Abstract
Background: Respiratory syncytial (RSV) subtype-A is thought to have a more severe clinical course than RSV–B in bronchiolitis but to what extent the clinical severity depends on the RSV-A infecting genotype remains controversial. Moreover, while patient innate immune system has a key role to clear RSV infection, it participates in disease pathogenesis as well. The RSV-A genotype distribution has changed over the past 12 epidemic seasons; genotype NA1 predominated up to 2011-2012, replaced in 2012 by the novel genotype ON1.
Aim: to test the hypothesis that genotype-specific viral loads and clinical severity were related to the Interferon (IFN) response elicited by the specific RSV strain
Methods: Quantitative expression of RSV RNA (viral load) and of two IFN-stimulated genes, MXA and ISG56 (markers of type I and III IFN activation) were measured in nasopharyngeal washings from 96 full-term infants hospitalized with bronchiolitis caused by NA1 (N=50) and ON1(N=46).
Results: ON1 patients had higher viral loads, despite presenting a milder clinical course with respect to NA1. In neither groups, the amount of RSV load correlated with clinical severity. Significantly higher levels of both MXA and ISG56 genes were found in NA1 than in ON1 patients.
Conclusions: An elevated level of IFN-stimulated genes was observed in infants infected with RSV-A genotype NA1, that caused a more severe bronchiolitis course. Similarly to other viral infections, IFN activation may be effective in controlling the amount of RSV replication but may cause detrimental effects on the host.
Footnotes
Cite this article as: European Respiratory Journal 2018 52: Suppl. 62, OA3604.
This is an ERS International Congress abstract. No full-text version is available. Further material to accompany this abstract may be available at www.ers-education.org (ERS member access only).
- Copyright ©the authors 2018