Zika M Oligopeptide ZAMP Confers Cell Death-Promoting Capability to a Soluble Tumor-Associated Antigen through Caspase-3/7 Activation

Vanwalscappel, Bénédicte; Haddad, Juliano G.; Almokdad, Roba; Decotter, Jason; Gadéa, Gilles; Desprès, Philippe

doi:10.3390/ijms21249578

Cited by 7 publications

(10 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Further studies have shown that the nuclear localization of ZIKA-C is related to ribosomal stress (RS) and apoptosis, and the 22 C-terminal residues of ZIKV-C are essential for nuclear localization, RS and apoptosis ( Slomnicki et al, 2017 ). Moreover, DENV2-C was found to have a similar apoptosis-inducing mechanism with ZIKA-C. New study demonstrates that the last C-terminal residues M-31/41 of the ZIKV M ectodomain have death-promoting activity through caspase-3/7 activation, which opens up attractive perspectives for ZAMP (Zika Apoptosis M Peptide) as an innovation anticancer agent ( Vanwalscappel et al, 2020 ). ZIKV-prM protein can induce apoptotic cell death, and the Pr region located on the N-terminal side of prM protein is responsible for prM-induced apoptosis ( Li et al, 2019 ).…”

Section: Apoptosis During Flavivirus-infectionmentioning

confidence: 97%

The Dual Regulation of Apoptosis by Flavivirus

et al. 2021

View full text Add to dashboard Cite

Apoptosis is a form of programmed cell death, which maintains cellular homeostasis by eliminating pathogen-infected cells. It contains three signaling pathways: death receptor pathway, mitochondria-mediated pathway, and endoplasmic reticulum pathway. Its importance in host defenses is highlighted by the observation that many viruses evade, hinder or destroy apoptosis, thereby weakening the host’s immune response. Flaviviruses such as Dengue virus, Japanese encephalitis virus, and West Nile virus utilize various strategies to activate or inhibit cell apoptosis. This article reviews the research progress of apoptosis mechanism during flaviviruses infection, including flaviviruses proteins and subgenomic flaviviral RNA to regulate apoptosis by interacting with host proteins, as well as various signaling pathways involved in flaviviruses-induced apoptosis, which provides a scientific basis for understanding the pathogenesis of flaviviruses and helps in developing an effective antiviral therapy.

show abstract

Section: Apoptosis During Flavivirus-infectionmentioning

confidence: 97%

The Dual Regulation of Apoptosis by Flavivirus

et al. 2021

View full text Add to dashboard Cite

show abstract

“…Viral compounds have been identified as capable of inducing apoptosis on their own. Among flaviviruses, the overexpression of viral proteins, both of structural and non-structural origin, or of peptides derived from these proteins, such as the peptide called apoptoM, have demonstrated their cytotoxic capacity [30][31][32][33]. Unfortunately, the exact mechanisms of their pro-apoptotic action remain poorly understood.…”

Section: Virus-induced Apoptosismentioning

confidence: 99%

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

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.

show abstract

“…The ZIKV-C induces ribosomal stress and apoptosis, and the C protein of DENV has the same function (136). ZIKV-M oligopeptide ZAMP can induce apoptosis by activating caspase-3/7 (137). Interestingly, the subgenomic flaviviral RNA (sfRNA) of ZIKV promotes the spread of ZIKV by inhibiting cell apoptosis in mosquito tissues (138).…”

Section: Apoptosismentioning

confidence: 99%

Flaviviruses: Innate Immunity, Inflammasome Activation, Inflammatory Cell Death, and Cytokines

et al. 2022

View full text Add to dashboard Cite

The innate immune system is the host’s first line of defense against the invasion of pathogens including flavivirus. The programmed cell death controlled by genes plays an irreplaceable role in resisting pathogen invasion and preventing pathogen infection. However, the inflammatory cell death, which can trigger the overflow of a large number of pro-inflammatory cytokines and cell contents, will initiate a severe inflammatory response. In this review, we summarized the current understanding of the innate immune response, inflammatory cell death pathway and cytokine secretion regulation during Dengue virus, West Nile virus, Zika virus, Japanese encephalitis virus and other flavivirus infections. We also discussed the impact of these flavivirus and viral proteins on these biological processes. This not only provides a scientific basis for elucidating the pathogenesis of flavivirus, but also lays the foundation for the development of effective antiviral therapies.

show abstract

Zika M Oligopeptide ZAMP Confers Cell Death-Promoting Capability to a Soluble Tumor-Associated Antigen through Caspase-3/7 Activation

Cited by 7 publications

References 39 publications

The Dual Regulation of Apoptosis by Flavivirus

The Dual Regulation of Apoptosis by Flavivirus

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

Flaviviruses: Innate Immunity, Inflammasome Activation, Inflammatory Cell Death, and Cytokines

Contact Info

Product

Resources

About