Evidence map›Paper›PMID 39561198›Full record

ArticlePloS one2024

Genomic variability in Zika virus in GBS cases in Colombia.

Nelson Rivera-Franco, Diana López-Alvarez, Andrés Castillo, Erica Aristizabal, Daniela Puiu, Steven L Salzberg, Carlos A Pardo, Beatriz Parra, NEAS

Abstract read
In one paragraph

Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Nelson Rivera-FrancoLaboratorio de Técnicas y Análisis Ómicos-TAOLab/CiBioFi, Facultad de Ciencias Naturales y Exactas, Universidad del Valle, Cali, Valle del Cauca, Colombia.
Diana López-AlvarezLaboratorio de Técnicas y Análisis Ómicos-TAOLab/CiBioFi, Facultad de Ciencias Naturales y Exactas, Universidad del Valle, Cali, Valle del Cauca, Colombia.
Andrés CastilloLaboratorio de Técnicas y Análisis Ómicos-TAOLab/CiBioFi, Facultad de Ciencias Naturales y Exactas, Universidad del Valle, Cali, Valle del Cauca, Colombia.
Erica AristizabalGrupo VIREM-Virus Emergentes y Enfermedad, Escuela de Ciencias Básicas, Facultad de Salud, Universidad del Valle, Cali, Valle del Cauca, Colombia.
Daniela PuiuCenter for Computational Biology, Johns Hopkins University, Baltimore, Maryland, United States of America.
Steven L SalzbergCenter for Computational Biology, Johns Hopkins University, Baltimore, Maryland, United States of America.ORCID https://orcid.org/0000-0002-8859-7432
Carlos A PardoDepartment of Neurology & Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, United States of America.
Beatriz ParraGrupo VIREM-Virus Emergentes y Enfermedad, Escuela de Ciencias Básicas, Facultad de Salud, Universidad del Valle, Cali, Valle del Cauca, Colombia.ORCID https://orcid.org/0000-0002-5371-7449
NEAS

Funding

Emerging Neuroviruses and Neurological Inflammatory DiseasesR01NS110122 · NINDS · JOHNS HOPKINS UNIVERSITY · PI PARDO-VILLAMIZAR, CARLOS A · 2019 to 2023
$1.7M
NINDS NIH HHS R01 NS110122
6 · The paper itself

Abstract

Major clusters of Guillain-Barré Syndrome (GBS) emerged during the Zika virus (ZIKV) outbreaks in the South Pacific and the Americas from 2014 to 2016. The factors contributing to GBS susceptibility in ZIKV infection remain unclear, although considerations of viral variation, patient susceptibility, environmental influences, and other potential factors have been hypothesized. Studying the role of viral genetic factors has been challenging due to the low viral load and rapid viral clearance from the blood after the onset of Zika symptoms. The prolonged excretion of ZIKV in urine by the time of GBS onset, when the virus is no longer present in the blood, provides an opportunity to unravel whether specific ZIKV mutations are related to the development of GBS in certain individuals. This study aimed to investigate the association between specific ZIKV genotypes and the development of GBS, taking advantage of a unique collection of ZIKV-positive urine samples obtained from GBS cases and controls during the 2016 ZIKV outbreak in Colombia. Utilizing Oxford-Nanopore technology, we conducted complete genome sequencing of ZIKV in biological samples from 15 patients with GBS associated with ZIKV and 17 with ZIKV infection without neurological complications. ZIKV genotypes in Colombia exhibited distribution across three clades (average bootstrap of 90.9±14.9%), with two clades dominating the landscape. A comparative analysis of ZIKV genomes from GBS and non-neurological complications, alongside 1368 previously reported genomes, revealed no significant distinctions between the two groups. Both genotypes were similarly distributed among observed clades in Colombia. Furthermore, no variations were identified in the amino acid composition of the viral genome between the two groups. Our findings suggest that GBS in ZIKV infection is perhaps associated with patient susceptibility and/or other para- or post-infectious immune-mediated mechanisms rather than with specific ZIKV genome variations.

Indexed as

Genome, ViralGenotypeGuillain-Barre SyndromeZika VirusZika Virus InfectionAdultColombiaDisease OutbreaksFemaleGenetic VariationHumansMaleMiddle AgedPhylogenyYoung Adult

Identifiers

PMID39561198
PMCPMC11575819

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.