The neonatal anti-viral response fails to control measles virus spread in neurons despite interferon-gamma expression and a Th1-like cytokine profile
Journal of Neuroimmunology
Interferon-gamma, Measles virus, Microglia, Natural killer cells, Neonatal, T cells
Neonates are highly susceptible to viral infections in the periphery, potentially due to deviant cytokine responses. Here, we investigated the role of interferon-gamma (IFN?), a key anti-viral in the neonatal brain. We found that (i) IFN? which is critical for viral control and survival in adults, delays mortality in neonates, (ii) IFN? limits infiltration of macrophages, neutrophils, and T cells in the neonatal brain, (iii) neonates and adults differentially express pathogen recognition receptors and Type I interferons in response to the infection, (iv) both neonates and adults express IFN? and other Th1-related factors, but expression of many cytokines/chemokines and IFN?-responsive genes is age-dependent, and (v) administration of IFN? extends survival and reduces CD4 T cell infiltration in the neonatal brain. Our findings suggest age-dependent expression of cytokine/chemokine profiles in the brain and distinct dynamic interplays between lymphocyte populations and cytokines/chemokines in MV-infected neonates.
Ganesan, P., Chandwani, M., Creisher, P., Bohn, L., & O'Donnell, L. (2018). The neonatal anti-viral response fails to control measles virus spread in neurons despite interferon-gamma expression and a Th1-like cytokine profile. Journal of Neuroimmunology, 316, 80-97. https://doi.org/10.1016/j.jneuroim.2017.12.018