IFN-γ and TNF are produced by CD8 T cells following RSV infection and contribute to both the acceleration of viral clearance and the induction of immunopathology.
Analysis of innate and adaptive immune responses revealed an early increase in the number of IL-17+ γδ T cells in CX3CR1-deficient mice that outnumbered IFN-γ+ γδ T cells as well as IFN-γ+ NK cells, IFN-γ being host protective in the context of RSV infection.
Thus, despite the involvement of different IFNs in the pathophysiology of RSV infection, genetic variants in IFNG and related genes might not alter the risk for the development of severe RSV-associated diseases.
2'-5' Oligoadenylate synthetase plays a critical role in interferon-gamma inhibition of respiratory syncytial virus infection of human epithelial cells.
Patients hospitalized because of RSV infection had increased numbers of CD16(+) and CD56(bright) cells and had RSV-specific increases in Th1 (interleukin [IL]-2 and interferon-gamma) and Th2 (IL-4 and IL-6) cytokines and CC chemokines (macrophage inflammatory protein [MIP]-1alpha, MIP-1beta, and RANTES [regulated on activation, normally T cell expressed and secreted]) mRNA expression.
Effect of lack of Interleukin-4, Interleukin-12, Interleukin-18, or the Interferon-gamma receptor on virus replication, cytokine response, and lung pathology during respiratory syncytial virus infection in mice.
In conclusion, the results of the present study indicate that the TLR4 signaling pathway, in conjunction with MYD88, TRAM, TRIF and the transcription factor AP‑1, may activate immune responses to RSV infection in airway epithelial cells.
In the present study, the effect of respiratory syncytial virus (RSV) infection on the expression of ICAM-1 in human pulmonary type II-like epithelial (A549) cells was evaluated.
Furthermore, the survival of bronchial epithelial cells was dramatically decreased when their endogenous NGF supply was depleted prior to RSV infection.