Prenatal brain MRI of fetuses with Zika virus infection

Guillemette-Artur, Prisca; Besnard, Marianne; Eyrolle-Guignot, Dominique; Jouannic, Jean‐Marie; Garel, Catherine

doi:10.1007/s00247-016-3619-6

Cited by 63 publications

(39 citation statements)

References 23 publications

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“…Besides the similar pattern of distribution of calcifications described here, malformation of cortical development with predominance of pachygyria or polymicrogyriain the frontal lobes and delayed myelination were seen. As well, Guillemette-Arturet al 25 recently reported very similar findings in a three-patient series using fetal MRI, including subependymal pseudocysts.…”

Section: Discussionsupporting

confidence: 63%

Presumed Zika virus-related congenital brain malformations: the spectrum of CT and MRI findings in fetuses and newborns

Castro

Pereira

Dias

et al. 2017

Arq. Neuro-Psiquiatr.

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The new epidemic of Zika virus infection raises grave concerns, especially with the increasingly-recognized link between emerging cases of microcephaly and this infectious disease. Besides small cranial dimensions, there are striking morphologic anomalies in the fetal brain. Key anomalies include cortical developmental malformations and a peculiar distribution of pathologic calcifications. These potentially indicate a new pattern of congenital central nervous system infection. Methods: Eight women underwent fetal MRI. Four infants also underwent postnatal CT. Five of the women underwent amniocentesis. Results: All neonates were born with microcephaly. On fetal MRI, ventriculomegaly, marked reduction of white matter thickness, severe sylvian fissure simplification, abnormal sulcation, and diffuse volumetric loss of cerebellar hemispheres were consistently seen. On postnatal CT, diffuse subcortical and basal ganglia calcifications were observed. The Zika virus was detected in two amniocenteses by polymerase chain reaction assays. Conclusion: We hope to assist the medical community in recognizing the spectrum of encephalic changes related to congenital Zika virus infection.Keywords:Zika virus; microcephaly; tomography, X-ray computed; magnetic resonance imaging. RESUMOOs novos casos epidêmicos de infecção pelo vírus Zika suscitam grande preocupação, sobretudo com o crescente reconhecimento da ligação entre casos emergentes de microcefalia e esta doença infecciosa. Além da cabeça de pequenas dimensões, existem profundas alterações morfológicas no encéfalo fetal. Anomalias mais típicas incluem malformações do desenvolvimento cortical e uma distribuição peculiar de calcificações patológicas. Estes dados potencialmente indicam um novo padrão de infecção congênita do sistema nervoso central. Métodos: Oito mulheres foram submetidas a RM fetal. Quatro crianças também realizaram TC pós-natal. Cinco mulheres foram submetidas a amniocentese. Resultados: Todos os neonatos nasceram com microcefalia. Na RM fetal, ventriculomegalia, acentuada redução da espessura da substância branca, acentuada simplificação da fissura sylviana, sulcação anormal e redução volumétrica difusa dos hemisférios cerebelares foram constantes. Na TC pós-natal, calcificações difusas subcorticais e nos núcleos da base foram observadas. O vírus Zika foi detectado por PCR em duas amniocenteses. Conclusão: Esperamos dar suporte à comunidade médica em reconhecer este padrão de imagem potencialmente específico.Palavras-chave: Zika vírus; microcefalia; tomografia computadorizada por raios X; imagem por ressonância magnética.

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Section: Discussionsupporting

confidence: 63%

Presumed Zika virus-related congenital brain malformations: the spectrum of CT and MRI findings in fetuses and newborns

Castro

Pereira

Dias

et al. 2017

Arq. Neuro-Psiquiatr.

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“…Twenty-eight items [29, 30, 34, 36–38, 40, 41, 44, 51, 52, 54–58, 61, 63, 64, 67, 69, 72, 75, 77, 79, 81, 85, 91–93] in 25 groups addressed biological plausibility (S4 Table). These studies suggest a teratogenic effect of Zika virus on the developing brain.…”

Section: Resultsmentioning

confidence: 99%

Zika Virus Infection as a Cause of Congenital Brain Abnormalities and Guillain–Barré Syndrome: Systematic Review

et al. 2017

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BackgroundThe World Health Organization (WHO) stated in March 2016 that there was scientific consensus that the mosquito-borne Zika virus was a cause of the neurological disorder Guillain–Barré syndrome (GBS) and of microcephaly and other congenital brain abnormalities based on rapid evidence assessments. Decisions about causality require systematic assessment to guide public health actions. The objectives of this study were to update and reassess the evidence for causality through a rapid and systematic review about links between Zika virus infection and (a) congenital brain abnormalities, including microcephaly, in the foetuses and offspring of pregnant women and (b) GBS in any population, and to describe the process and outcomes of an expert assessment of the evidence about causality.Methods and FindingsThe study had three linked components. First, in February 2016, we developed a causality framework that defined questions about the relationship between Zika virus infection and each of the two clinical outcomes in ten dimensions: temporality, biological plausibility, strength of association, alternative explanations, cessation, dose–response relationship, animal experiments, analogy, specificity, and consistency. Second, we did a systematic review (protocol number CRD42016036693). We searched multiple online sources up to May 30, 2016 to find studies that directly addressed either outcome and any causality dimension, used methods to expedite study selection, data extraction, and quality assessment, and summarised evidence descriptively. Third, WHO convened a multidisciplinary panel of experts who assessed the review findings and reached consensus statements to update the WHO position on causality. We found 1,091 unique items up to May 30, 2016. For congenital brain abnormalities, including microcephaly, we included 72 items; for eight of ten causality dimensions (all except dose–response relationship and specificity), we found that more than half the relevant studies supported a causal association with Zika virus infection. For GBS, we included 36 items, of which more than half the relevant studies supported a causal association in seven of ten dimensions (all except dose–response relationship, specificity, and animal experimental evidence). Articles identified nonsystematically from May 30 to July 29, 2016 strengthened the review findings. The expert panel concluded that (a) the most likely explanation of available evidence from outbreaks of Zika virus infection and clusters of microcephaly is that Zika virus infection during pregnancy is a cause of congenital brain abnormalities including microcephaly, and (b) the most likely explanation of available evidence from outbreaks of Zika virus infection and GBS is that Zika virus infection is a trigger of GBS. The expert panel recognised that Zika virus alone may not be sufficient to cause either congenital brain abnormalities or GBS but agreed that the evidence was sufficient to recommend increased public health measures. Weaknesses are the limited assessment of ...

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“…The finding that HSV-1 receptors are expressed at only low levels in gestation, but rise markedly during the postnatal period, is notable because the fetal human brain is not generally subject to infection with HSV-1, in contrast to other viruses (e.g., cytomegalovirus, rubella, Zika virus) that can establish damaging brain infection during gestation (Driggers et al 2016; Guillemette-Artur et al 2016; McCarthy et al 2011; Naeye and Blanc 1965). Although exposed to HSV-1 in utero of HSV-1-positive mothers, overt pathology appears to be generally limited to postnatal ages.…”

Section: Discussionmentioning

confidence: 99%

Distribution of cellular HSV-1 receptor expression in human brain

Lathe

Haas

2016

J. Neurovirol.

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Herpes simplex virus type 1 (HSV-1) is a neurotropic virus linked to a range of acute and chronic neurological disorders affecting distinct regions of the brain. Unusually, HSV-1 entry into cells requires the interaction of viral proteins glycoprotein D (gD) and glycoprotein B (gB) with distinct cellular receptor proteins. Several different gD and gB receptors have been identified, including TNFRSF14/HVEM and PVRL1/nectin 1 as gD receptors and PILRA, MAG, and MYH9 as gB receptors. We investigated the expression of these receptor molecules in different areas of the adult and developing human brain using online transcriptome databases. Whereas all HSV-1 receptors showed distinct expression patterns in different brain areas, the Allan Brain Atlas (ABA) reported increased expression of both gD and gB receptors in the hippocampus. Specifically, for PVRL1, TNFRFS14, and MYH9, the differential z scores for hippocampal expression, a measure of relative levels of increased expression, rose to 2.9, 2.9, and 2.5, respectively, comparable to the z score for the archetypical hippocampus-enriched mineralocorticoid receptor (NR3C2, z = 3.1). These data were confirmed at the Human Brain Transcriptome (HBT) database, but HBT data indicate that MAG expression is also enriched in hippocampus. The HBT database allowed the developmental pattern of expression to be investigated; we report that all HSV1 receptors markedly increase in expression levels between gestation and the postnatal/adult periods. These results suggest that differential receptor expression levels of several HSV-1 gD and gB receptors in the adult hippocampus are likely to underlie the susceptibility of this brain region to HSV-1 infection.

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Prenatal brain MRI of fetuses with Zika virus infection

Cited by 63 publications

References 23 publications

Presumed Zika virus-related congenital brain malformations: the spectrum of CT and MRI findings in fetuses and newborns

Presumed Zika virus-related congenital brain malformations: the spectrum of CT and MRI findings in fetuses and newborns

Zika Virus Infection as a Cause of Congenital Brain Abnormalities and Guillain–Barré Syndrome: Systematic Review

Distribution of cellular HSV-1 receptor expression in human brain

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