Activation of ATF3 via the Integrated Stress Response Pathway Regulates Innate Immune Response to Restrict Zika Virus DOI Creative Commons
Pheonah Badu, Gabriele Baniulyte, Morgan A. Sammons

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2023, Volume and Issue: unknown

Published: July 27, 2023

Abstract Zika virus (ZIKV) is a re-emerging mosquito-borne flavivirus that can have devastating health consequences. The developmental and neurological effects from ZIKV infection arise in part the triggering cellular stress pathways perturbing transcriptional programs. To date, underlying mechanisms of control directing viral restriction virus-host interaction are understudied. Activating Transcription Factor 3 (ATF3) stress-induced effector modulates expression genes involved myriad processes, including inflammation antiviral responses, to restore homeostasis. While ATF3 known be upregulated during infection, mode by which activated specific role unknown. In this study, we show via inhibitor RNA interference approaches initiates integrated response pathway activate ATF4 turn induces expression. Additionally, using CRISPR-Cas9 system delete ATF3, found acts limit gene A549 cells. We also determined enhances such as STAT1 other components innate immunity induce an ATF3-dependent anti-ZIKV response. Our study reveals crosstalk between immune highlights important for establishing effect infection. Importance co-opts support processes reprogram host profile. Such viral-directed changes pro- or anti-viral outcomes remain previously showed transcription factor, significantly infected mammalian cells, along with genes. now define intracellular responsible activation elucidate impact on stimulates antagonize This establishes link viral-induced regulation defense thus expands our knowledge virus-mediated interferon stimulated

Language: Английский

Activation of ATF3 via the integrated stress response pathway regulates innate immune response to restrict Zika virus DOI Creative Commons
Pheonah Badu, Gabriele Baniulyte, Morgan A. Sammons

et al.

Journal of Virology, Journal Year: 2024, Volume and Issue: unknown

Published: Aug. 30, 2024

ABSTRACT Zika virus (ZIKV) is a re-emerging mosquito-borne flavivirus that can have devastating health consequences. The developmental and neurological effects of ZIKV infection arise in part from the triggering cellular stress pathways perturbing transcriptional programs. To date, underlying mechanisms control directing viral restriction virus-host interaction are understudied. Activating Transcription Factor 3 (ATF3) stress-induced effector modulates expression genes involved myriad processes, including inflammation antiviral responses, to restore homeostasis. While ATF3 known be upregulated during infection, mode by which activated, specific role unknown. In this study, we show via inhibitor RNA interference approaches initiates integrated response pathway activate ATF4 turn induces expression. Additionally, using CRISPR-Cas9 system delete ATF3, found acts limit gene A549 cells. We also determined enhances such as STAT1 other components innate immunity induce an ATF3-dependent anti-ZIKV response. Our study reveals crosstalk between immune highlights important for establishing effect infection. IMPORTANCE co-opts support processes reprogram host profile. Such viral-directed changes pro- or anti-viral outcomes remain previously showed transcription factor, significantly ZIKV-infected mammalian cells, along with genes. now define intracellular responsible activation elucidate impact on stimulates antagonize This establishes link viral-induced regulation defense thus expands our knowledge virus-mediated interferon-stimulated

Language: Английский

Citations

4
Activation of ATF3 via the Integrated Stress Response Pathway Regulates Innate Immune Response to Restrict Zika Virus DOI Creative Commons
Pheonah Badu, Gabriele Baniulyte, Morgan A. Sammons

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2023, Volume and Issue: unknown

Published: July 27, 2023

Abstract Zika virus (ZIKV) is a re-emerging mosquito-borne flavivirus that can have devastating health consequences. The developmental and neurological effects from ZIKV infection arise in part the triggering cellular stress pathways perturbing transcriptional programs. To date, underlying mechanisms of control directing viral restriction virus-host interaction are understudied. Activating Transcription Factor 3 (ATF3) stress-induced effector modulates expression genes involved myriad processes, including inflammation antiviral responses, to restore homeostasis. While ATF3 known be upregulated during infection, mode by which activated specific role unknown. In this study, we show via inhibitor RNA interference approaches initiates integrated response pathway activate ATF4 turn induces expression. Additionally, using CRISPR-Cas9 system delete ATF3, found acts limit gene A549 cells. We also determined enhances such as STAT1 other components innate immunity induce an ATF3-dependent anti-ZIKV response. Our study reveals crosstalk between immune highlights important for establishing effect infection. Importance co-opts support processes reprogram host profile. Such viral-directed changes pro- or anti-viral outcomes remain previously showed transcription factor, significantly infected mammalian cells, along with genes. now define intracellular responsible activation elucidate impact on stimulates antagonize This establishes link viral-induced regulation defense thus expands our knowledge virus-mediated interferon stimulated

Language: Английский

Citations

5