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Journal of Virology, July 2005, p. 9157-9167, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.9157-9167.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Genetic Variability and Molecular Evolution of the Human Respiratory Syncytial Virus Subgroup B Attachment G Protein

Kalina T. Zlateva, Philippe Lemey, Elien Moës,{dagger} Anne-Mieke Vandamme, and Marc Van Ranst*

Laboratory of Clinical and Epidemiological Virology, Department of Microbiology and Immunology, Rega Institute for Medical Research, University of Leuven, Leuven, Belgium

Received 10 November 2004/ Accepted 2 April 2005

Human respiratory syncytial virus (HRSV) is the most important cause of acute respiratory disease in infants. Two major subgroups (A and B) have been identified based on antigenic differences in the attachment G protein. Antigenic variation between and within the subgroups may contribute to reinfections with these viruses by evading the host immune responses. To investigate the circulation patterns and mechanisms by which HRSV-B viruses evolve, we analyzed the G protein genetic variability of subgroup B sequences isolated over a 45-year period, including 196 Belgian strains obtained over 22 epidemic seasons (1982 to 2004). Our study revealed that the HRSV-B evolutionary rate (1.95 x 10–3 nucleotide substitutions/site/year) is similar to that previously estimated for HRSV-A (1.83 x 10–3 nucleotide substitutions/site/year). However, natural HRSV-B isolates appear to accommodate more drastic changes in their attachment G proteins. The most recent common ancestor of the currently circulating subgroup B strains was estimated to date back to around the year 1949. The divergence between the two major subgroups was calculated to have occurred approximately 350 years ago. Furthermore, we have identified 12 positively selected sites in the G protein ectodomain, suggesting that immune-driven selective pressure operates in certain codon positions. HRSV-A and -B strains have similar phylodynamic patterns: both subgroups are characterized by global spatiotemporal strain dynamics, where the high infectiousness of HRSV permits the rapid geographic spread of novel strain variants.

* Corresponding author. Mailing address: Laboratory of Clinical and Epidemiological Virology, Department of Microbiology and Immunology, Rega Institute for Medical Research, University of Leuven, Minderbroedersstraat 10, B-3000 Leuven, Belgium. Phone: 32 16 347908. Fax: 32 16 347900. E-mail: marc.vanranst{at}uz.kuleuven.ac.be.

{dagger} Present address: School of Biology, University of St. Andrews, St. Andrews, United Kingdom.

Journal of Virology, July 2005, p. 9157-9167, Vol. 79, No. 14
0022-538X/05/$08.00+0     doi:10.1128/JVI.79.14.9157-9167.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



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