Genetic Variation in Attachment Glycoprotein Genes of Human Respiratory Syncytial Virus Subgroups A and B in Children in Recent Five Consecutive Years

Abstract

Human respiratory syncytial virus (HRSV) outranks other viral agents as the cause of respiratory tract diseases in children worldwide. Molecular epidemiological study of the virus provides useful information for the development of globally effective vaccine. We investigated the circulating pattern and genetic variation in the attachment glycoprotein genes of HRSV in Beijing during 5 consecutive seasons from 2007 to 2012. Out of 19,942 tested specimens, 3,160 (15.8%) were HRSV antigen-positive. The incidence of HRSV infection in males was significantly higher than in females. Of the total 723 (23.1%) randomly selected HRSV antigen-positive samples, 462 (63.9%) and 239 (33.1%) samples were identified as subgroup A and B, respectively. Subgroups A and B co-circulated in the 5 consecutive HRSV seasons, which showed a shifting mixed pattern of subgroup dominance. Complete G gene sequences were obtained from 190 HRSV-A and 72 HRSV-B by PCR for phylogenetic analysis. Although 4 new genotypes, NA3 and NA4 for HRSV-A and BA-C and CB1 for HRSV-B, were identified here, they were not predominant; NA1 and BA9 were the prevailing HRSV-A and -B genotypes, respectively. We provide the first report of a 9 consecutive nucleotide insertion in 3 CB1 genotype strains. One Beijing strain of ON1 genotype with a 72 nucleotide insertion was found among samples collected in February 2012. The reversion of codon states in glycosylation sites to previous ones were found from HRSV strains in this study, suggesting an immune-escape strategy of this important virus.

Prevalence of human respiratory syncytial virus circulating in Iran

“…Based on its reaction with monoclonal antibodies against glycoprotein G and fusion protein F, RSV has two main genetic subtypes, A and B. There are 11 genotypes in subtype A (GA1-7, SAA1, ON1, and NA1-2) and 20 in subtype B (GB1-4, BA1-10, SAB1-4, and URU1-2) [12]. Although these subtypes can co-circulate, subtype A tends to be predominant, which might reflect time or geographical factors; virus circulation and evolution can be affected by several other factors including virus infectivity and spontaneous mutations as well as host group immunity [13,14].…”

“…Although these subtypes can co-circulate, subtype A tends to be predominant, which might reflect time or geographical factors; virus circulation and evolution can be affected by several other factors including virus infectivity and spontaneous mutations as well as host group immunity [13,14]. Gender-related susceptibility to RSV infection, with male children reportedly more at risk than females, remains controversial [12]; however, comparatively higher percentages of respiratory infections are reported in women, which might be due to increased exposure to airborne infections through frequent contact with children and elderly family members.…”

Rapid replacement of prevailing genotype of human respiratory syncytial virus by genotype ON1 in Beijing, 2012–2014

“…By phylogenetic analyses for nucleotide sequences of HVR2, HRSV-A have been classified into 11 genotypes (GA1-GA5, GA6-GA7, SAA1, NA1-NA2 and ON1) and HRSV-B into 22 genotypes (GB1-GB4, BA1-BA6, BA7-BA10, BA-C, SAB1-SAB3, SAB4, URU1, URU2 and CB1) (Cui et al, 2013b). In 2003, Trento et al (2003 reported three new HRSV-B strains isolated in 1999, named BA genotype, with the characteristic of a major change in the HVR2 introduced by a duplication of 60 nucleotides.…”

Retrospective phylogenetic analysis of circulating BA genotype of human respiratory syncytial virus with 60 bp duplication from New Delhi, India during 2007–2010

“…The G protein is one of the targets of host immune response and thus a vaccine candidate. hRSV group B strains have been classified into 13 reported genotypes GB1, GB2, GB3, GB4, SAB1, SAB2, SAB3, SAB4, URU1, URU2, JAB1, CB1 and BA [5,8,9,21,23,25]. The BA genotype has 60 nucleotide duplication in the second hypervariable region of the G protein gene.…”