Journal of Neuroinfectious Diseases
Open Access

Chandipura virus (CHPV) is an arthropod-borne virus belonging to the family Rhabdoviridae and genus Vesiculovirus. First isolated in 1965 from a patient in Chandipura village, Maharashtra, India, the virus has since been linked to sporadic outbreaks of acute encephalitis, particularly among children. While relatively lesser known compared to arboviruses like dengue or Zika, CHPV has attracted attention due to its rapid progression, high mortality rates, and potential for large outbreaks. Endemic mainly in India, the virus has also been detected in other regions of Asia and Africa, suggesting a broader geographical range [1,2].

Discussion

Chandipura virus is primarily transmitted through the bite of sandflies (Phlebotomus species), although mosquitoes and other insects may act as secondary vectors. The virus is maintained in a zoonotic cycle, with evidence of infection in cattle and other animals, but humans—especially children—are highly susceptible. Environmental factors such as heavy rainfall, deforestation, and poor sanitation favor vector breeding, increasing the risk of outbreaks in rural and peri-urban communities [3,4].

The clinical presentation of CHPV infection is striking for its rapid onset and severe outcomes. Infected individuals, particularly children under 15 years of age, develop acute febrile illness characterized by high fever, vomiting, convulsions, and altered consciousness. The disease often progresses quickly to encephalitis, with mortality rates reported as high as 50–75% in some outbreaks. Survivors may suffer from long-term neurological sequelae, including motor and cognitive impairments [5-8]. The short incubation period and aggressive course of the illness leave little time for effective intervention, making early recognition critical.

Epidemiologically, Chandipura virus has caused several outbreaks in India since the early 2000s, particularly in states such as Andhra Pradesh, Gujarat, and Maharashtra. These outbreaks often occur during the monsoon season, coinciding with peak sandfly activity. Hundreds of cases, mostly in children, have been reported, with high fatality rates. The burden of the disease is believed to be underreported due to limited diagnostic facilities and misclassification of cases as other encephalitic illnesses [9,10].

Conclusion

Chandipura virus is an emerging but neglected pathogen that poses a serious health threat in endemic regions, particularly to children. Its rapid progression to encephalitis and high mortality rates make it a formidable public health challenge. The lack of specific treatment and preventive vaccines underscores the importance of vector control, community awareness, and early case detection. As outbreaks continue to be reported in India and the possibility of wider spread exists, strengthening surveillance, investing in research, and developing effective interventions are essential. Addressing the threat of Chandipura virus not only protects vulnerable populations but also contributes to global preparedness against emerging infectious diseases.

References

1. Soria J, Metcalf T, Mori N, Newby RE, Montano SM, et al. (2019) Mortality in hospitalized patients with tuberculous meningitis. BMC Infect Dis 19: 1-7.

   Indexed at, Google Scholar, Cross Ref

2. Torok ME (2015) Tuberculosis meningitis: Advances in diagnosis and treatment. Br Med Bull 113: 117-131.

   Indexed at, Google Scholar, Cross Ref

3. Iype T, Pillai AK, Cherian A, Nujum ZT, Pushpa C, et al. (2014) Major outcomes of patients with tuberculous meningitis on directly observed thrice a week regime. Ann Indian Acad Neurol 17: 281-286.

   Indexed at, Google Scholar, Cross Ref

4. Sharma SR, Lynrah KG, Sharma N, Lyngdoh M (2013) Directly observed treatment, short course in tuberculous meningitis: Indian perspective. Ann Indian Acad Neurol 16: 82-84.

   Indexed at, Google Scholar, Cross Ref

5. Marais S, Pepper DJ, Schutz C, Wilkinson RJ, Meintjes G (2011) Presentation and outcome of tuberculous meningitis in a high HIV prevalence setting. PLoS One 6.

   Indexed at, Google Scholar, Cross Ref

6. Vincent A (2002) Unraveling the pathogenesis of myasthenia gravis. Nat Rev Immunol 2: 797-804.

   Indexed at, Google Scholar, Cross Ref

7. Gasperi C, Melms A, Schoser B, Zhang Y, Meltoranta J, et al. (2014) Anti-agrin autoantibodies in myasthenia gravis. Neurology 82: 1976-1983.

   Indexed at, Google Scholar, Cross Ref

8. Hong Y, Zisimopoulou P, Trakas N, Karagiorgou K, Stergiou C, et al. (2017) Multiple antibody detection in ‘seronegative’myasthenia gravis patients. Eur J Neurol 24: 844-850.

   Indexed at, Google Scholar, Cross Ref

9. Hewer R, Matthews I, Chen S, McGrath V, Evans M, et al. (2006) A sensitive non-isotopic assay for acetylcholine receptor autoantibodies. Clin Chim Acta 364: 159-166.

   Indexed at, Google Scholar, Cross Ref

10. Matthews I, Chen S, Hewer R, McGrath V, Furmaniak J, et al. (2004) Musclespecific receptor tyrosine kinase autoantibodies-a new immunoprecipitation assay. Clin Chim Acta 348: 95-99.

    Indexed at, Google Scholar, Cross Ref