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Chandipura virus – what we know & do not know

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  • Chandipura virus – what we know & do not know

    This is well worth reading in full;
    In essence Dr. John questions whether Chandipura virus is involved in encephalitis cases or if some other causative agent is responsible.

    Chandipura virus – what we know & do not know
    T. Jacob John
    Indian J Med Res 132, August 2010, pp 125-127


    The Chandipura virus was discovered in 1966 by Bhatt and Rodrigues, scientists of the Virus Research Centre (VRC) established by the Rockefeller Foundation in 1952 in Poona (now Pune)1. They were investigating persons with fever in Chandipura in northern Maharashtra, near Nagpur, for dengue or chikungunya virus aetiology1. The virus thus detected was hitherto unknown, and Bhatt and Rodrigues named it Chandipura after the geographic location of its discovery1.


    In 1983, Rodrigues
    et al2 reported the isolation of Chandipura virus from the blood of an 11 yr old child who died with acute encephalopathy syndrome. In 1988, a 35 yr old man had uneventful mediastinal surgery in our hospital in Vellore for a benign lesion; a week later he developed fever and intense headache and neck-stiffness; cerebrospinal fluid (CSF) examination showed lymphocytosis. The diagnosis was aseptic meningitis. In CSF we found a rapidly growing cytopathogenic virus in Vero cell culture (unpublished). The virus was enveloped – knowas shown by loss of infectivity when treated with a lipid solvent; thus it was not an enterovirus, the most common cause of viral meningitis. Unable to identify it, we sent it to Centers for Disease Control (CDC) in the USA. Scientists in CDC were baffled at first as electron microscopy showed what looked like rabies virus. The patient had fully recovered in a week; his second CSF sample had no virus but had virus-neutralizing antibody. With this information, CDC scientists explored further and classified it as a member of Rhabdoviridae family and finally identified it as Chandipura virus (Pallansch M, personal communication). We surmised that the patient got infected while in the hospital, most probably by mosquito-bite, most likely Aedes aegypti. NIV scientists had earlier proved the vectorial capacity of mosquitoes to transmit Chandipura virus3.


    Until the NIV reports on Chandipura virus causing ‘encephalitis’ epidemics with high case fatality, it was believed to be an inconsequential agent causing at best no illness or at worst short-lived febrile illness, with very rare instances of viral meningitis and possibly acute encephalopathy. Some experts have raised doubts about the validity of evidences for Chandipura virus aetiology of epidemic encephalopathy17-21. An arbovirus expert in CDC has stated: “Chandipura virus, an infrequently recognized rhabdovirus, was attributed to large outbreaks of viral encephalitis; however, compelling
    evidence suggests that the relationship of illness and
    the virus are questionable”17

    Yet another study of acute encephalitis in Andhra Pradesh has provided intriguing results20. In a hospital in Hyderabad all cases of encephalitis in children from May 2005 to April 2006 were prospectively investigated20. Of the 90 cases, 25 yielded evidence of Chandipura virus infection by PCR, IgM antibody or seroconversion; however, no virus could be isolated20. Among contacts of cases who were <15 yr of age, 71-73 per cent and among those who were >15 yr, 94-97 per cent had antibody evidence of past Chandipura virus infection20. Thus Chandipura virus infection seems to nearly saturate the population by about 15 yr of age. Yet, reported outbreaks of acute brain disease supposedly caused by it have been inexplicably very few. However, basic studies on Chandipura virus must continue and as much details of its biology learned since it is a common agent of infection in a variety of species of hosts in India. Moreover, it is a vesiculovirus and much can be learned about the host-virus interactions of the genus, to which belongs rabies virus also.

    Earlier anepidemic acute encephalopathy syndrome was reported in Haryana, with measles virus directly isolated from the CSF of several children22. Could very similar, if not identical, clinical disease affecting the brain and causing high case-fatality be caused by two very common viruses, measles and Chandipura?


    In short, it is possible that the true aetiology was neither measles nor Chandipura virus in these outbreaks. Investigations to discover the true aetiology in future outbreaks should not be confined to confirming or excluding infection with Chandipura and measles virus. The temptation to quickly seek to identify the causative agent in outbreaks of unknown diagnosis/aetiology has misled many in the past. Instead every such outbreak should be thoroughly investigated using tools of epidemiology first, or at least in parallel with, investigating for aetiology. Often detailed epidemiology will lead to the correct aetiology.
    Twitter: @RonanKelly13
    The views expressed are mine alone and do not represent the views of my employer or any other person or organization.

  • #2
    Re: Chandipura virus – what we know &amp; do not know


    Acta Tropica
    Volume 124, Issue 1, October 2012, Pages 1–14

    Chandipura Virus: An emerging tropical pathogen
    Sunil Menghania, 1, , Rupesh Chikhalea, , , Ami Ravalb, , , Pankaj Wadibhasmea, 2, , Pramod Khedekara, 3,
    a University Department of Pharmaceutical Sciences, Mahatma Jyotiba Fuley Shaikshanik Parisar, Rashtrasant Tukadoji Maharaj Nagpur University, Amravati Road, Nagpur 440033, Maharashtra, India
    b Cerebral Vascular Disease Research Laboratories, Department of Neurology, Leonard M. Miller School of Medicine, University of Miami, Miami, FL 33136, USA, How to Cite or Link Using DOI

    Chandipura Virus (CHPV), a member of Rhabdoviridae, is responsible for an explosive outbreak in rural areas of India. It affects mostly children and is characterized by influenza-like illness and neurologic dysfunctions. It is transmitted by vectors such as mosquitoes, ticks and sand flies. An effective real-time one step reverse-transcriptase PCR assay method is adopted for diagnosis of this virus. CHPV has a negative sense RNA genome encoding five different proteins (N, P, M, G, and L). P protein plays a vital role in the virus's life cycle, while M protein is lethal in nature. There is no specific treatment available to date, symptomatic treatment involves use of mannitol to reduce brain edema. A Vero cell based vaccine candidate against CHPV was evaluated efficiently as a preventive agent against it. Prevention is the best method to suppress CHPV infection. Containment of disease transmitting vectors, maintaining good nutrition, health, hygiene and awareness in rural areas will help in curbing the menace of CHPV. Thus, to control virus transmission some immense preventive measures need to be attempted until a good anti-CHPV agent is developed.
    Twitter: @RonanKelly13
    The views expressed are mine alone and do not represent the views of my employer or any other person or organization.