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. 2005 May;43(5):2266-73.
doi: 10.1128/JCM.43.5.2266-2273.2005.

Genetic and antigenic variability of human respiratory syncytial virus (groups a and b) isolated over seven consecutive seasons in Argentina (1995 to 2001)

Monica C Galiano  1 , Concepcion Palomo, Cristina M Videla, Juan Arbiza, José A Melero, Guadalupe Carballal
Affiliations

Genetic and antigenic variability of human respiratory syncytial virus (groups a and b) isolated over seven consecutive seasons in Argentina (1995 to 2001)

Monica C Galiano et al. J Clin Microbiol. 2005 May.

Abstract

The genetic and antigenic variability of human respiratory syncytial virus (HRSV) strains isolated in Buenos Aires from 1995 to 2001 was evaluated by partial nucleotide sequencing of the G gene and enzyme-linked immunosorbent assay analysis with anti-G monoclonal antibodies. Phylogenetic analyses showed that 37 group A strains clustered into five genotypes, whereas 20 group B strains clustered into three genotypes. Group A showed more genetic variability than group B. A close correlation between genotypes and antigenic patterns was observed. Changes detected in the G protein of viruses from both groups included (i) amino acid substitutions and(ii) differences in protein length due to either changes in stop codon usage or sequence duplications. Three B strains from 1999 exhibited a duplication of 20 amino acids, while one B strain from 2001 had 2 amino acids duplicated. The comparison among Argentinean HRSV strains and viruses isolated in other geographical areas during different epidemics is discussed.

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Figures

FIG. 1.
FIG. 1.
Phylogenetic trees of group A (A) and B (B) HRSV strains. Prototype strains A/Long (8) and B/CH18537 (18) were included in the analysis. Selected worldwide sequences representing described genotypes were retrieved from GenBank and included in the trees for their comparison (9, 11, 12, 24, 25, 27, 30-32, 39, 44). Trees were built using the neighbor-joining algorithm through the MEGA program. BA HRSV strains and genotypes are shown in boldface. Numbers in italics correspond to bootstrap values supporting the adjacent nodes; only bootstrap values greater than 70% are displayed.
FIG. 2.
FIG. 2.
Correlation between the genetic and antigenic analyses of group A strains isolated in Buenos Aires. Strains Mon/3/88 and Long, used to raise monoclonal antibodies, are also included. Trees were built with the neighbor-joining algorithm, using the last 350 nucleotides, which code for the C-terminal segment of the G protein. Antigenic patterns corresponding to each virus are displayed near the tree. Antigenic patterns were defined by the combination of reactivities with the eight strain-specific MAbs. Reactivity with strain-specific MAbs is represented in black (reactive), gray (weakly reactive), or white (nonreactive).
FIG. 3.
FIG. 3.
Frequencies of nucleotide changes in sequences of HRSV G protein (BA viruses) of group A (a) and group B (b). Sequences in the vRNA sense were compared pairwise for each virus, and the percentage of different changes shown in each figure was calculated. Since the ancestor sequence for each pair of viruses is unknown, changes involving the same nucleotides (i.e., AG or GA) were added together as in reference .
FIG. 4.
FIG. 4.
Amino acid alignment of the second variable region of the G protein for group A (A) and group B (B) Argentinean strains. Strains A/Mon/3/88 and B/CH18537 are shown as consensus sequences. The genotype and protein length are shown at the end of each sequence. Locations of some group A strain-specific epitopes, as deduced from amino acid changes selected in escape mutants (22, 33, 34), are highlighted in panel A (light gray). Reactivities by ELISA (see Fig. 2) with strain-specific MAbs shown in italics above sequences are indicated by dark gray.
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