Zika Virus–Associated Cognitive Impairment in Adolescent, 2016

Zucker, Jason; Neu, Natalie; Chiriboga, Claudia A.; Hinton, Veronica J.; Leonardo, Marc; Sheikh, Arif; Thakur, Kiran T.

doi:10.3201/eid2306.162029

Cited by 28 publications

(27 citation statements)

References 5 publications

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“…Our findings predict that many of these individuals may have changes in their DNA methylome that could ultimately affect the expression of key genes involved in a spectrum of neuropsychiatric disorders. Our findings, together with recent clinical reports describing a causal relationship between ZIKV infection in adolescents and severe depression ( 31 ) and psychosis ( 32 ), support the hypothesis that ZIKV might directly trigger neuropsychiatric and cognitive disease. Hence, while more is being learned about the consequences of severe symptomatic ZIKV infection, our results reinforce the concern that asymptomatic prenatal ZIKV infections could have long-term effects on neurodevelopment, justifying further rigorous study to identify infected individuals and mechanisms of disease induction.…”

Section: Discussionsupporting

confidence: 87%

Zika Virus Alters DNA Methylation of Neural Genes in an Organoid Model of the Developing Human Brain

et al. 2018

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Scientific research on human neural stem cells and cerebral organoids has confirmed the congenital neurotropic and neurodestructive nature of the Zika virus. However, the extent to which prenatal ZIKV infection is associated with more subtle brain alterations, such as epigenetic changes, remains ill defined. Here, we address the question of whether ZIKV infection induces DNA methylation changes with the potential to cause brain disorders later in life.

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Section: Discussionsupporting

confidence: 87%

Zika Virus Alters DNA Methylation of Neural Genes in an Organoid Model of the Developing Human Brain

et al. 2018

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“…However, there are concerns that in utero affected offspring born without apparent symptoms may develop mental illnesses in later life ( Torales and Barrios, 2017 ). Zika virus-associated cognitive impairment and psychiatric symptoms like anxiety, racing thoughts, and an inability to turn off thoughts have also been reported in an acutely infected adolescent ( Zucker et al, 2017 ). Thus, the development of animal models to test interventions against in utero ZIKV infection and sequelae in offspring is of high importance.…”

Section: Introductionmentioning

confidence: 99%

Zika Virus Causes Persistent Infection in Porcine Conceptuses and may Impair Health in Offspring

et al. 2017

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Outcomes of Zika virus (ZIKV) infection in pregnant women vary from the birth of asymptomatic offspring to abnormal development and severe brain lesions in fetuses and infants. There are concerns that offspring affected in utero and born without apparent symptoms may develop mental illnesses. Therefore, animal models are important to test interventions against in utero infection and health sequelae in symptomatic and likely more widespread asymptomatic offspring. To partially reproduce in utero infection in humans, we directly inoculated selected porcine conceptuses with ZIKV. Inoculation resulted in rapid trans-fetal infections, persistent infection in conceptuses, molecular pathology in fetal brains, fetal antibody and type I interferon responses. Offspring infected in utero showed ZIKV in their fetal membranes collected after birth. Some in utero affected piglets were small, depressed, had undersized brains, and showed seizures. Some piglets showed potentially increased activity. Our data suggest that porcine model of persistent in utero ZIKV infection has a strong potential for translational research and can be used to test therapeutic interventions in vivo.

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“…Although the full spectrum of clinical complications after infection with ZIKV remains unclear, the incidence of neurological manifestations is increasing, including reports of cognitive sequelae 45,46 . Our study also detected increased motor activity in ZIKV-infected mice post recovery.…”

Section: Discussionmentioning

confidence: 99%

T cells promote microglia-mediated synaptic elimination and cognitive dysfunction during recovery from neuropathogenic flaviviruses

et al. 2019

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T cells clear virus from the CNS and dynamically regulate brain functions, including spatial learning, through cytokine signaling. Here we determined whether hippocampal T cells that persist after recovery from infection with West Nile virus (WNV) or Zika virus (ZIKV) impact hippocampal-dependent learning and memory. Using newly established models of viral encephalitis recovery in adult animals, we show that in mice that have recovered from WNV or ZIKV infection, T cell-derived interferon-γ (IFN-γ) signaling in microglia underlies spatial-learning defects via virus-target-specific mechanisms. Following recovery from WNV infection, mice showed presynaptic termini elimination with lack of repair, while for ZIKV, mice showed extensive neuronal apoptosis with loss of postsynaptic termini. Accordingly, animals deficient in CD8+ T cells or IFN-γ signaling in microglia demonstrated protection against synapse elimination following WNV infection and decreased neuronal apoptosis with synapse recovery following ZIKV infection. Thus, T cell signaling to microglia drives post-infectious cognitive sequelae that are associated with emerging neurotropic flaviviruses.

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Zika Virus–Associated Cognitive Impairment in Adolescent, 2016

Cited by 28 publications

References 5 publications

Zika Virus Alters DNA Methylation of Neural Genes in an Organoid Model of the Developing Human Brain

Zika Virus Alters DNA Methylation of Neural Genes in an Organoid Model of the Developing Human Brain

Zika Virus Causes Persistent Infection in Porcine Conceptuses and may Impair Health in Offspring

T cells promote microglia-mediated synaptic elimination and cognitive dysfunction during recovery from neuropathogenic flaviviruses

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