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Zika Virus infection and Guillain-Barré syndrome in Northeastern Mexico: A case-control study

BACKGROUND: Beginning August 2017, we conducted a prospective case-control investigation in Monterrey, Mexico to assess the association between Zika virus (ZIKV) and Guillain-Barré syndrome (GBS). METHODS: For each of 50 GBS case-patients, we enrolled 2–3 afebrile controls (141 controls in total) ma...

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Detalles Bibliográficos
Autores principales: Gongora-Rivera, Fernando, Grijalva, Israel, Infante-Valenzuela, Adrian, Cámara-Lemarroy, Carlos, Garza-González, Elvira, Paredes-Cruz, Martin, Grajales-Muñiz, Concepción, Guerrero-Cantera, José, Vargas-Ramos, Ignacio, Soares, Jesus, Abrams, Joseph Y., Styczynski, Ashley R., Camacho-Ortiz, Adrián, Villarino, Margarita E., Belay, Ermias D., Schonberger, Lawrence B., Sejvar, James J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7098590/
https://www.ncbi.nlm.nih.gov/pubmed/32214354
http://dx.doi.org/10.1371/journal.pone.0230132
Descripción
Sumario:BACKGROUND: Beginning August 2017, we conducted a prospective case-control investigation in Monterrey, Mexico to assess the association between Zika virus (ZIKV) and Guillain-Barré syndrome (GBS). METHODS: For each of 50 GBS case-patients, we enrolled 2–3 afebrile controls (141 controls in total) matched by sex, age group, and presentation to same hospital within 7 days. RESULTS: PCR results for ZIKV in blood and/or urine were available on all subjects; serum ZIKV IgM antibody for 52% of case-patients and 80% of controls. Subjects were asked about antecedent illness in the two months prior to neurological onset (for case-patients) or interview (for controls). Laboratory evidence of ZIKV infection alone (PCR+ or IgM+) was not significantly different between case-patients and controls (OR: 1.26, 95% CI: 0.45–3.54) but antecedent symptomatic ZIKV infection [a typical ZIKV symptom (rash, joint pain, or conjunctivitis) plus laboratory evidence of ZIKV infection] was higher among case-patients (OR: 12.45, 95% CI: 1.45–106.64). GBS case-patients with laboratory evidence of ZIKV infection were significantly more likely to have had typical ZIKV symptoms than controls with laboratory evidence of ZIKV infection (OR: 17.5, 95% CI: 3.2–96.6). This association remained significant even when only GBS case-patients who were afebrile for 5 days before onset were included in the analysis, (OR 9.57 (95% CI: 1.07 to 85.35). CONCLUSIONS: During ZIKV epidemics, this study indicates that increases in GBS will occur primarily among those with antecedent symptomatic ZIKV.