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High Resolution Analysis of Respiratory Syncytial Virus Infection In Vivo

Authors
  • Aljabr, Waleed1
  • Armstrong, Stuart2, 3
  • Rickett, Natasha Y.2, 3
  • Pollakis, Georgios2
  • Touzelet, Olivier
  • Cloutman-Green, Elaine
  • Matthews, David A.
  • Hiscox, Julian A.2, 3
  • 1 King Fahad Medical City, Research Center, 59046 Riyadh 11525, Saudi Arabia
  • 2 (J.A.H.)
  • 3 National Institute of Health Research, Health Protection Research Unit in Emerging and Zoonotic Infections, Liverpool L3 5RF, UK
Type
Published Article
Journal
Viruses
Publisher
MDPI AG
Publication Date
Oct 10, 2019
Volume
11
Issue
10
Identifiers
DOI: 10.3390/v11100926
PMID: 31658630
PMCID: PMC6832471
Source
PubMed Central
Keywords
License
Green

Abstract

Human respiratory syncytial virus (HRSV) is a major cause of pediatric infection and also causes disease in the elderly and those with underlying respiratory problems. There is no vaccine for HRSV and anti-viral therapeutics are not broadly applicable. To investigate the effect of HRSV biology in children, nasopharyngeal aspirates were taken from children with different viral loads and a combined high throughput RNAseq and label free quantitative proteomics approach was used to characterize the nucleic acid and proteins in these samples. HRSV proteins were identified in the nasopharyngeal aspirates from infected children, and their abundance correlated with viral load (Ct value), confirming HRSV infection. Analysis of the HRSV genome indicated that the children were infected with sub-group A virus and that minor variants in nucleotide frequency occurred in discrete clusters along the HRSV genome, and within a patient clustered distinctly within the glycoprotein gene. Data from the samples were binned into four groups; no-HRSV infection (control), high viral load (Ct < 20), medium viral load (Ct = 20–25), and low viral load (Ct > 25). Cellular proteins associated with the anti-viral response (e.g., ISG15) were identified in the nasopharyngeal aspirates and their abundance was correlated with viral load. These combined approaches have not been used before to study HRSV biology in vivo and can be readily applied to the study the variation of virus host interactions.

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