RESUMO
In 2015-2016, a Zika virus (ZIKV) outbreak occurred in the Americas. In 2017, we conducted a ZIKV serosurvey in Suriname in which 770 participants were recruited from 1 urban area and 2 rural villages in the tropical rainforest. All collected samples were tested for presence of ZIKV antibodies using a ZIKV immunoglobulin G enzyme-linked immunosorbent assay and a virus neutralization assay. We found that 35.1% of the participants had neutralizing antibodies against ZIKV. In 1 remote village in the rainforest, 24.5% of the participants had neutralizing antibodies against ZIKV, suggesting that ZIKV was widely spread across Suriname.
Assuntos
Infecção por Zika virus/epidemiologia , Infecção por Zika virus/imunologia , Zika virus/imunologia , Adolescente , Adulto , Anticorpos Neutralizantes/imunologia , Anticorpos Antivirais/imunologia , Surtos de Doenças , Feminino , Humanos , Imunoglobulina G/imunologia , Masculino , Pessoa de Meia-Idade , Testes de Neutralização/métodos , Estudos Soroepidemiológicos , Suriname/epidemiologia , Adulto JovemRESUMO
BACKGROUND: Between September 2000 and November 2005, approximately 10% of the retrospectively examined human adenovirus (HAdV)-positive pediatric cases of acute respiratory disease (ARD) requiring hospitalization at the Hospital Nacional de Pediatria Juan P. Garrahan in Buenos Aires, Argentina, were found to have a HAdV-B2 infection. OBJECTIVE: To characterize genetically and antigenically the HAdV-B2 virus isolates. STUDY DESIGN: Restriction enzyme analysis (REA), hexon and fiber gene sequencing and virus neutralization assays (VN) were carried out on 8 HAdV-B2 respiratory virus isolates. RESULTS: REA showed that the 8 examined HAdV-B2 virus isolates were HAdV11, belonging to two genomic variants: HAdV11a and a BclI variant of HAdV11c which we designated 11c4. Molecular analysis of the hexon genes showed that both REA variants had a HAdV11-like hexon gene. Confirming previous reports, the 7 HAdV11a virus isolates were found to have HAdV14-like fiber genes and therefore are HAdV H11/F14. The fiber gene of the HAdV11c4 virus isolates most closely resembled that of various strains of HAdV7. In VN assays, the 4 tested HAdV11a strains were serotyped as HAdV11-14. The HAdV11c4 strain was serotyped as HAdV11 but also showed a weak but significant reactivity with antiserum to HAdV7. Compared with the other HAdV-positive cases in our study, infection with HAdV11 caused a similarly severe disease. CONCLUSIONS: Our results provide evidence to the long term world-wide circulation of HAdV H11/F14 as a causative agent of ARD. Combined, our molecular and serology data support the rationale to base the molecular typing and designation of recombinant viruses on the sequences of the hexon and fiber genes.