Targeting aryl hydrocarbon receptor signaling enhances type I interferon-independent resistance to herpes simplex virus

Jincheng Chen; Juan Liang; Hui Xu; Wenqi Liu; Shuyan Liu; Lian Duan; Fang Li; Zhaoqin Wang; Yingxia Liu; Brian McSharry; Carl G Feng; Guoliang Zhang

doi:10.1128/Spectrum.00473-21

Targeting aryl hydrocarbon receptor signaling enhances type I interferon-independent resistance to herpes simplex virus

Jincheng Chen, Juan Liang, Hui Xu, Wenqi Liu, Shuyan Liu, Lian Duan, Fang Li, Zhaoqin Wang, Yingxia Liu, Brian McSharry, Carl G Feng, Guoliang Zhang

Dentistry and Medical Sciences

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Abstract

The aryl hydrocarbon receptor (AHR) is a ligand-activated transcript factor that plays an important role in regulating immunity and cell differentiation. However, its role in cell-autonomous antiviral resistance has not been fully elucidated. Here, we show that interruption of AHR signaling in human cells by a chemical antagonist or genetic targeting led to significant reductions in the replication of herpes simplex virus 1 (HSV-1) and cytomegalovirus (CMV), revealing an unexpected proviral function of AHR. Interestingly, the enhanced viral control in the absence of AHR is independent of type I interferon (IFN) signaling. Together, these results reveal a previously unknown function of AHR in promoting viral replication in vitro and suggest a potential intervention point for treating viral disease.IMPORTANCE This study describes how a virus might utilize host aryl hydrocarbon receptor signaling to promote its replication, even in the presence of type I interferons.

Original language	English
Article number	e00473-21
Number of pages	9
Journal	Microbiology spectrum
Volume	9
Issue number	2
DOIs	https://doi.org/10.1128/Spectrum.00473-21
Publication status	Published - 31 Oct 2021

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10.1128/Spectrum.00473-21

183296711 published articleFinal published version, 1.98 MBLicence: CC BY

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title = "Targeting aryl hydrocarbon receptor signaling enhances type I interferon-independent resistance to herpes simplex virus",

abstract = "The aryl hydrocarbon receptor (AHR) is a ligand-activated transcript factor that plays an important role in regulating immunity and cell differentiation. However, its role in cell-autonomous antiviral resistance has not been fully elucidated. Here, we show that interruption of AHR signaling in human cells by a chemical antagonist or genetic targeting led to significant reductions in the replication of herpes simplex virus 1 (HSV-1) and cytomegalovirus (CMV), revealing an unexpected proviral function of AHR. Interestingly, the enhanced viral control in the absence of AHR is independent of type I interferon (IFN) signaling. Together, these results reveal a previously unknown function of AHR in promoting viral replication in vitro and suggest a potential intervention point for treating viral disease.IMPORTANCE This study describes how a virus might utilize host aryl hydrocarbon receptor signaling to promote its replication, even in the presence of type I interferons.",

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author = "Jincheng Chen and Juan Liang and Hui Xu and Wenqi Liu and Shuyan Liu and Lian Duan and Fang Li and Zhaoqin Wang and Yingxia Liu and Brian McSharry and Feng, {Carl G} and Guoliang Zhang",

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doi = "10.1128/Spectrum.00473-21",

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AU - Chen, Jincheng

AU - Liang, Juan

AU - Xu, Hui

AU - Liu, Wenqi

AU - Liu, Shuyan

AU - Duan, Lian

AU - Li, Fang

AU - Wang, Zhaoqin

AU - Liu, Yingxia

AU - McSharry, Brian

AU - Feng, Carl G

AU - Zhang, Guoliang

PY - 2021/10/31

Y1 - 2021/10/31

N2 - The aryl hydrocarbon receptor (AHR) is a ligand-activated transcript factor that plays an important role in regulating immunity and cell differentiation. However, its role in cell-autonomous antiviral resistance has not been fully elucidated. Here, we show that interruption of AHR signaling in human cells by a chemical antagonist or genetic targeting led to significant reductions in the replication of herpes simplex virus 1 (HSV-1) and cytomegalovirus (CMV), revealing an unexpected proviral function of AHR. Interestingly, the enhanced viral control in the absence of AHR is independent of type I interferon (IFN) signaling. Together, these results reveal a previously unknown function of AHR in promoting viral replication in vitro and suggest a potential intervention point for treating viral disease.IMPORTANCE This study describes how a virus might utilize host aryl hydrocarbon receptor signaling to promote its replication, even in the presence of type I interferons.

AB - The aryl hydrocarbon receptor (AHR) is a ligand-activated transcript factor that plays an important role in regulating immunity and cell differentiation. However, its role in cell-autonomous antiviral resistance has not been fully elucidated. Here, we show that interruption of AHR signaling in human cells by a chemical antagonist or genetic targeting led to significant reductions in the replication of herpes simplex virus 1 (HSV-1) and cytomegalovirus (CMV), revealing an unexpected proviral function of AHR. Interestingly, the enhanced viral control in the absence of AHR is independent of type I interferon (IFN) signaling. Together, these results reveal a previously unknown function of AHR in promoting viral replication in vitro and suggest a potential intervention point for treating viral disease.IMPORTANCE This study describes how a virus might utilize host aryl hydrocarbon receptor signaling to promote its replication, even in the presence of type I interferons.

KW - aryl hydrocarbon receptor

KW - herpes simplex virus 1

KW - type 1interferons

KW - viral replication

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DO - 10.1128/Spectrum.00473-21

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JO - Microbiology spectrum

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Targeting aryl hydrocarbon receptor signaling enhances type I interferon-independent resistance to herpes simplex virus

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