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HIV Triggers a cGAS-Dependent, Vpu- and Vpr-Regulated Type I Interferon Response in CD4+ T Cells.

Abstract：

:Several pattern-recognition receptors sense HIV-1 replication products and induce type I interferon (IFN-I) production under specific experimental conditions. However, it is thought that viral sensing and IFN induction are virtually absent in the main target cells of HIV-1 in vivo. Here, we show that activated CD4+ T cells sense HIV-1 infection through the cytosolic DNA sensor cGAS and mount a bioactive IFN-I response. Efficient induction of IFN-I by HIV-1 infection requires proviral integration and is regulated by newly expressed viral accessory proteins: Vpr potentiates, while Vpu suppresses cGAS-dependent IFN-I induction. Furthermore, Vpr also amplifies innate sensing of HIV-1 infection in Vpx-treated dendritic cells. Our results identify cGAS as mediator of an IFN-I response to HIV-1 infection in CD4+ T cells and demonstrate that this response is modulated by the viral accessory proteins Vpr and Vpu. Thus, viral innate immune evasion is incomplete in the main target cells of HIV-1.

journal_name

Cell Rep

journal_title

Cell reports

authors

Vermeire J,Roesch F,Sauter D,Rua R,Hotter D,Van Nuffel A,Vanderstraeten H,Naessens E,Iannucci V,Landi A,Witkowski W,Baeyens A,Kirchhoff F,Verhasselt B

doi

10.1016/j.celrep.2016.09.023

subject

Has Abstract

pub_date

2016-10-04 00:00:00

pages

413-424

issue

2

issn

2211-1247

pii

S2211-1247(16)31245-1

journal_volume

17

pub_type

杂志文章

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