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Chandipura virus (CHPV), initially thought to be an orphan virus, was later reported to cause sporadic cases of fever with arthralgia,1 Reye's syndrome,2 and epidemic coma. Epidemic coma was reported as epidemic brain attack of childhood (EBAC) (supported by clinical features, normal CSF in all cases, neuroimaging, and response to treatment)3,4,5 or Chandipura encephalitis (supported by virus isolation, identification by electron microscopy, immunofluorescence, and PCR).6,7,8,9
CHPV is ubiquitous in the Indian sub‐continent (at least since 1955),1 Srilanka,10 and Africa (Nigeria, Senegal).11,12 Human cases have only been reported from India. CHPV can infect many other mammalian species. The high prevalence of specific antibodies and viral RNA in the population of India combine to obscure any potential role of this virus in paediatric illnesses, and the matter remains unresolved.13 Chandipura virus has been employed for several years in academic virology laboratories as a substitute for the animal pathogen, vesicular stomatitis virus, in research on interferon, for assay of retroviruses by pseudotype formation, and as a vehicle for antigen presentation. There have been no adverse consequences.14,15
Isolation and detection of CHPV, serological status, and presence of viral antigen in brain biopsy by immunofluorescence assay, while providing reasonable evidence of an association between CHPV and the outbreak,16 fulfil neither the Bradford Hill criteria nor modified Koch's postulates.3,17 Since there is histopathological evidence of an inflammatory reaction in the brains of mice,16 but not in humans, it could be a passenger virus, a concomitant virus, or a pathogenic virus in humans.3
In an outbreak of EBAC, clinicians critically argued against the diagnosis of encephalitis and a pathogenic role of CHPV since the linkage between CHPV and EBAC was not proved.3,5,17 In subsequent papers,6,9,18,19 virologists avoided arguing against the ischaemia hypothesis or defending the diagnosis of encephalitis or the aetiological role of CHPV by ignoring that report, and did not even reference the articles.3,4,5,17,21
Evidence of atypical measles encephalitis in an identical epidemic by the same authors20 was subsequently believed to be a laboratory contamination with measles vaccine virus.21 Evidence from multiple studies from multiple laboratories is necessary before accepting CHPV as a human pathogen (as has been done for SARS).
Evidence of the presence of the virus, its genome, or antigen or antigen–antibody complex in the middle cerebral artery in at least some cases would confirm the aetiologic role of the CHPV in EBAC.
Competing interests: none declared