scholarly journals Zika Virus Infection and Immuno-Cross-Reactivity to Dengue: An Issue in the Pathogenesis of Congenital Microcephaly

2016 ◽  
Vol 4 (4) ◽  
Author(s):  
Sora Yasri ◽  
Viroj Wiwanikit
2017 ◽  
Vol 89 (8) ◽  
pp. 1477-1479 ◽  
Author(s):  
Alvina Clara Felix ◽  
Nathalia C. Santiago Souza ◽  
Walter M. Figueiredo ◽  
Angela A. Costa ◽  
Marta Inenami ◽  
...  

2020 ◽  
Vol 101 ◽  
pp. 191-193 ◽  
Author(s):  
Álvaro A. Faccini-Martínez ◽  
Ricardo Rivero ◽  
Evelin Garay ◽  
Alejandra García ◽  
Salim Mattar ◽  
...  

Science ◽  
2016 ◽  
Vol 353 (6301) ◽  
pp. 823-826 ◽  
Author(s):  
K. Stettler ◽  
M. Beltramello ◽  
D. A. Espinosa ◽  
V. Graham ◽  
A. Cassotta ◽  
...  

EBioMedicine ◽  
2017 ◽  
Vol 24 ◽  
pp. 189-194 ◽  
Author(s):  
Chunfeng Li ◽  
Xingliang Zhu ◽  
Xue Ji ◽  
Natalie Quanquin ◽  
Yong-Qiang Deng ◽  
...  

2016 ◽  
Vol 141 (1) ◽  
pp. 73-81 ◽  
Author(s):  
Peter Štrafela ◽  
Alenka Vizjak ◽  
Jerica Mraz ◽  
Jernej Mlakar ◽  
Jože Pižem ◽  
...  

Context.—The 2015 outbreak of Zika virus in Brazil resulted in a 20-times increased prevalence of congenital microcephaly in stillborns and neonates and was instrumental in raising the suspicion of a causal association between Zika virus and microcephaly. Objective.—To provide a comprehensive description of the neuropathologic features of congenital Zika virus infection. Design.—Autopsy evaluation of the brain from a fetus of 32 weeks and 6 days of gestation, with a prenatal diagnosis of microcephaly associated with polymerase chain reaction–confirmed, fetal, Zika virus infection. Results.—Multiple severe pathology findings were present. These included lissencephaly, except for the occipital lobes, where some pachygyria was observed. Also present was reduction and thinning of white matter, ventriculomegaly of the lateral ventricles, and coalescent calcifications in the cortical-subcortical white matter border associated with glioneuronal outbursting into the subarachnoid space above and heterotopias below. There were small, scattered calcifications in the basal ganglia, with fewer in the white matter and germinal matrix, and none in the cerebellum and brainstem. The cerebellum and pontine base were atrophic because of Wallerian degeneration or maldevelopment of descending tracts and pontocerebellar connections. Conclusion.—Our findings are in agreement with neuroimaging of Zika virus–associated fetal and infant micrencephalic brains and, to some extent, with neuroimaging of other intrauterine infections causing microcephaly.


2017 ◽  
Vol 5 (4) ◽  
pp. 686-696
Author(s):  
Anne-Marie Rick ◽  
Gretchen Domek ◽  
Maureen Cunningham ◽  
Daniel Olson ◽  
Molly M Lamb ◽  
...  

2019 ◽  
Vol 1 (1) ◽  
pp. 49-56
Author(s):  
Mariam M. Mirambo ◽  
Lucas Matemba ◽  
Mtebe Majigo ◽  
Stephen E. Mshana

Background: Zika virus infection during pregnancy has been recently associated with congenital microcephaly and other severe neural tube defects. However, the magnitude of confirmed cases and the scope of these anomalies have not been extensively documented. This review focuses on the magnitude of laboratory-confirmed congenital Zika virus cases among probable cases and describing the patterns of congenital anomalies allegedly caused by the Zika virus, information which will inform further research in this area. Methods: We conducted a literature search for English-language articles about congenital Zika virus infection using online electronic databases (PubMed/MEDLINE, POPLINE, Embase, Google Scholar, and Web of Knowledge). The search terms used were, “zika”, “pregnancy”, [year], “microcephaly”, “infants”, “children”, “neonates”, “foetuses”, “neural tube defect”, and “CNS manifestations” in different combinations. All articles reporting cases or case series between January 2015 and December 2016 were included. Data were entered into a Microsoft Excel database and analysed to obtain proportions of the confirmed cases and patterns of anomalies. Results: A total of 24 articles (11 case series, 9 case reports, and 4 others) were found to be eligible and included in this review. These articles reported 919 cases, with or without microcephaly, presumed to have congenital Zika virus infection. Of these cases, 884 (96.2%) had microcephaly. Of the 884 cases of microcephaly, 783 (88.6%) were tested for Zika virus infection, and 216 (27.6%; 95% confidence interval, 24.5% to 30.8%) were confirmed to be Zika virus-positive. In addition to microcephaly, other common abnormalities reported – out of 442 cases investigated – were calcifications of brain tissue (n=240, 54.3%), ventriculomegaly (n=93, 20.8%), cerebellar hypoplasia (n=52, 11.7%), and ocular manifestations (n=46, 10.4%). Conclusion: Based on the available literature, Zika virus infection during pregnancy might lead to a wide array of outcomes other than microcephaly. There is a need for more epidemiological studies in Zika-endemic areas, particularly in Africa, to ascertain the role of Zika virus in causing congenital neurological defects.


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