Background: Respiratory syncytial virus (hRSV) infections primarily cause acute respiratory illness and pediatric hospitalizations. We examined the hRSV molecular epidemiology in a pediatric cohort over a 4-year period and described the interrelationship with clinical data.
Methods: A cross-sectional study was conducted from 2014 to 2017 on children with acute respiratory illness. Respiratory viruses were detected using a multiplex real-time polymerase chain reaction and molecular typing was performed by nucleotide sequencing.
Results: Three hundred fifty-three children with hRSV were included; 207 (36%) samples were submitted to partial G gene sequencing. A total of 58.3% (n = 120) were males, the median age was 2.3 months (interquartile range 1-4), and 36.4% (n = 75) of the children required intensive care unit assistance. Coinfection was detected in 27 (5.7%) children, mainly hRSV and rhinovirus (14.2%). A total of 95.6% of patients had no comorbidities, and prematurity (4.4%) was more frequent among those with comorbidities. hRSV-B was detected in 109 patients (53%) and hRSV-A in 98 patients (47%), with changes in incidence over the period. All the hRSV-A sequences were classified as ON1-like, with genetic lineage GA2.3.5 forming distinct clusters. hRSV-B sequences were identified as BA-like, comprising 3 genetic lineages, GB5.0.2, GB5.0.4a and GB5.0.5a, with variation over time, and a higher severity was associated with hRSV type B GB5.0.2 and GB5.0.4a lineages compared with the GB5.0.5a.
Conclusions: Both hRSV subtypes showed similar severity and were not linked to comorbidities. Severe cases were more common in young patients and those infected with GB5.0.2 and GB5.0.4a genotypes. Understanding hRSV's molecular evolution is crucial for tracking new variants and assessing their impact on the effectiveness of emerging vaccines and monoclonal antibodies.
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