scholarly journals Zika virus infection as a cause of congenital brain abnormalities and Guillain-Barré syndrome: systematic review

2016 ◽  
Author(s):  
Fabienne Krauer ◽  
Maurane Riesen ◽  
Ludovic Reveiz ◽  
Olufemi T Oladapo ◽  
Ruth Martínez-Vega ◽  
...  

AbstractBackgroundThe World Health Organization 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 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 re-assess 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) Guillain-Barré syndrome 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 10 dimensions; temporality, biological plausibility, strength of association, alternative explanations, cessation, dose-response, 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, a multidisciplinary panel of experts assessed the review findings and reached consensus on causality. We found 1091 unique items up to May 30, 2016. For congenital brain abnormalities, including microcephaly, we included 72 items; for eight of 10 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 Guillain-Barré syndrome, 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 non-systematically from May 30-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 61 microcephaly; and b) the most likely explanation of available evidence from outbreaks of Zika virus infection and Guillain-Barré syndrome is that Zika virus infection is a trigger of Guillain-Barré syndrome. The expert panel recognised that Zika virus alone may not be sufficient to cause either congenital brain abnormalities or Guillain-Barré syndrome but agreed that the evidence was sufficient to recommend increased public health measures. Weaknesses are the limited assessment of the role of dengue virus and other possible co-factors, the small number of comparative epidemiological studies, and the difficulty in keeping the review up to date with the pace of publication of new research.ConclusionsRapid and systematic reviews with frequent updating and open dissemination are now needed, both for appraisal of the evidence about Zika virus infection and for the next public health threats that will emerge. This rapid systematic review found sufficient evidence to say that Zika virus is a cause of congenital abnormalities and is a trigger of Guillain-Barré situation.

PLoS Medicine ◽  
2017 ◽  
Vol 14 (1) ◽  
pp. e1002203 ◽  
Author(s):  
Fabienne Krauer ◽  
Maurane Riesen ◽  
Ludovic Reveiz ◽  
Olufemi T. Oladapo ◽  
Ruth Martínez-Vega ◽  
...  

2020 ◽  
Vol 14 (4) ◽  
pp. e0008264 ◽  
Author(s):  
Sonja E. Leonhard ◽  
Cristiane C. Bresani-Salvi ◽  
Joanna D. Lyra Batista ◽  
Sergio Cunha ◽  
Bart C. Jacobs ◽  
...  

2018 ◽  
Vol 25 (4) ◽  
pp. 644-650 ◽  
Author(s):  
A. Uncini ◽  
D. C. González-Bravo ◽  
Y. Y. Acosta-Ampudia ◽  
E. C. Ojeda ◽  
Y. Rodríguez ◽  
...  

2016 ◽  
Vol 95 (5) ◽  
pp. 1157-1160 ◽  
Author(s):  
Mateus Santana do Rosário ◽  
Isadora Cristina de Siqueira ◽  
Sueli Guerreiro Rodrigues ◽  
Lívia Caricio Martins ◽  
Nikos Vasilakis ◽  
...  

2016 ◽  
Vol 7 ◽  
Author(s):  
Thomas Langerak ◽  
Harvey Yang ◽  
Mark Baptista ◽  
Laura Doornekamp ◽  
Tessa Kerkman ◽  
...  

2014 ◽  
Vol 19 (9) ◽  
Author(s):  
E Oehler ◽  
L Watrin ◽  
P Larre ◽  
I Leparc-Goffart ◽  
S Lastère ◽  
...  

Binary file ES_Abstracts_Final_ECDC.txt matches


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
John D. Morrey ◽  
Alexandre L. R. Oliveira ◽  
Hong Wang ◽  
Katherine Zukor ◽  
Mateus Vidigal de Castro ◽  
...  

AbstractClinical evidence is mounting that Zika virus can contribute to Guillain-Barré syndrome which causes temporary paralysis, yet the mechanism is unknown. We investigated the mechanism of temporary acute flaccid paralysis caused by Zika virus infection in aged interferon αβ-receptor knockout mice used for their susceptibility to infection. Twenty-five to thirty-five percent of mice infected subcutaneously with Zika virus developed motor deficits including acute flaccid paralysis that peaked 8-10 days after viral challenge. These mice recovered within a week. Despite Zika virus infection in the spinal cord, motor neurons were not destroyed. We examined ultrastructures of motor neurons and synapses by transmission electron microscopy. The percent coverage of motor neurons by boutons was reduced by 20%; more specifically, flattened-vesicle boutons were reduced by 46%, and were normalized in recovering mice. Using electromyographic procedures employed in people to help diagnose Guillain-Barré syndrome, we determined that nerve conduction velocities between the sciatic notch and the gastrocnemius muscle were unchanged in paralyzed mice. However, F-wave latencies were increased in paralyzed mice, which suggests that neuropathy may exist between the sciatic notch to the nerve rootlets. Reversible synaptic retraction may be a previously unrecognized cofactor along with peripheral neuropathy for the development of Guillain-Barré syndrome during Zika virus outbreaks.


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