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HIV-1 blocks the signaling adaptor MAVS to evade antiviral host defense after sensing of abortive HIV-1 RNA by the host helicase DDX3. / Gringhuis, Sonja I.; Hertoghs, Nina; Kaptein, Tanja M. et al.

In: Nature immunology, Vol. 18, No. 2, 2017, p. 225-235.

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@article{3a4d6ac3efd348159f0e753238491f17,
title = "HIV-1 blocks the signaling adaptor MAVS to evade antiviral host defense after sensing of abortive HIV-1 RNA by the host helicase DDX3",
abstract = "The mechanisms by which human immunodeficiency virus 1 (HIV-1) avoids immune surveillance by dendritic cells (DCs), and thereby prevents protective adaptive immune responses, remain poorly understood. Here we showed that HIV-1 actively arrested antiviral immune responses by DCs, which contributed to efficient HIV-1 replication in infected individuals. We identified the RNA helicase DDX3 as an HIV-1 sensor that bound abortive HIV-1 RNA after HIV-1 infection and induced DC maturation and type I interferon responses via the signaling adaptor MAVS. Notably, HIV-1 recognition by the C-type lectin receptor DC-SIGN activated the mitotic kinase PLK1, which suppressed signaling downstream of MAVS, thereby interfering with intrinsic host defense during HIV-1 infection. Finally, we showed that PLK1-mediated suppression of DDX3-MAVS signaling was a viral strategy that accelerated HIV-1 replication in infected individuals",
author = "Gringhuis, {Sonja I.} and Nina Hertoghs and Kaptein, {Tanja M.} and Zijlstra-Willems, {Esther M.} and Ramin Sarrami-Fooroshani and Sprokholt, {Joris K.} and {van Teijlingen}, {Nienke H.} and Kootstra, {Neeltje A.} and Thijs Booiman and {van Dort}, {Karel A.} and Ribeiro, {Carla M. S.} and Agata Drewniak and Geijtenbeek, {Teunis B. H.}",
year = "2017",
doi = "10.1038/ni.3647",
language = "English",
volume = "18",
pages = "225--235",
journal = "Nature immunology",
issn = "1529-2908",
publisher = "Nature Publishing Group",
number = "2",

}

RIS

TY - JOUR

T1 - HIV-1 blocks the signaling adaptor MAVS to evade antiviral host defense after sensing of abortive HIV-1 RNA by the host helicase DDX3

AU - Gringhuis, Sonja I.

AU - Hertoghs, Nina

AU - Kaptein, Tanja M.

AU - Zijlstra-Willems, Esther M.

AU - Sarrami-Fooroshani, Ramin

AU - Sprokholt, Joris K.

AU - van Teijlingen, Nienke H.

AU - Kootstra, Neeltje A.

AU - Booiman, Thijs

AU - van Dort, Karel A.

AU - Ribeiro, Carla M. S.

AU - Drewniak, Agata

AU - Geijtenbeek, Teunis B. H.

PY - 2017

Y1 - 2017

N2 - The mechanisms by which human immunodeficiency virus 1 (HIV-1) avoids immune surveillance by dendritic cells (DCs), and thereby prevents protective adaptive immune responses, remain poorly understood. Here we showed that HIV-1 actively arrested antiviral immune responses by DCs, which contributed to efficient HIV-1 replication in infected individuals. We identified the RNA helicase DDX3 as an HIV-1 sensor that bound abortive HIV-1 RNA after HIV-1 infection and induced DC maturation and type I interferon responses via the signaling adaptor MAVS. Notably, HIV-1 recognition by the C-type lectin receptor DC-SIGN activated the mitotic kinase PLK1, which suppressed signaling downstream of MAVS, thereby interfering with intrinsic host defense during HIV-1 infection. Finally, we showed that PLK1-mediated suppression of DDX3-MAVS signaling was a viral strategy that accelerated HIV-1 replication in infected individuals

AB - The mechanisms by which human immunodeficiency virus 1 (HIV-1) avoids immune surveillance by dendritic cells (DCs), and thereby prevents protective adaptive immune responses, remain poorly understood. Here we showed that HIV-1 actively arrested antiviral immune responses by DCs, which contributed to efficient HIV-1 replication in infected individuals. We identified the RNA helicase DDX3 as an HIV-1 sensor that bound abortive HIV-1 RNA after HIV-1 infection and induced DC maturation and type I interferon responses via the signaling adaptor MAVS. Notably, HIV-1 recognition by the C-type lectin receptor DC-SIGN activated the mitotic kinase PLK1, which suppressed signaling downstream of MAVS, thereby interfering with intrinsic host defense during HIV-1 infection. Finally, we showed that PLK1-mediated suppression of DDX3-MAVS signaling was a viral strategy that accelerated HIV-1 replication in infected individuals

U2 - 10.1038/ni.3647

DO - 10.1038/ni.3647

M3 - Article

C2 - 28024153

VL - 18

SP - 225

EP - 235

JO - Nature immunology

JF - Nature immunology

SN - 1529-2908

IS - 2

ER -

ID: 3277702