Genetic diversity of respiratory syncytial virus isolated during an epidemic period from children of northeastern Brazil

✍ Scribed by Fernanda Edna Araújo Moura; Andrea Blanc; Sandra Frabasile; Adriana Delfraro; María José de Sierra; Lorena Tome; Eduardo Antônio Gonçalves Ramos; Marilda Mendonça Siqueira; Juan Arbiza

• Publisher: John Wiley and Sons
• Year: 2004
• Tongue: English
• Weight: 92 KB
• Volume: 74
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.20159

✦ Synopsis

Abstract

Outbreaks of human respiratory syncytial virus (HRSV) are the leading cause of serious acute lower respiratory viral disease in many countries in different continents. Data on clinical and epidemiological aspects of HRSV infections in this country have been reported, but there is lack of data regarding the molecular epidemiology of this virus in Salvador. The genetic variability of HRSV isolated during an outbreak in Salvador, Brazil (1999) has been analysed. Partial sequences of the G protein gene of 13 isolates from antigenic group A and 4 isolates from antigenic group B of HRSV were determined. Nucleotide sequences of C‐terminal G gene were compared to sequences of HRSV isolates from countries of South America and from the rest of the world available at the GenBank. Brazilian group A and B isolates were clustered into previously characterised genotypes: GA5, GA2, GA7, and GB3, SAB3, respectively. This is the first study of GA7 and SAB3 genotypes circulation in South American countries. It is interesting to point out that viruses isolated in Salvador appear to be closer related with those from Montevideo‐Uruguay and Buenos Aires, Argentina strains, suggesting circulation of similar strains among different South American countries in different seasons. Moreover, viruses closely related genetically circulated in the same year in Salvador and distant places such as Mozambique, supporting the previous suggestion on the complexity of HRSV strain circulation patterns, and the high capability of HRSV spreading world‐wide. J. Med. Virol. 74:156–160, 2004. © 2004 Wiley‐Liss, Inc.