Spread and clinical severity of respiratory syncytial virus A genotype ON1 in Germany, 2011–2017

Abstract

Background The Respiratory Syncytial Virus (RSV) A genotype ON1, which was first detected in Ontario (Canada) in 2010/11, appeared in Germany in 2011/12. Preliminary observations suggested a higher clinical severity in children infected with this new genotype. We investigated spread and disease severity of RSV-A ON1 in pediatric in- and outpatient settings. Methods During 2010/11 to 2016/17, clinical characteristics and respiratory samples from children with acute respiratory tract infections (RTI) were obtained from ongoing surveillance studies in 33 pediatric practices (PP), one pediatric hospital ward (PW) and 23 pediatric intensive care units (PICU) in Germany. RSV was detected in the respiratory samples by PCR; genotypes were identified by sequencing. Within each setting, clinical severity markers were compared between RSV-A ON1 and RSV-A non-ON1 genotypes. Results A total of 603 children with RSV-RTI were included (132 children in PP, 288 in PW, and 183 in PICU). Of these children, 341 (56.6%) were infected with RSV-A, 235 (39.0%) with RSV-B, and one child (0.2%) with both RSV-A and RSV-B; in 26 (4.3%) children, the subtype could not be identified. In the 341 RSV-A positive samples, genotype ON1 was detected in 247 (72.4%), NA1 in 92 (26.9%), and GA5 in 2 children (0.6%). RSV-A ON1, rarely observed in 2011/12, was the predominant RSV-A genotype in all settings by 2012/13 and remained predominant until 2016/17. Children in PP or PW infected with RSV-A ON1 did not show a more severe clinical course of disease compared with RSV-A non-ON1 infections. In the PICU group, hospital stay was one day longer (median 8 days, inter-quartile range (IQR) 7–12 vs. 7 days, IQR 5–9; p = 0.02) and duration of oxygen treatment two days longer (median 6 days, IQR 4–9 vs. 4 days, IQR 2–6; p = 0.03) for children infected with RSV-A ON1. Conclusions In children, RSV-A ON1 largely replaced RSV-A non-ON1 genotypes within two seasons and remained the predominant RSV-A genotype in Germany during subsequent seasons. A higher clinical severity of RSV-A ON1 was observed within the group of children receiving PICU treatment, whereas in other settings clinical severity of RSV-A ON1 and non-ON1 genotypes was largely similar. Electronic supplementary material The online version of this article (10.1186/s12879-019-4266-y) contains supplementary material, which is available to authorized users.

Respiratory Syncytial Virus in Greece, 2016–2018

“…Genotyping of the strains showed that one single ge­notype per subtype was detected, and RSV-A ON1 predominated during 2016–2017, and RSV-B BA predominated in the next season. Similarly, in Germany, a predominance of RSV-A (53.2%) was seen during 2016–2017, with ON1 being the only genotype detected [19]. However, the predominance of RSV subtypes in other European countries during the same winter seasons varied.…”

Identification and seasonality of rhinovirus and respiratory syncytial virus in asthmatic children in tropical climate

“…In countries of temperate zones, upper respiratory tract infections being more frequent in autumn and spring, rising during winter, following weather changes [ 11 ]. A study conducted in Germany suggests that humidity and temperature are associated with hospitalizations due to lower respiratory tract infections by the Influenza virus, RSV, and RV [ 12 ]. Another study carried out in the Colombia, showed that the occurrence of acute respiratory infection in children was associated with air temperature and relative humidity [ 13 ].…”

The specific features of the developing T cell compartment of the neonatal lung are a determinant of respiratory syncytial virus immunopathogenesis

“…to assess the adaptive mechanisms and virus clearance (Fig 6A). Additionally, neonates were infected with RSV-ON1-H1 strain, a primary clinical isolate recently circulating in central Europe (see following section) [36]. BAL cellularity is provided in S8 Fig; no significant difference was found between the absolute counts of RSV-infected adults and neonates.…”

“…While immune-mediated mechanisms are central determinants of RSV severity, there are indications that viral factors play also a role [37]. We evaluated the pulmonary T cell response in neonates infected with RSV A2, a well characterized prototypical strain of RSV, in comparison to the RSV-ON1-H1, a primary clinical isolate which was the major genotype circulating in central Europe during the RSV seasons of 2012 to 2017 (Fig 6A) [36]. Whereas infection of neonates with RSV-ON1-H1 strain led to a milder disease, as indicated by milder histological lesions (Fig 8A ), the viral loads and virus clearance was comparable between both strains, again reinforcing the hypothesis for immune-mediated RSV pathogenesis (Fig 8B).…”