Zika virus infection in 18 travellers returning from Surinam and the Dominican Republic, The Netherlands, November 2015–March 2016

Duijster, Janneke; Goorhuis, Abraham; Genderen, Perry J.J. van; Visser, Leo G.; Reimerink, Johan; Grobusch, Martin P.; Eijk, Annemiek A. van der; Kerkhof, J H C T van den; Reusken, Chantal; Hahné, Susan

doi:10.1007/s15010-016-0906-y

Cited by 37 publications

(22 citation statements)

References 15 publications

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“…We included 31 items [55–57, 67, 78, 100–112, 115–117, 120–122] in 26 groups (S6 Table). At the individual level, symptoms of Zika virus infection were reported before the onset of GBS symptoms in cases in French Polynesia, Brazil, El Salvador, Panama, Puerto Rico, and Venezuela, and in returning travellers from Haiti, Suriname, and Central America.…”

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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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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“…World Health Oganization (PAHO/WHO), 2015; Sarmiento-Ospina et al, 2016;Arzuza-Ortega et al, 2016;Duijster et al, 2016). Notably, patients with severe non-pregnancy-related complications of ZIKV often deteriorated suddenly after an initially mild disease phase as the viral load began to decrease (Cao-Lormeau et al, 2016;Mecharles et al, 2016;Sarmiento-Ospina et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

Zika Virus Infection in Dexamethasone-immunosuppressed Mice Demonstrating Disseminated Infection with Multi-organ Involvement Including Orchitis Effectively Treated by Recombinant Type I Interferons

et al. 2016

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BackgroundDisseminated or fatal Zika virus (ZIKV) infections were reported in immunosuppressed patients. Existing interferon-signaling/receptor-deficient mouse models may not be suitable for evaluating treatment effects of recombinant interferons.MethodsWe developed a novel mouse model for ZIKV infection by immunosuppressing BALB/c mice with dexamethasone.ResultsDexamethasone-immunosuppressed male mice (6–8 weeks) developed disseminated infection as evidenced by the detection of ZIKV-NS1 protein expression and high viral loads in multiple organs. They had ≥ 10% weight loss and high clinical scores soon after dexamethasone withdrawal (10 dpi), which warranted euthanasia at 12 dpi. Viral loads in blood and most tissues at 5 dpi were significantly higher than those at 12 dpi (P < 0.05). Histological examination revealed prominent inflammatory infiltrates in multiple organs, and CD45 + and CD8 + inflammatory cells were seen in the testis. These findings suggested that clinical deterioration occurred during viral clearance by host immune response. Type I interferon treatments improved clinical outcome of mice (100% vs 0% survival).ConclusionsBesides virus dissemination, inflammation of various tissues, especially orchitis, may be potential complications of ZIKV infection with significant implications on disease transmission and male fertility. Interferon treatment should be considered in patients at high risks for ZIKV-associated complications when the potential benefits outweigh the side effects of treatment.

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“…At present, more than 30 countries in Asia, Africa, Oceania, Micronesia and South America have reported indigenous human ZIKV cases [29]. The travel-related cases from epidemic and endemic regions were also reported in North America, Australia, Europe and Japan [30][31][32][33][34][35][36][37]. As of 27th July 2016, a total of 50 territories and countries in the Americas have reported ZIKV infections.…”

Section: Epidemiologymentioning

confidence: 99%

Zika virus disease: a current review of the literature

et al. 2016

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Zika virus infection in 18 travellers returning from Surinam and the Dominican Republic, The Netherlands, November 2015–March 2016

Cited by 37 publications

References 15 publications

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

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

Zika Virus Infection in Dexamethasone-immunosuppressed Mice Demonstrating Disseminated Infection with Multi-organ Involvement Including Orchitis Effectively Treated by Recombinant Type I Interferons

Zika virus disease: a current review of the literature

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