Name: DEBORA MARIA PIRES GONÇALVES BARREIRA
Publication date: 25/10/2019
Advisor:
Name |
Role |
|---|---|
| LILIANA CRUZ SPANO | Advisor * |
Examining board:
| Name |
Role |
|---|---|
| FAUSTO EDMUNDO LIMA PEREIRA | Internal Examiner * |
| LILIANA CRUZ SPANO | Advisor * |
| MOISES PALACI | Internal Examiner * |
Summary: Human Norovirus, belonging to three genogroups and more than 30 genotypes, are the main cause of sporadic gastroenteritis and outbreaks in the world. They are characterized by significant evolution due to mutation and recombination events, and generation of pandemic spread variants. The aim of this study was to determine the genetic diversity of norovirus in individuals with gastroenteritis in our geographic area. Three groups of samples are part of this study: (i) fecal specimens obtained prospectively from children with diarrhea (n = 307) collected between October 2014 and September 2018; (ii) norovirus positive specimens (n = 78) obtained from children and adults from February 2003 to June 2004 and December 2007 to June 2011; and (iii) norovirus positive specimens (n = 2) associated with an outbreak of gastroenteritis in a hospital unit in 2012. Norovirus detection was performed using RT-qPCR for ORF1-ORF-2 junction region. The genotypes were determined by the phylogenetic analysis of partial polymerase and capsid sequences. Complete sequencing of the capsid protein (VP1) GII.4 Sydney 2012 and nearly complete of the polymerase GII.P16 of the new recombinant GII.4 Sydney [P16] were obtained and phylogenetic analysis was performed. Noroviruses were detected in 24.4% (75/307) of the specimens in the prospective study and the phylogenetic analysis (n = 52) demonstrated the predominance of the recombinant GII.4 Sydney [P16] (n = 27), described for the first time in Brazil, followed by the genotypes GII.4 Sydney[P31] (n = 10) and GII.17[P17] (n = 5), in addition to seven other recombinants in fewer cases (GII.2[P16], GII .6[P7], GII.3[P16], GII.4 Sydney[PNA], GII.1[Pg], GII.4 Sydney[P4 New Orleans] and GI.7[P7]). There were amino acid substitutions in proteins: (i) GII.P16 polymerase of strains that circulated in 2016 and 2017 compared to pre-2015 sequences (available on GenBank); and in (ii) VP1 of GII.4 Sydney strains associated with GII.P16 (2016 and 2018) compared to those associated with GII.P31 before 2015. Different GII.4 variants were detected in all collection periods samples, coinciding with the circulation in the world. The recombinant GII.4 Sydney[P31] was responsible for the outbreak in the hospital, which occurred in the same year as its first description in the world. Our study shows the great genetic diversity of norovirus circulating in our geographical area and highlights the unprecedented report of the emerging recombinant GII.4 Sydney[P16] in Brazil.
