Neurologic Alterations Due to Respiratory Virus Infections

Bohmwald, Karen; Gálvez, Nicolás M. S.; Ríos, Mariana; Kalergis, Alexis M.

Recently, an in vitro study using neuronal N2a cells as hRSV-infection model-which are a neuroblastoma cell line that can differentiate into cells that possess neuronal characteristic-was performed (Yuan et al., 2018) . The data presented by the authors indicated that this virus infects these cells and that viral titers increased up until 96 h post-infection, suggesting that hRSV replicates in this cell line (Yuan et al., 2018 ; Figure 1) . Additionally, they evaluated if toll-like receptor 4 (TLR4) and nucleolin (C23) are able to recognize the F-hRSV protein in N2a cells, as was reported in the literature. Using confocal microscopy, they found that this interaction also occurs in the hRSV-infected cells (Yuan et al., 2018) . According to this, they also observed that hRSV-infection increases the protein levels of TLR4 and C23 in N2a cells (Yuan et al., 2018) . To evaluate the contribution of infected neurons, in encephalopathies associated with hRSV-infection, the secretion of pro-inflammatory cytokines in the supernatant of N2a-hRSV infected cells was assessed by ELISA. The data obtained showed an increase of IL-6 and TNF-α in N2a hRSV-infected cells when compared to the control cells (Yuan et al., 2018) . Despite this new knowledge, there is no in vivo evidence that shows whether hRSV infects neurons or other resident cells. More research in this field is required to achieve a better understanding of the mechanism involved in the CNS disease induced by hRSVinfection.