Evaluation of viral load in infants hospitalized with bronchiolitis caused by respiratory syncytial virus

Abstract

The relationship between viral load, disease severity and antiviral immune activation in infants suffering from respiratory syncytial virus (RSV)-associated bronchiolitis has not been well identified. The main objective of this study was to determine the existence of a correlation between RSV load and disease severity and also between different clinical markers and mRNA levels of the interferon stimulated gene (ISG)56 in infants hospitalized for bronchiolitis. We also evaluated whether viral load tended to be persistent over the course of the RSV infection. The levels of RSV-RNA were quantified in nasopharyngeal washings, collected from 132 infants infected with RSV as a single (90.15%) or as a dual infection with other respiratory viruses (9.85%). Results indicated that viral load was positively related to the clinical severity of bronchiolitis, the length of hospital stay, the levels of glycemia and the relative gene expression of ISG56, whereas an inverse correlation was observed with the levels of hemoglobin. We also found that the RSV load significantly decreased between the first and second nasopharingeal washings sample in most subjects. These results suggest that infants with high RSV load on hospital admission are more likely to have both more severe bronchiolitis and a higher airway activation of antiviral immune response.

The interdependencies of viral load, the innate immune response, and clinical outcome in children presenting to the emergency department with respiratory syncytial virus-associated bronchiolitis

“…In the latter study, sample quality was not measured and therefore could not be corrected by RNase P copy number. Additionally, samples were collected from hospitalized infants only and later into the course of infection compared to the current study [17] Others have reported similar associations between viral load and disease severity, but the associations are weak and come either from hospitalized infants [20–23] or infants healthy enough to stay home [19, 24]–rarely both [26]. Additionally, most of the samples were collected later in the course of infection than those analyzed here.…”

Infantile respiratory syncytial virus and human rhinovirus infections: respective role in inception and persistence of wheezing

“…The lack of protective antibodies at the site of infection in young infants with bronchiolitis favours viral replication, leading to high RSV viral load, a factor that has been shown to correlate positively with the clinical severity of the disease and the length of hospital stay [34]. Viral replication directly increases the number of infected cells and, therefore, the extension of the damage to the airway.…”

Respiratory syncytial virus infection: an innate perspective

“…Importantly, the two are not independent variables. A high viral load has been associated with high release of pro-inflammatory immune mediators and more severe symptoms 19– 23 . Thus, it is possible that the development of severe disease is due to an early lack of control of the virus, which leads to epithelial cell damage and a high release of pro-inflammatory mediators that recruit and activate leukocytes in the lung and induce an excessive immune response that results in immunopathology 20, 24– 26 .…”