Molecular epidemiology of human respiratory syncytial virus subgroups A and B identified in adults with hematological malignancy attending an Irish hospital between 2004 and 2009

Abstract

Human respiratory syncytial virus (HRSV) is an important cause of respiratory infection in patients with hematological malignancy, particularly hematopoietic stem cell transplant recipients. This study investigated the genetic variability of the attachment (G) protein gene among HRSV isolates collected from adult patients with hematological malignancy. Between December 2004 and March 2009, 60 samples collected from 58 adults attending an Irish hospital were positive for HRSV by direct immunofluorescence. Nucleotide sequence analysis of the G gene showed a slightly higher frequency of HRSV subgroup A (52%) than HRSV subgroup B (48%). Genetic variability was higher among subgroup A viruses (up to 13% at nucleotide level) than among subgroup B viruses (up to 4%). Phylogenetic analysis revealed two genotypes of HRSV subgroup A, GA2 and GA5, which cocirculated between 2004/2005 and 2007/2008, although GA2 alone was identified in season 2008/2009. Genotype BA was the only genotype of HRSV subgroup B identified. Genotype-specific amino acid substitutions were identified, with two and seven changes for GA2 and GA5, respectively. Furthermore, one to four potential N-glycosylation sites were found among HRSV subgroup A isolates while two to three were identified in HRSV B isolates. Predicted O-glycosylation sites included 25-34 and 40-43 in HRSV subgroups A and B, respectively. The average synonymous mutation-to-non-synonymous mutation ratios (dS/dN) implied neutral selection pressure on both HRSV subgroup isolates. This study provides data for the first time on the molecular epidemiology of HRSV isolates over five successive epidemic seasons among patients attending an Irish hospital.

Whole Genome Sequencing and Evolutionary Analysis of Human Respiratory Syncytial Virus A and B from Milwaukee, WI 1998-2010

“…GA2 and GA5 co-circulated in two different seasons (1998 and 2006) after which apparently only GA2 persisted, still infecting people in the Milwaukee area in 2010. These results are consistent with other published studies for RSV A [29], [46] where they also had shown that several genotypes are present now, were present in 1996, and were even present much earlier as can be seen by the fact that published sequences from as far back as 1956 fall into these same genotypes (Figure 3). These genotypes appear to have much more distant origins and continue to co-circulate with each genotype steadily accumulating unique mutations.…”

Circulation of HRSV in Belgium: From Multiple Genotype Circulation to Prolonged Circulation of Predominant Genotypes

“…The GB13 genotype, first detected in Belgium in 2001/2002 has replaced all other genotypes and co-circulated with GB12 in the season 2002/2003 and 2006/2007. This gradual replacement of circulating genotypes by GB13 has been observed in different countries and GB13 represents 100% of the isolated HRSV-B strains after 2006 [25], [28]. Since 2006/2007, GA2 has been predominating over GA5, whereas the genotype distribution pattern of the previous seasons (1996/1997–2005/2006) demonstrated annual or biennial replacement of GA5 by GA2 or vice versa.…”

“…GA2 and GA5 are characterised by genotype specific amino acid mutations [24], [25]. All Belgian GA2 strains had the previous reported T269 and S289 amino acid substitution (Figure S1).…”

Evaluation of respiratory syncytial virus group A and B genotypes among nosocomial and community-acquired pediatric infections in southern Brazil

“…It has also been reported in Europe and Asia [12,29,30]. The rapid and worldwide spread of the BA genotype implies that it may have a selective advantage over other circulating strains [31]. However, there may be mutations elsewhere in the genome that confer more efficient replication when compared with other RSV-B genotypes.…”