ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor

Cellular integrated stress response (ISR), the mitochondrial unfolded protein response (UPRmt), and IFN signaling are associated with viral infections. Activating transcription factor 4 (ATF4) plays a pivotal role in these pathways and controls the expression of many genes involved in redox processe...

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Main Authors: Adrien Corne, Florine Adolphe, Jérôme Estaquier, Sébastien Gaumer, Jean-Marc Corsi
Format: Article
Language:English
Published: MDPI AG 2024-02-01
Series:Biology
Subjects:
Online Access:https://www.mdpi.com/2079-7737/13/3/146
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author Adrien Corne
Florine Adolphe
Jérôme Estaquier
Sébastien Gaumer
Jean-Marc Corsi
author_facet Adrien Corne
Florine Adolphe
Jérôme Estaquier
Sébastien Gaumer
Jean-Marc Corsi
author_sort Adrien Corne
collection DOAJ
description Cellular integrated stress response (ISR), the mitochondrial unfolded protein response (UPRmt), and IFN signaling are associated with viral infections. Activating transcription factor 4 (ATF4) plays a pivotal role in these pathways and controls the expression of many genes involved in redox processes, amino acid metabolism, protein misfolding, autophagy, and apoptosis. The precise role of ATF4 during viral infection is unclear and depends on cell hosts, viral agents, and models. Furthermore, ATF4 signaling can be hijacked by pathogens to favor viral infection and replication. In this review, we summarize the ATF4-mediated signaling pathways in response to viral infections, focusing on human immunodeficiency virus 1 (HIV-1). We examine the consequences of ATF4 activation for HIV-1 replication and reactivation. The role of ATF4 in autophagy and apoptosis is explored as in the context of HIV-1 infection programmed cell deaths contribute to the depletion of CD4 T cells. Furthermore, ATF4 can also participate in the establishment of innate and adaptive immunity that is essential for the host to control viral infections. We finally discuss the putative role of the ATF4 paralogue, named ATF5, in HIV-1 infection. This review underlines the role of ATF4 at the crossroads of multiple processes reflecting host–pathogen interactions.
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spelling doaj.art-ff406ca31b054679b7a6af84379a7e752024-03-27T13:22:05ZengMDPI AGBiology2079-77372024-02-0113314610.3390/biology13030146ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription FactorAdrien Corne0Florine Adolphe1Jérôme Estaquier2Sébastien Gaumer3Jean-Marc Corsi4Laboratoire de Génétique et Biologie Cellulaire, Université Versailles-Saint-Quentin-en-Yvelines, Université Paris-Saclay, 78000 Versailles, FranceLaboratoire de Génétique et Biologie Cellulaire, Université Versailles-Saint-Quentin-en-Yvelines, Université Paris-Saclay, 78000 Versailles, FranceCHU de Québec Research Center, Laval University, Quebec City, QC G1V 4G2, CanadaLaboratoire de Génétique et Biologie Cellulaire, Université Versailles-Saint-Quentin-en-Yvelines, Université Paris-Saclay, 78000 Versailles, FranceLaboratoire de Génétique et Biologie Cellulaire, Université Versailles-Saint-Quentin-en-Yvelines, Université Paris-Saclay, 78000 Versailles, FranceCellular integrated stress response (ISR), the mitochondrial unfolded protein response (UPRmt), and IFN signaling are associated with viral infections. Activating transcription factor 4 (ATF4) plays a pivotal role in these pathways and controls the expression of many genes involved in redox processes, amino acid metabolism, protein misfolding, autophagy, and apoptosis. The precise role of ATF4 during viral infection is unclear and depends on cell hosts, viral agents, and models. Furthermore, ATF4 signaling can be hijacked by pathogens to favor viral infection and replication. In this review, we summarize the ATF4-mediated signaling pathways in response to viral infections, focusing on human immunodeficiency virus 1 (HIV-1). We examine the consequences of ATF4 activation for HIV-1 replication and reactivation. The role of ATF4 in autophagy and apoptosis is explored as in the context of HIV-1 infection programmed cell deaths contribute to the depletion of CD4 T cells. Furthermore, ATF4 can also participate in the establishment of innate and adaptive immunity that is essential for the host to control viral infections. We finally discuss the putative role of the ATF4 paralogue, named ATF5, in HIV-1 infection. This review underlines the role of ATF4 at the crossroads of multiple processes reflecting host–pathogen interactions.https://www.mdpi.com/2079-7737/13/3/146ISRAIDSimmunitymitochondriaER stressUPR
spellingShingle Adrien Corne
Florine Adolphe
Jérôme Estaquier
Sébastien Gaumer
Jean-Marc Corsi
ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor
Biology
ISR
AIDS
immunity
mitochondria
ER stress
UPR
title ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor
title_full ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor
title_fullStr ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor
title_full_unstemmed ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor
title_short ATF4 Signaling in HIV-1 Infection: Viral Subversion of a Stress Response Transcription Factor
title_sort atf4 signaling in hiv 1 infection viral subversion of a stress response transcription factor
topic ISR
AIDS
immunity
mitochondria
ER stress
UPR
url https://www.mdpi.com/2079-7737/13/3/146
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