Immunity & infection
The human respiratory syncytial virus (hRSV) is the most common infectious agent that affects children before two years of age. Outbreaks due to hRSV cause a significant increase in hospitalizations during the winter season associated with bronchiolitis and pneumonia. Recently, neurologic alterations have been associated with hRSV infection in children, which include seizures, central apnea, and encephalopathy. Also, hRSV RNA has been detected in cerebrospinal fluids (CSF) from patients with neurological symptoms after hRSV infection. Furthermore, previous work demonstrated that hRSV can be detected in the lungs and brains of mice exposed to the virus. The effects of hRSV infection within the central nervous system (CNS) are unknown. In this work using a murine model of hRSV-infected mice, we show that hRSV infection causes an alteration in the permeability of the blood-brain barrier (BBB), which allows the infiltration whether immune cells and the expression of pro-inflammatory cytokines in the CNS. Additionally, we show that the virus infects murine astrocytes both in vivo and in vitro. Murine astrocytes hRSV-infected presented an increased production of nitric oxide (NO) and TNF-α. hRSV infection caused an acute and chronic behavior impairment (up to two months), as well as altered expression of cytokines, such as IL-4, IL-10, and CCL2. Our results suggest that hRSV infection can impair the proper CNS function and induce local inflammation. Furthermore, this study provides a better understanding of the neuropathy caused by hRSV in humans and the possible detrimental effects on behavior.