CHOP Pro-Apoptotic Transcriptional Program in Response to ER Stress Is Hacked by Zika Virus

Turpin, Jonathan; El-Safadi, Daed; Lebeau, Grégorie; Frumence, Étienne; Desprès, Philippe; Viranaïcken, Wildriss; Krejbich-Trotot, Pascale

doi:10.3390/ijms22073750

Cited by 20 publications

(27 citation statements)

References 59 publications

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“…A privileged role for Bcl-2-family of anti-apoptotics was confirmed by the use of the inhibitor ABT-737, which abrogated ZIKV-mediated protection, led to restoration of apoptosis and reduced viral infection [90]. As previously mentioned, we also found that ZIKV was able to subvert the CHOP pro-apoptotic program and thus override ERdependent apoptosis [94]. This viral ability to inhibit one of the main cellular defense responses to infection legitimately raises the question of its effect on the outcome of infection and, if unsuccessful, the possibility that the virus will not be properly eliminated.…”

Section: Is Delayed and Impaired Apoptosis Responsible For Zikv Persistence And Unusual Transmission Pathways?supporting

confidence: 81%

“…However, if we and others have noticed a significant increase in the transcriptional expression of CHOP [88], there is a lack of information concerning the CHOP protein presence in ZIKV infected cells. Thus, in the A549 model, we showed that the CHOP factor and its pro-apoptotic translational program were not induced [94]. Assessment of its role in the virally induced UPR-dependent apoptosis is therefore difficult.…”

Section: Is Early Apoptosis In Development Responsible For the Irreversible Damage Produced By Zikv Infection?mentioning

confidence: 87%

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Apoptosis During ZIKA Virus Infection: Too Soon or Too Late?

Turpin¹,

Safadi²,

Lebeau³

et al. 2021

Preprint

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Cell death by apoptosis is a major cellular response, in the control of tissue homeostasis and as a defense mechanism in case of cellular aggression like an infection. Cell self-destruction is part of antiviral responses, aimed at limiting the spread of a virus. Although it may contribute to the deleterious effects in infectious pathology, apoptosis remains a key mechanism for viral clearance and resolution of infection. The control mechanisms of cell death processes by viruses have been extensively studied. Apoptosis can be triggered by different viral determinants, through different pathways, as a result of virally induced cell stresses and innate immune responses. Zika virus (ZIKV) induces Zika disease in humans which has caused severe neurological forms, birth defects and microcephaly in newborns during the last epidemics. ZIKV also surprised by revealing an ability to persist in the genital tract and in semen, thus being sexually transmitted. Mechanisms of diverting antiviral responses such as the interferon response, the role of cytopathic effects and apoptosis in the etiology of the disease have been widely studied and debated. In this review, we examined the interplay between ZIKV infection of different cell types and apoptosis and how the virus deals with this cellular response. We illustrate a duality in the effects of ZIKV-controlled apoptosis, depending on whether it occurs too early or too late, respectively in neuropathogenesis, or in long-term viral persistence. We further discuss a prospective role for apoptosis in ZIKV-related therapies, and the use of ZIKV as an oncolytic agent.

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Section: Is Delayed and Impaired Apoptosis Responsible For Zikv Persistence And Unusual Transmission Pathways?supporting

confidence: 81%

Section: Is Early Apoptosis In Development Responsible For the Irreversible Damage Produced By Zikv Infection?mentioning

confidence: 87%

Apoptosis During ZIKA Virus Infection: Too Soon or Too Late?

Turpin¹,

Safadi²,

Lebeau³

et al. 2021

Preprint

Self Cite

View full text Add to dashboard Cite

show abstract

“…However, if we and others have noticed a significant increase in the transcriptional expression of CHOP [104], there is a lack of information concerning the CHOP protein presence in ZIKV infected cells. Thus, in the A549 model, we showed that the CHOP factor and its pro-apoptotic translational program were not induced [92]. Assessment of its role in the virally induced UPR-dependent apoptosis is therefore difficult.…”

Section: Zika Virus and Apoptosismentioning

confidence: 87%

Apoptosis during ZIKA Virus Infection: Too Soon or Too Late?

Turpin

Safadi

Lebeau

et al. 2022

IJMS

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Cell death by apoptosis is a major cellular response in the control of tissue homeostasis and as a defense mechanism in the case of cellular aggression such as an infection. Cell self-destruction is part of antiviral responses, aimed at limiting the spread of a virus. Although it may contribute to the deleterious effects in infectious pathology, apoptosis remains a key mechanism for viral clearance and the resolution of infection. The control mechanisms of cell death processes by viruses have been extensively studied. Apoptosis can be triggered by different viral determinants through different pathways as a result of virally induced cell stresses and innate immune responses. Zika virus (ZIKV) induces Zika disease in humans, which has caused severe neurological forms, birth defects, and microcephaly in newborns during the last epidemics. ZIKV also surprised by revealing an ability to persist in the genital tract and in semen, thus being sexually transmitted. Mechanisms of diverting antiviral responses such as the interferon response, the role of cytopathic effects and apoptosis in the etiology of the disease have been widely studied and debated. In this review, we examined the interplay between ZIKV infection of different cell types and apoptosis and how the virus deals with this cellular response. We illustrate a duality in the effects of ZIKV-controlled apoptosis, depending on whether it occurs too early or too late, respectively, in neuropathogenesis, or in long-term viral persistence. We further discuss a prospective role for apoptosis in ZIKV-related therapies, and the use of ZIKV as an oncolytic agent.

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“…In the middle and late stages of virus infection, a large number of viruses replicate in the target cells, and activate mitochondrial and endoplasmic reticulum stress and other apoptosis pathways, leading to cell apoptosis. The flaviviruses infection is capable of triggering multiple apoptotic pathways, such as mitochondria-dependence ( Suzuki et al., 2018 ), death receptor ( Liao et al., 2010 ), and endoplasmic reticulum ( ER ) stress ( Huang et al., 2016 ; Turpin et al., 2021 ). JEV triggered apoptosis of N18 (a mouse neuroblastoma cell line) cells through the mitochondrial pathway ( Tsao et al., 2008 ), possibly by inducing proteolysis of endogenous p21 BAX to produce p18 BAX in SH-SY5Y cells (human neuroblastoma) ( Wongchitrat et al., 2019 ).…”

Section: Discussionmentioning

confidence: 99%

“…JEV plays a role in cell apoptosis through p38-dependent and transcription factor C/EBP homologous protein ( CHOP ) mediated pathways ( Su et al., 2002 ). ZIKV impaired the expression of CHOP/DDIT3, which is the main factor of ER-stress-driven apoptosis ( Turpin et al., 2021 ). JEV infection decreased Forkhead box O ( FoxO ) expression both in vitro and in vivo.…”

Section: Discussionmentioning

confidence: 99%

Role of apoptosis in Duck Tembusu virus infection of duckling brains in vivo

Yang

Huang

et al. 2022

Poultry Science

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The Duck Tembusu virus ( DTMUV ) is a novel flavivirus that occurs mainly in poultry. DTMUV infection can cause common neurological symptoms in ducklings, but the pathogenesis of DTMUV has not been elucidated yet. In this study, a DTMUV-infected duckling model was constructed to investigate the apoptosis in the duckling brains. After DTMUV infection, apoptotic cells were observed by transmission electron microscopy. It was found that the abundances of apoptosis-related genes and proteins were not obviously changed in the early stage of infection but significantly changed in the middle and late stages of the disease. Terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling assay staining results were also consistent with the above phenomena. Interestingly, although apoptosis occurred in the duckling brains infected by DTMUV, some antiapoptotic genes in the brain increased in varying degrees. In conclusion, DTMUV infection could induce apoptosis in ducklings’ brains, and the occurrence of apoptosis was accompanied by the virus infection process with certain regularity. This study provides a scientific basis for elucidating the apoptotic mechanism of brain lesions induced by DTMUV infection.

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CHOP Pro-Apoptotic Transcriptional Program in Response to ER Stress Is Hacked by Zika Virus

Cited by 20 publications

References 59 publications

Apoptosis During ZIKA Virus Infection: Too Soon or Too Late?

Apoptosis During ZIKA Virus Infection: Too Soon or Too Late?

Apoptosis during ZIKA Virus Infection: Too Soon or Too Late?

Role of apoptosis in Duck Tembusu virus infection of duckling brains in vivo

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