Japanese encephalitis virus, a neurotropic
flavivirus, causes sporadic
encephalitis with nearly 25% fatal casereports. JEV infects neural
stem/
progenitor cells (NSPCs) and decreases their proliferation.
Statin, a commonlyused class of
cholesterol lowering
drug, has been shown to possess potent anti-inflammatory and
neuroprotective effects in
acute brain injury and chronic neurodegenerative conditions. Here, we aimed to check theefficacy of
atorvastatin in alleviating the symptoms of
Japanese encephalitis (JE). Using BALB/c
mouse modelof JEV
infection, we observed that
atorvastatin effectively reduces
viral load in the
subventricular zone (SVZ)of infected pups and decreases the resultant
cell death. Furthermore,
atorvastatin abrogates microglial activation and
production of proinflammatory cyto/
chemokine production post JEV
infection in vivo. It alsoreduced
interferon-b response in the neurogenic environs. The neuroprotective
role of
atorvastatin is againevident from the rescued neurosphere size and decreased
cell death in vitro. It has also been observed that uponatorvastatin
administration,
cell cycle regulatory proteins and
cell survival proteins are also restored to theirrespective expression level as observed in uninfected
animals. Thus the
antiviral, immunomodulatory andneuroprotective
roles of
atorvastatin reflect in our experimental observations. Therefore, this
drug broadens apath for
future therapeutic measures against JEV
infection.