Guillain-Barré syndrome and dengue-like disease in 2015: temporal relationship in Piauí state and implications on Zika virus surveillance

Vieira, Marcelo Adriano da Cunha e Silva; Cruz, Ana Cecília Ribeiro; Barros, Ananda Naya Mesquita; Costa, Dorcas Lamounier; Silva, Eliana Vieira Pinto da; Batista, Francisca Miriane de Araújo; Azevedo, Raimunda do Socorro da Silva; Rodrigues, Sueli Guerreiro; Araújo-Júnior, Rui Cipriano; Vasconcelos, Pedro Fernando da Costa

doi:10.1590/s1678-9946201759022

Cited by 4 publications

(4 citation statements)

References 17 publications

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“…During this review period, we included 17 case reports 44, 218– 233 , 22 case series 118, 234– 254 , seven case-control studies 4, 255– 260 , one ecological study 264 , one modelling study 265 and eight outbreak reports 201, 203, 206, 266– 270 that reported on ZIKV infection and GBS.…”

Section: Resultsmentioning

confidence: 99%

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

et al. 2019

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Background: The Zika virus (ZIKV) caused a large outbreak in the Americas leading to the declaration of a Public Health Emergency of International Concern in February 2016. A causal relation between infection and adverse congenital outcomes such as microcephaly was declared by the World Health Organization (WHO) informed by a systematic review structured according to a framework of ten dimensions of causality, based on the work of Bradford Hill. Subsequently, the evidence has continued to accumulate, which we incorporate in regular updates of the original work, rendering it a living systematic review. Methods: We present an update of our living systematic review on the causal relation between ZIKV infection and adverse congenital outcomes and between ZIKV and GBS for four dimensions of causality: strength of association, dose-response, specificity, and consistency. We assess the evidence published between January 18, 2017 and July 1, 2019. Results: We found that the strength of association between ZIKV infection and adverse outcomes from case-control studies differs according to whether exposure to ZIKV is assessed in the mother (OR 3.8, 95% CI: 1.7-8.7, I2=19.8%) or the foetus/infant (OR 37.4, 95% CI: 11.0-127.1, I2=0%). In cohort studies, the risk of congenital abnormalities was 3.5 times higher after ZIKV infection (95% CI: 0.9-13.5, I2=0%). The strength of association between ZIKV infection and GBS was higher in studies that enrolled controls from hospital (OR: 55.8, 95% CI: 17.2-181.7, I2=0%) than in studies that enrolled controls at random from the same community or household (OR: 2.0, 95% CI: 0.8-5.4, I2=74.6%). In case-control studies, selection of controls from hospitals could have biased results. Conclusions: The conclusions that ZIKV infection causes adverse congenital outcomes and GBS are reinforced with the evidence published between January 18, 2017 and July 1, 2019.

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Section: Resultsmentioning

confidence: 99%

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

et al. 2019

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“…Given the recent outbreaks of DENV, CHIKV and ZIKV, and the related increase in GBS cases, GBS should be considered as a sentinel surveillance for these arboviruses. 106 Cytomegalovirus and GBS CMV presents four basic structural elements, namely an outer lipid envelope, tegument, a nucleocapsid and an internal nucleoprotein core, where genome resides. Seroprevalence in the general population in the USA reaches 50%, 107 although in developing countries may be over 80%.…”

Section: Viral Infections and Gbsmentioning

confidence: 99%

Guillain–Barré syndrome, transverse myelitis and infectious diseases

et al. 2018

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Guillain-Barré syndrome (GBS) and transverse myelitis (TM) both represent immunologically mediated polyneuropathies of major clinical importance. Both are thought to have a genetic predisposition, but as of yet no specific genetic risk loci have been clearly defined. Both are considered autoimmune, but again the etiologies remain enigmatic. Both may be induced via molecular mimicry, particularly from infectious agents and vaccines, but clearly host factor and co-founding host responses will modulate disease susceptibility and natural history. GBS is an acute inflammatory immune-mediated polyradiculoneuropathy characterized by tingling, progressive weakness, autonomic dysfunction, and pain. Immune injury specifically takes place at the myelin sheath and related Schwann-cell components in acute inflammatory demyelinating polyneuropathy, whereas in acute motor axonal neuropathy membranes on the nerve axon (the axolemma) are the primary target for immune-related injury. Outbreaks of GBS have been reported, most frequently related to Campylobacter jejuni infection, however, other agents such as Zika Virus have been strongly associated. Patients with GBS related to infections frequently produce antibodies against human peripheral nerve gangliosides. In contrast, TM is an inflammatory disorder characterized by acute or subacute motor, sensory, and autonomic spinal cord dysfunction. There is interruption of ascending and descending neuroanatomical pathways on the transverse plane of the spinal cord similar to GBS. It has been suggested to be triggered by infectious agents and molecular mimicry. In this review, we will focus on the putative role of infectious agents as triggering factors of GBS and TM.

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“…Figure 3 presents the schematic work plan by WP. Box 3 summarizes the primary research objectives of WP 1-12. absolute risk of miscarriage, still birth, microcephaly, and other clinical manifestations of adverse outcomes to fetuses born to pregnant women with ZIKV infection by gestational age; and to define the full spectrum of congenital Zika syndrome at birth and the subsequent manifestations and neurodevelopmental milestones in the first 3 years of life [4][5][6][7][8][9][10][11][12][13][14]. This will help develop an improved case definition of congenital Zika syndrome for surveillance purposes and birth-defect registries, and help us understand the extent of disability and the social and economic burden to affected families.…”

Section: Concept and Methodologymentioning

confidence: 99%

ZikaPLAN: Zika Preparedness Latin American Network

Wilder‐Smith

Preet

Renhorn

et al. 2017

Global Health Action

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The ongoing Zika virus (ZIKV) outbreak in Latin America, the Caribbean, and the Pacific Islands has underlined the need for a coordinated research network across the whole region that can respond rapidly to address the current knowledge gaps in Zika and enhance research preparedness beyond Zika. The European Union under its Horizon 2020 Research and Innovation Programme awarded three research consortia to respond to this need. Here we present the ZikaPLAN (Zika Preparedness Latin American Network) consortium. ZikaPLAN combines the strengths of 25 partners in Latin America, North America, Africa, Asia, and various centers in Europe. We will conduct clinical studies to estimate the risk and further define the full spectrum and risk factors of congenital Zika virus syndrome (including neurodevelopmental milestones in the first 3 years of life), delineate neurological complications associated with ZIKV due to direct neuroinvasion and immune-mediated responses in older children and adults, and strengthen surveillance for birth defects and Guillain-Barré Syndrome. Laboratory-based research to unravel neurotropism and investigate the role of sexual transmission, determinants of severe disease, and viral fitness will underpin the clinical studies. Social messaging and engagement with affected communities, as well as development of wearable repellent technologies against Aedes mosquitoes will enhance the impact. Burden of disease studies, data-driven vector control, and vaccine modeling as well as risk assessments on geographic spread of ZIKV will form the foundation for evidence-informed policies. While addressing the research gaps around ZIKV, we will engage in capacity building in laboratory and clinical research, collaborate with existing and new networks to share knowledge, and work with international organizations to tackle regulatory and other bottlenecks and refine research priorities. In this way, we can leverage the ZIKV response toward building a long-term emerging infectious diseases response capacity in the region to address future challenges.

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Guillain-Barré syndrome and dengue-like disease in 2015: temporal relationship in Piauí state and implications on Zika virus surveillance

Cited by 4 publications

References 17 publications

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

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

Guillain–Barré syndrome, transverse myelitis and infectious diseases

ZikaPLAN: Zika Preparedness Latin American Network

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