title: Analysis of respiratory syncytial virus strain variation in successive epidemics in one city.
abstract: The variability of respiratory syncytial virus isolates from five successive epidemics in an urban population was determined. A total of 187 isolates of respiratory syncytial virus from the southern part of Birmingham, United Kingdom, were classified into subgroups A and B and were then further assigned to genetic lineages. Allocation of isolates into lineages was achieved by reverse transcription of infected cell RNA and then PCR amplification of selected regions of the genome; PCR products were examined by restriction mapping or nucleotide sequencing of parts of the nucleoprotein gene, the small hydrophobic protein gene, and the attachment protein gene. Previous work has shown that estimations of genetic diversity by analysis of genes coding for proteins likely (attachment protein) and unlikely (nucleoprotein and small hydrophobic protein) to be under immune pressure gave concordant results. Six genetic lineages of subgroup A isolates have been defined by this procedure; these isolates differ by up to 20% in the amino acid sequences of their attachment proteins; likewise, subgroup B isolates can be divided into two categories by restriction mapping of parts of their nucleoprotein and attachment protein genes. The same genetic lineages appeared to be present worldwide during the same period. The analysis of isolates from successive epidemics showed that different lineages predominated in each epidemic and that not all lineages were present in every epidemic. Some lineages appeared to increase in numbers over several years and then decline, possibly indicating a buildup of resistance in the community to a particular genotype.
authors.affiliation: Department of Biological Sciences, University of Warwick, Coventry, United Kingdom.
authors.forename: P A
authors.initials: PA
authors.lastname: Cane
authors.forename: D A
authors.initials: DA
authors.lastname: Matthews
authors.forename: C R
authors.initials: CR
authors.lastname: Pringle
mesh_terms: D002213:Capsid / Q000235:genetics; D004196:Disease Outbreaks; D005814:Genes, Viral / Q000235:genetics*; D014644:Genetic Variation; D005838:Genotype; D015707:HN Protein; D006801:Humans; D007231:Infant, Newborn; D016133:Polymerase Chain Reaction; D018357:Respiratory Syncytial Virus Infections / Q000453:epidemiology / Q000382:microbiology*; D012136:Respiratory Syncytial Viruses / Q000145:classification / Q000235:genetics* / Q000302:isolation & purification; D015183:Restriction Mapping; D013997:Time Factors; D006113:United Kingdom / Q000453:epidemiology; D014758:Viral Core Proteins / Q000235:genetics; D014759:Viral Envelope Proteins; D014764:Viral Proteins / Q000235:genetics
chemical_list: D015707:HN Protein; D014758:Viral Core Proteins; D014759:Viral Envelope Proteins; D014764:Viral Proteins; C116204:attachment protein G