Table 1

Respiratory viruses, inflammatory markers, and clinical manifestations

Respiratory viruses Inflammatory markers Clinical manifestations
Influenza↓ IL-5
↑ interferon (IFN)-γ
↑ MCP-1/CCL2, RANTES/CCL5, macrophage inhibitory protein-1α (MIP)-1α,/CCL3, MCP-3/CCL7, eotaxin/CCL11
↑ IL-1β and ?IL-13
Though influenza-infected airways do not demonstrate significant eosinophilic response due to inhibitory effects of IFN γ, non-T2 cytokine IL-1β and T2 cytokine IL-13 may contribute to airway hyper-reactivity. Influenza still induces goblet cell metaplasia and mucus hypersecretion.
Human rhinovirus (RV)↑IL-5
↑eosinophil cationic protein (ECP)
↑IL-10
↑IL-13
Cytokine profile favoring eosinophilic inflammation with potential downregulation of T1 inflammation by IL-10. Increased IL-13 associated with airways hyper-reactivity.
Bronchiolitis in young children with symptoms of wheezing associated with increased risk of asthma diagnosis in later childhood.
Respiratory syncytial virus↑MIP-1α/CCL3, MIP-1β/CCL4
↑leukotriene C4 (LTC4)
↑ECP
↑IL-4
↑VEGF
↑G-CSF
↑IL-10
↑IL-6
↑IFN-γ
Mixed type 1 and type 2 inflammatory response though the elevation of IL-4 does drive eosinophilic inflammation, airway hyper-reactivity and goblet cell hypersecretion.
Most common cause of bronchiolitis (small airways inflammation, mucus production, and wheeze) in infants. Infection with respiratory syncytial virus (RSV) is associated with prolonged type 2 inflammation even after recovery which may play into development of atopy.