Table 1.
Virulence factors involved in molecular mechanisms of interactions between Staphylococcus aureus and non-influenza respiratory viruses.
| Virulence factors | Cellular target | Effects | Synergism | References |
|---|---|---|---|---|
| Staphylococcus aureus | ||||
| SEA/SEB | Unknown | Increase of IL-1β, IL-6 and IL-8 secretion | Increase of ICAM-1 expression Enhancement of rhinovirus replication |
[53,83–85] |
| LTA | Unknown | Increase of IL-6, IL-12/IL-23 and IFN-γ secretion | Increase of susceptibility to coronavirus | [98] |
| Human rhinovirus | ||||
| Capsid | Membrane TLR2 | NFκB activation Increase of IL-6, IL-8, INFβ and IFN-γ secretion |
Increase of cFn and ICAM-1 expression Increase of S. aureus adhesion and internalization to/in host cells | [48,51–56] |
| ssRNA | Endosomal TLR7/8 | |||
| Cytoplasmic RIG-I | Increase of IFN-β, IFN-γ, RANTES, IL-8, IP-10 and ENA78 secretion | |||
| dsRNA | Cytoplasmic MDA5 | |||
| Endosomal TLR3 | RIG-I and MDA5 upregulation NFκB activation Increase of IL-6, IL-8, INF-β and IFN-γ secretion |
|||
| Unknown | Rac1 activation NOX1 production Stimulation of ROS generation |
Loss of ZO-1 tight junctions Induce S. aureus invasion of the epithelium |
[78,81] | |
| Respiratory Syncytial Virus | ||||
| Viral envelope | Membrane TLR2 | NFκB activation Increase of pro-inflammatory cytokine secretion IRFs activation Increase of type I IFNs secretion |
Alteration of neutrophil recruitment Inhibition of B cells response Decrease of S. aureus clearance |
[87,90,93,94,99] |
| Viral F protein | Membrane TLR4 | |||
| ssRNA | Endosomal TLR3 | |||
| Cytoplasmic RIG-I | ||||
| Cytoplasmic Nod2 | ||||
| dsRNA | Endosomal TLR7 | |||
| Cytoplasmic MDA5 | ||||
| Unknown | NKG2D | Increase of IFN-γ secretion | ||
| Unknown | Unknown | Increase of Lewis blood group antigen expression | Increase of toxin-producing S. aureus binding to epithelial cells | [88,89,91] |