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Published on: April 28, 2019
Neuropathogenesis by Chandipura virus: An acute encephalitis syndrome in India
1National Brain Research Centre, Manesar 122051, Haryana, India.
Insights
Chandipura virus (CHPV) causes acute encephalitis, leading to deaths in India. Cellular stress and reactive oxygen species (ROS) are key factors in CHPV neuropathogenesis and neuronal death.
Area of Science:
- Virology
- Neuroscience
- Pathology
Background:
- Chandipura virus (CHPV) is a significant cause of acute encephalitis syndrome (AES) and mortality in India.
- While CHPV neuropathogenesis is known, its precise entry into the central nervous system (CNS) and the mechanisms driving neuronal death remain unclear.
Purpose of the Study:
- To elucidate the entry mechanisms of CHPV into the CNS.
- To identify the triggers responsible for neuronal death during CHPV infection.
Main Methods:
- Review of existing literature on CHPV and related viruses (Rabies, Vesicular Stomatitis Virus).
- Analysis of proposed pathways for viral entry into the CNS, including retrograde transport and blood-brain barrier disruption.
- Examination of cellular stress responses, stress granule formation, and reactive oxygen species (ROS) generation in neurons post-CHPV infection.
Main Results:
- CHPV may enter the CNS via retrograde transport from peripheral or olfactory neurons, similar to related rhabdoviruses.
- Disruption of the blood-brain barrier is also implicated as a potential entry route.
- CHPV infection induces cellular stress, leading to the formation of stress granules and the generation of ROS.
- Stress granules are linked to viral replication and ROS production, which collectively contribute to neurodegeneration.
Conclusions:
- CHPV infection triggers cellular stress responses and ROS production within neurons.
- These phenomena, including stress granule formation, play a cohesive role in CHPV-induced neuropathogenesis and neurodegeneration.
- Understanding these mechanisms is crucial for developing targeted therapies against CHPV encephalitis.
Abstract:
Chandipura virus (CHPV) has been contributing to the rising number of premature deaths due to acute encephalitis syndrome for over a decade in India. CHPV belongs to the family Rhabdoviridae. Neuropathogenesis of CHPV has been well established but the exact route of entry into the central nervous system (CNS) and the triggering factor for neuronal death are still unknown. Rabies virus and vesicular stomatitis virus, which are related closely to CHPV, enter the CNS retrogradely from peripheral or olfactory neurons. Disruption of the blood-brain barrier has also been connoted in the entry of CHPV into the CNS. CHPV upon entering the neurons triggers cellular stress factors and release of reactive oxygen species (ROS). The stress granules produced in response to cellular stress have been implicated in viral replication and ROS generation, which stimulates neuronal death. Both these phenomena cohesively explain the neuropathogenesis and neurodegeneration following CHPV infection.
