cells, rather than in target cells to block viral entry. Overall, our results argue against the idea that IFITM proteins distinguish co-receptors CCR5 and CXCR4 to inhibit entry but emphasize that the predominant role of IFITMs on HIV-1 is in producer cells that intrinsically impair the viral infectivity.
has issue date	2018-08-07(xsd:dateTime)
bibo:doi	10.3390/v10080413
bibo:pmid	30087232
has license	cc-by
sha1sum (hex)	73aec7f72de1b225ab650b78a7633aab4ebd97bc
schema:url	https://doi.org/10.3390/v10080413
resource representing a document's title	The Inhibition of HIV-1 Entry Imposed by Interferon Inducible Transmembrane Proteins Is Independent of Co-Receptor Usage
has PubMed Central identifier	PMC6115839
has PubMed identifier	30087232
schema:publication	Viruses
resource representing a document's body	covid:73aec7f72de1b225ab650b78a7633aab4ebd97bc#body_text
is schema:about of	named entity 'producer' named entity 'HIV-1' named entity 'filoviruses' named entity 'enveloped viruses' named entity 'inhibit' named entity 'tested' named entity 'strains' named entity 'Consistent' named entity 'orthologs' named entity 'restrict' named entity 'replication' named entity 'HIV-1' covid:arg/73aec7f72de1b225ab650b78a7633aab4ebd97bc named entity 'usage' named entity 'reinforcing' named entity 'cells' named entity 'transmembrane proteins' named entity 'HIV-1 infection' named entity 'inhibition' named entity 'CD4' named entity 'PBMCs' named entity 'cells' named entity 'manner' named entity 'virus' named entity 'observed' named entity 'expressing' named entity 'argue' named entity 'However' named entity 'Inhibition' named entity 'CCR5' named entity 'viruses' named entity 'flaviviruses' named entity 'retroviruses' named entity 'HIV-1' named entity 'infectivity' named entity 'enveloped viruses' named entity 'HIV-1' named entity 'HIV-1 infection' named entity 'viruses' named entity 'viruses' named entity 'CXCR4' named entity 'CCR5' named entity 'endogenous' named entity 'filoviruses' named entity 'IFITM1' named entity 'IFITM3' named entity 'co-receptor' named entity 'peripheral blood mononuclear cells' named entity 'Transmembrane Proteins' named entity 'HIV-1' named entity 'CD4' named entity 'Env' named entity 'HIV-1' named entity 'transduced' named entity 'IFITM3' named entity 'innate immunity' named entity 'Reagent' named entity 'luciferase' named entity 'HIV-1' named entity 'IFITM3' named entity 'endogenous' named entity 'HIV-1' named entity 'CD4' named entity 'IFITM1' named entity 'IFN' named entity 'PBMCs' named entity 'HIV-1' named entity 'HIV-1 infection' named entity 'monocytes' named entity 'HEK293T cells' named entity 'Env' named entity 'transfection' named entity 'CXCR4' named entity 'lipid' named entity 'IFN' named entity 'potency' named entity 'CD4 +' named entity 'IFITM1' named entity 'IFN' named entity 'IFITM1'

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