2018
DOI: 10.1038/nm.4510
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A previously undetected pathology of Zika virus infection

Abstract: In a nonhuman primate model of Zika virus infection, structural and cellular pathology deficits that could have a long-lasting impact on neural development and neurocognitive function are detected in offspring of infected mothers.

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Cited by 2 publications
(3 citation statements)
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“…A recent epidemic with similar consequences is Zika virus infection, which causes microcephaly with cognitive disability. The Zika virus impairs Musashi-1 function in neural progenitors, leading to decreased neurogenesis in both the cortex and the dentate gyrus and therefore an overall decrease in size ( Chavali et al, 2017 ; Christian et al, 2018 ). Moreover, the Zika virus disorganizes the granule cell layer and strata, in addition to predisposes infants to brain calcifications ( Christian et al, 2018 ).…”
Section: Main Textmentioning
confidence: 99%
See 1 more Smart Citation
“…A recent epidemic with similar consequences is Zika virus infection, which causes microcephaly with cognitive disability. The Zika virus impairs Musashi-1 function in neural progenitors, leading to decreased neurogenesis in both the cortex and the dentate gyrus and therefore an overall decrease in size ( Chavali et al, 2017 ; Christian et al, 2018 ). Moreover, the Zika virus disorganizes the granule cell layer and strata, in addition to predisposes infants to brain calcifications ( Christian et al, 2018 ).…”
Section: Main Textmentioning
confidence: 99%
“…Accompanying these structural deficits to the brain are insults to neural circuit development. The Zika virus promotes gliosis, impairs myelination, disrupts synaptogenesis, and alters the levels of SHH and FGF ( Christian et al, 2018 ; Thawani et al, 2018 ). But, during normal development it should be noted that even before secreted molecules such as SHH, FGF, and REELIN impact cell placement, lineage history and birthdate initiate a spatial and temporal order of cellular invasion of a territory ( Sudarov et al, 2011 ).…”
Section: Main Textmentioning
confidence: 99%
“…In recent years, advances in multiparameter flow cytometry, high-throughput technologies, and robust imaging techniques have produced an abundance of quantitative data and illuminated the need for new theoretical approaches that can unravel complex biological interactions. In addition, the emergence of new data on multi-pathogen infections (reviewed in [9]), important viral-induced pathologies (e.g., by Zika virus (ZV) [10,11], Ebola virus (EV) [12], or BK virus (BKV) [13]) and better data on virus-induced autoimmunity (e.g., by EBV [4]) has opened the door for novel investigative designs. For over 20 years, mathematical models have been developed to assess infection kinetics during acute or chronic viral infection to better understand virus replication, elucidate mechanisms of viral persistence and control by host immune responses, disentangle pathogen-pathogen interplay, and evaluate the clinical potential of different antiviral therapies [cite].…”
Section: Introductionmentioning
confidence: 99%