Neurologic Alterations Due to Respiratory Virus Infections

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

Mice studies are mainly performed with MHV, a virus that belongs to the BCoV genus and is genetically related to HCoV-OC43; likewise, the disease at CNS as elucidated by both viruses are similar, as they both induce demyelination (Jacomy and Talbot, 2003; Bergmann et al., 2006 ; Figure 3 ). Jacomy and Talbot (2003) were among the first to describe a mouse model to characterize the CNS disease in their publication the year 2003. Therein, they exhibit that BALB/c and C57BL/6 mice could be infected through nasal instillation with MHV, although they chose to use intracerebral inoculation to favor CNS infection (Jacomy and Talbot, 2003) . They also determined that viral RNA could be detected in brain, heart, spleen, lungs, liver and muscles (Jacomy and Talbot, 2003) . Likewise, the year 2004 Glass et al. (2004) described a systemic non-lethal model of infection for SARS-CoV in C57BL/6 mice that eventually reached the brain. Finally, in Jacomy et al. (2006) described that HCoV-OC43 could infect glial and neuronal cells of both rat and mice (Figure 3) . Therein, they also showed that surviving animals exhibited decreased motor functions. Recently, Wheeler et al. (2018) described that microglia is essential for the regulation of MHV infection, as depletion of this cell type led to faster viral replication, enhancing its capacity to avoid adaptive immunity. According to this, glial primary cultures of MHV-A59-infected cells showed an increase in the secretion of IL-12 p40, TNF-α, IL-15 and IL-6 compared with a non-neurotropic MHV, suggesting that the infection with a neurotropic virus activates glial cells and induces a pro-inflammatory state (Li et al., 2004 ; Figure 3) .