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

Research output: Contribution to journalArticlepeer-review

2 Downloads (Pure)

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 languageEnglish
Article numbere00473-21
Number of pages9
JournalMicrobiology spectrum
Volume9
Issue number2
DOIs
Publication statusPublished - 31 Oct 2021

Fingerprint

Dive into the research topics of 'Targeting aryl hydrocarbon receptor signaling enhances type I interferon-independent resistance to herpes simplex virus'. Together they form a unique fingerprint.

Cite this