Oligodendrocytes are susceptible to Zika virus infection in a mouse model of perinatal exposure: Implications for <scp>CNS</scp> complications

Schultz, Verena; Barrie, Jennifer A.; Donald, Claire L.; Crawford, Colin L.; Mullin, Margaret; Anderson, Thomas; Solomon, Tom; Barnett, Susan C.; Linington, Christopher; Kohl, Alain; Willison, Hugh J.; Edgar, Julia M.

doi:10.1002/glia.24010

Cited by 20 publications

(20 citation statements)

References 69 publications

(85 reference statements)

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“…In a mouse model of intracranial infection at different stages of embryonic development, co-immunoreactivity throughout the brain of cleaved caspase-3 and ZIKV are indicators of deleterious cell death [8]. In a recent study, oligodendrocyte loss in spinal cord and white matter has been linked to neurodevelopmental defects and perinatal ZIKV induced pathogenesis in mice [98]. In another chick embryo model, virus-induced apoptosis of cranial neural crest cells was shown to be responsible for aberrations in cranial osteogenesis and to lead to birth defects [99].…”

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

confidence: 99%

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

confidence: 99%

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

Turpin¹,

Safadi²,

Lebeau³

et al. 2021

Preprint

View full text Add to dashboard Cite

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Section: Zika Virus and Apoptosismentioning

confidence: 99%

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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“…While the mechanism for these delayed effects is unclear, murine models suggest that Zika infection of oligodendrocytes and subsequent cell death in the post-natal period leads to secondary immune demyelination. 129 It is also possible that ZIKV has persistent replicating ability in the CNS, which could increase the risk of neurological issues in children with intrauterine Zika exposure. 130 Together, these data present a strong case that clinically normal infants at birth whose mothers had a known Zika infection during pregnancy should be closely followed for the signs of neurodevelopmental delays years after initial diagnosis.…”

Section: Neuroinvasive Zikv Infectionmentioning

confidence: 99%

Acute neurologic emerging flaviviruses

Caldwell

Boruah

Thakur

2022

Therapeutic Advances in Infection

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The COVID-19 pandemic has shed light on the challenges we face as a global society in preventing and containing emerging and re-emerging pathogens. Multiple intersecting factors, including environmental changes, host immunological factors, and pathogen dynamics, are intimately connected to the emergence and re-emergence of communicable diseases. There is a large and expanding list of communicable diseases that can cause neurological damage, either through direct or indirect routes. Novel pathogens of neurotropic potential have been identified through advanced diagnostic techniques, including metagenomic next-generation sequencing, but there are also known pathogens which have expanded their geographic distribution to infect non-immune individuals. Factors including population growth, climate change, the increase in animal and human interface, and an increase in international travel and trade are contributing to the expansion of emerging and re-emerging pathogens. Challenges exist around antimicrobial misuse giving rise to antimicrobial-resistant infectious neurotropic organisms and increased susceptibility to infection related to the expanded use of immunomodulatory treatments. In this article, we will review key concepts around emerging and re-emerging pathogens and discuss factors associated with neurotropism and neuroinvasion. We highlight several neurotropic pathogens of interest, including West Nile virus (WNV), Zika Virus, Japanese Encephalitis Virus (JEV), and Tick-Borne Encephalitis Virus (TBEV). We emphasize neuroinfectious diseases which impact the central nervous system (CNS) and focus on flaviviruses, a group of vector-borne pathogens that have expanded globally in recent years and have proven capable of widespread outbreak.

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Oligodendrocytes are susceptible to Zika virus infection in a mouse model of perinatal exposure: Implications for CNS complications

Cited by 20 publications

References 69 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?

Acute neurologic emerging flaviviruses

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