Viral infection and neural stem/progenitor cell's fate: Implications in brain development and neurological disorders

National Brain Research Centre, Manesar, Haryana, India.
Neurochemistry International (Impact Factor: 3.09). 02/2011; 59(3):357-66. DOI: 10.1016/j.neuint.2011.02.020
Source: PubMed


Viral infections in the prenatal (during pregnancy) and perinatal period have been a common cause of brain malformation. Besides the immediate neurological dysfunctions, virus infections may critically affect CNS development culminating in long-term cognitive deficits. Most of these neurotropic viruses are most damaging at a critical stage of the host, when the brain is in a dynamic stage of development. The neuropathology can be attributed to the massive neuronal loss induced by the virus as well as lack of CNS repair owing to a deficit in the neural stem/progenitor cell (NSPC) pool or aberrant formation of new neurons from NSPCs. Being one of the mitotically active populations in the post natal brain, the NSPCs have emerged as the potential targets of neurotropic viruses. The NSPCs are self-renewing and multipotent cells residing in the neurogenic niches of the brain, and, therefore, hampering the developmental fate of these cells may adversely affect the overall neurogenesis pattern. A number of neurotropic viruses utilize NSPCs as their cellular reservoirs and often establish latent and persistent infection in them. Both HIV and Herpes virus infect NSPCs over long periods of time and reactivation of the virus may occur later in life. The virus infected NSPCs either undergoes cell cycle arrest or impaired neuronal or glial differentiation, all of which leads to impaired neurogenesis. The disturbances in neurogenesis and CNS development following neurotropic virus infections have direct implications in the viral pathogenesis and long-term neurobehavioral outcome in infected individuals.

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Available from: Sulagna Das, Apr 21, 2015
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    • "Being a neurotropic virus, JEV targets mostly neurons and results in neuronal death through activation of pro-apoptotic pathway (Swarup et al. 2007). Several neurotropic viruses have been shown to either develop persistent infection in NSPCs or modulate their differentiation potential (Das and Basu 2011). Besides neurons, the mitotically active NSPC also act as potential target for JEV infection (Das and Basu 2008). "
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