Neurologic Manifestation of Chikungunya Virus

Brizzi, Kate

doi:10.1007/s11908-017-0561-1

Cited by 35 publications

(30 citation statements)

References 39 publications

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“…Despite the lack of association between CHIKV and GBS in the present study, evidence from other studies with different study designs than the ones considered in this review show evidence of causality. A study done during a CHIKV outbreak in Reunion Island in 2006 found an association between CHIKV and occurrence of GBS in the absence of any other plausible factor associated with the syndrome .…”

Section: Discussionmentioning

confidence: 99%

Systematic review of factors associated with the development of Guillain–Barré syndrome 2007–2017: what has changed?

Wachira

Peixoto

Oliveira

2018

Tropical Med Int Health

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Objective The objective of this study was to describe the factors associated with the development of Guillain–Barré syndrome, both infectious and non‐infectious, during and after the A(H1N1) influenza pandemic in 2009 and the recent Zika virus epidemic in the Americas. Method Systematic review of literature on factors associated with the development of the Guillain–Barré syndrome published between 2007 and 2017 listed in EBSCO, MEDLINE and LILACS databases. The quality of the studies was evaluated using the Newcastle Ottawa Scale. Results Thirty‐four articles met inclusion criteria and were selected for analysis. Their quality was considered good in relation to most of the items evaluated. Many aetiological agents had the results of association with Guillain–Barré syndrome, among them Campylobacter jejuni, influenza vaccine – both pandemic and seasonal vaccines, respiratory infection, gastrointestinal infection among others. The aetiological agents found are, in most part, the same reported prior to the study period. The association with surgeries, chikungunya virus (CHIKV), Zika virus and quadrivalent human papillomavirus vaccine stand out as new aetiological agents in the list of the various possible agents that trigger Guillain–Barré syndrome reported in the study period. There were no Brazilian studies identified during this period. Conclusions The results of the review reaffirmed C. jejuni as the major trigger of GBS, whereas the association of influenza vaccines and GBS is less clear; Zika virus infection in association with GBS was found in only one study.

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Section: Discussionmentioning

confidence: 99%

Systematic review of factors associated with the development of Guillain–Barré syndrome 2007–2017: what has changed?

Wachira

Peixoto

Oliveira

2018

Tropical Med Int Health

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“…Computational prediction of CHIKV recoding signals CHIKV sequences were imported from NCBI into the Dinman laboratory frameshifting database (http://prfdb.umd. edu) 6 (59). The conserved opal stop codon at the 3Ј end of the nsP3 gene and the U UUU UUA slippery site in the 6K gene were used to identify the sequences harboring the CHIKV TCR and Ϫ1 PRF stimulatory elements, respectively.…”

Section: Methodsmentioning

confidence: 99%

“…HEK293T or U-87 MG cells were seeded at 0.6 ϫ 10 5 cells in 0.5 ml/well for 24-well plates for Dual-Luciferase transfections; and 1 ϫ 10 6 cell in 2 ml/well for 6-well plates for BiFl transfections in appropriate complete growth media (Dulbecco's modified Eagle's medium or Eagle's minimum essential medium). Following a 24-h incubation period, control and experimental reporter plasmids were then transfected into cells using Lipo- 6 Please note that the JBC is not responsible for the long-term archiving and maintenance of this site or any other third party-hosted site.…”

Section: Plasmid Transfectionsmentioning

confidence: 99%

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Functional and structural characterization of the chikungunya virus translational recoding signals

Kendra¹,

Advani

Chen³

et al. 2018

Journal of Biological Chemistry

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Climate change and human globalization have spurred the rapid spread of mosquito-borne diseases to naïve populations. One such emerging virus of public health concern is chikungunya virus (CHIKV), a member of the Togaviridae family, genus Alphavirus. CHIKV pathogenesis is predominately characterized by acute febrile symptoms and severe arthralgia, which can persist in the host long after viral clearance. CHIKV has also been implicated in cases of acute encephalomyelitis, and its vertical transmission has been reported. Currently, no FDA-approved treatments exist for this virus. Recoding elements help expand the coding capacity in many viruses and therefore represent potential therapeutic targets in antiviral treatments. Here, we report the molecular and structural characterization of two CHIKV translational recoding signals: a termination codon read-through (TCR) element located between the nonstructural protein 3 and 4 genes and a programmed ؊1 ribosomal frameshift (؊1 PRF) signal located toward the 3 end of the CHIKV 6K gene. Using Dual-Luciferase and immunoblot assays in HEK293T and U87MG mammalian cell lines, we validated and genetically characterized efficient TCR and ؊1 PRF. Analyses of RNA chemical modification data with selective 2-hydroxyl acylation and primer extension (SHAPE) assays revealed that CHIKV ؊1 PRF is stimulated by a tightly structured, triple-stem hairpin element, consistent with previous observations in alphaviruses, and that the TCR signal is composed of a single large multibulged hairpin element. These findings illuminate the roles of RNA structure in translational recoding and provide critical information relevant for design of live-attenuated vaccines against CHIKV and related viruses.

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“…The infection of CHIKV causes debilitating rheumatic diseases and inflammatory disorders which are generally non-fatal. However, in rare cases CHIKV infection can cause neurodegenerative disorders such as meningoencephalitis, myelitis, and Guillain-Barre syndrome (Gerardin et al, 2016; Brizzi, 2017). …”

Section: The Relationship Between Viral Infections and Neuroinflammatmentioning

confidence: 99%

Neuroinflammation and Infection: Molecular Mechanisms Associated with Dysfunction of Neurovascular Unit

Tohidpour

Моргун

Boitsova

et al. 2017

Front. Cell. Infect. Microbiol.

127

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Neuroinflammation is a complex inflammatory process in the central nervous system, which is sought to play an important defensive role against various pathogens, toxins or factors that induce neurodegeneration. The onset of neurodegenerative diseases and various microbial infections are counted as stimuli that can challenge the host immune system and trigger the development of neuroinflammation. The homeostatic nature of neuroinflammation is essential to maintain the neuroplasticity. Neuroinflammation is regulated by the activity of neuronal, glial, and endothelial cells within the neurovascular unit, which serves as a “platform” for the coordinated action of pro- and anti-inflammatory mechanisms. Production of inflammatory mediators (cytokines, chemokines, reactive oxygen species) by brain resident cells or cells migrating from the peripheral blood, results in the impairment of blood-brain barrier integrity, thereby further affecting the course of local inflammation. In this review, we analyzed the most recent data on the central nervous system inflammation and focused on major mechanisms of neurovascular unit dysfunction caused by neuroinflammation and infections.

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Neurologic Manifestation of Chikungunya Virus

Cited by 35 publications

References 39 publications

Systematic review of factors associated with the development of Guillain–Barré syndrome 2007–2017: what has changed?

Systematic review of factors associated with the development of Guillain–Barré syndrome 2007–2017: what has changed?

Functional and structural characterization of the chikungunya virus translational recoding signals

Neuroinflammation and Infection: Molecular Mechanisms Associated with Dysfunction of Neurovascular Unit

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