“Severe Human Respiratory Syncytial Virus (hRSV)” appears to cause “Bronchiolitis” both via a reduced local interferon (IFN) - ? response and substance P-mediated inflammation.
Malcolm Semple and his team of other UK researchers at the “University of Liverpool” have discovered this after the conclusion of a research study. Findings of this study have been published in the journal “PLoS ONE” recently.
The researchers believe that the research study results clearly indicate about the infants’ susceptibility to severe hRSV bronchiolitis and this may depend on innate immune responses to the virus.
Malcolm Semple went on to explore the factors that may mediate proposed mechanisms for bronchiolitis. His research team then studied 197 infants admitted to hospital with hRSV. All these infants were subsequently divided into groups like 27 with no oxygen requirement, 114 who were dependent on oxygen, and 56 who needed mechanical ventilation.
In addition to collecting clinical data, the researchers also measured levels of IFN-?, substance P, interleukin (IL)-9, and urea, as well as hRSV load in nasopharyngeal aspirate (NPA) and ventilated bronchoalveolar lavage (BAL).
Researchers observed that the infants who were dependent on oxygen or required mechanical ventilation had lower IFN-? and substance P levels in NPA than other children. Although concentrations of IL-9 and viral loads were high in all groups, these factors did not vary with the severity of the disease.
Malcolm Semple and his researcher’s team also stresses that findings from samples collected via NPA correlated with findings from those obtained using BAL.
Multivariate analysis of the results obtained revealed that independent predictors of severe disease were low weight on admission, low gestation at birth, low NPA IFN-? levels, and low NPA substance P concentrations, at odds ratios of 0.016, 0.482, 0.724, and 0.744, respectively.
Writing in the journal “PLoS ONE”, the researchers conclude: “Our data directly supports two of the recently proposed mechanisms for severe hRSV disease, namely a reduced local IFN-? response and substance P-mediated inflammation.”
Malcolm Semple explained in his conclusive remark of the research study, “A difference in the innate response to primary hRSV infection, common to term infants susceptible to severe hRSV bronchiolitis, may explain why so many of these infants experience recurrent wheeze in childhood in association with viral respiratory tract infections“.
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