RSV Strain 2-20 Induces More Severe Disease in BALB/c Mice than RSV Strain 3-12 (39.25)

Abstract Respiratory syncytial virus (RSV) is the chief cause of bronchiolitis and viral pneumonia in infants. Mucus production contributes to morbidity and mortality in RSV disease. The TH2 cytokine IL-13 is a mediator of mucus production. RSV strain differences can play a role in differential immunologic phenotypes. The pathogenesis of RSV clinical isolate strains was examined in BALB/c mice. RSV strain 2-20 induced significant weight loss, lung IL-13 levels, and bronchiolitis in BALB/c mice. In contrast, RSV 3-12 exhibited a less severe phenotype similar to the RSV A2 laboratory strain. Mucin expressing cells in the lungs of BALB/c mice infected with RSV A2, 2-20, or 3-12 were quantified with a digital scanning microscope. RSV 2-20 induced greater mucin expression than RSV 3-12 and RSV A2. T cell and IFN-γ-expressing T cells were enumerated by flow cytometry. RSV 2-20 infection resulted in fewer IFN-γ-expressing T cells and lower overall T cell numbers in the lungs of BALB/c mice compared to RSV 3-12 and RSV A2 infection. These data correlate the heighted virulence and mucogenicity of RSV 2-20 with a diminished T cell response. RSV strain differences have an impact on RSV immunopathogenesis.