Subgroup prevalence and genotype circulation patterns of human respiratory syncytial virus in Belgium during ten successive epidemic seasons

Abstract

Human respiratory syncytial virus (HRSV) is the leading viral cause of severe respiratory illness for infants and young children worldwide. Two major antigenic groups (A and B) of HRSV exist, and viruses from both subgroups can cocirculate during epidemics; however, their frequencies might differ between seasons. The subgroup prevalence and genotype distribution patterns of HRSV strains were investigated in a community in Belgium during 10 successive epidemic seasons (1996 to 2006). A regular 3-year cyclic pattern of subgroup dominance was observed, consisting of two predominant HRSV-A seasons, followed by a single HRSV-B-dominant year. HRSV infections with both subgroups were more prevalent among children younger than 6 months and had a peak incidence in December. The most frequently detected genotypes were GA5 and GB13, the latter including strains with the 60-nucleotide duplication in the G gene. Furthermore, GA5 remained the dominant HRSV genotype in two consecutive epidemic seasons twice during the study period. Additional variability was detected among the GB13 isolates, due to the usage of a novel termination codon in the G gene. Dual infections with both HRSV subgroups were detected for 9 patients, and subsequent infections with the heterologous HRSV subgroup were documented for 15 patients. Among five patients with homologous reinfections, only one was caused by HRSV-B. Our results support the hypothesis that the overall prevalence of HRSV-A over HRSV-B could be due to a more-transient subgroup A-specific immune protection.

FIG. 1.

Seasonal frequency of antigen-positive HRSV infections (curves) and monthly distribution of typed HRSV-A (white bars) and HRSV-B (black bars) infections among hospitalized patients in Belgium (1996 to 2006). Initial letters of months are given along the y axis, beginning with July for each season.

FIG. 2.

Age distributions of HRSV-A and -B infections among hospitalized patients in Belgium from 1996 to 2006.

FIG. 3.

Unrooted neighbor-joining phylogenetic trees of the G genes of 119 HRSV-A (A) and 163 HRSV-B (B) strains obtained in Belgium from 1996 to 2006. Only bootstrap values above 75% are shown. The italicized numbers in parentheses at the terminal nodes correspond to the numbers of identical sequences. Brackets on the right delimit the HRSV-A and HRSV-B genotypes. The predicted length of the G protein is given in boldface after the genotype and, for exceptions, after the strain designation or grouping. The nomenclature is based on phylogenetic clustering with sequences previously assigned to specific genotypes. HRSV-A genotypes GA2 and GA5 are designated according to the classification systems of Peret et al. (32, 33) and Venter et al. (45). HRSV-B genotype designation GB2 represents the classification systems of Peret et al. (32) and Venter et al. (44, 45), while GB3, GB6, GB8, and GB10 to GB13 are based on the classification of Zlateva et al. (48).

FIG. 3.

Unrooted neighbor-joining phylogenetic trees of the G genes of 119 HRSV-A (A) and 163 HRSV-B (B) strains obtained in Belgium from 1996 to 2006. Only bootstrap values above 75% are shown. The italicized numbers in parentheses at the terminal nodes correspond to the numbers of identical sequences. Brackets on the right delimit the HRSV-A and HRSV-B genotypes. The predicted length of the G protein is given in boldface after the genotype and, for exceptions, after the strain designation or grouping. The nomenclature is based on phylogenetic clustering with sequences previously assigned to specific genotypes. HRSV-A genotypes GA2 and GA5 are designated according to the classification systems of Peret et al. (32, 33) and Venter et al. (45). HRSV-B genotype designation GB2 represents the classification systems of Peret et al. (32) and Venter et al. (44, 45), while GB3, GB6, GB8, and GB10 to GB13 are based on the classification of Zlateva et al. (48).