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Measles virus and Crohn’s disease
  1. M A AFZAL,
  2. P D MINOR
  1. Division of Virology
  2. National Institute for Biological Standards and Control
  3. South Mimms, Potters Bar
  4. Hertfordshire EN6 3QG, UK
  5. Gastrointestinal Unit
  6. Department of Medicine
  7. University of Edinburgh
  8. Western General Hospital
  9. Edinburgh, Scotland, UK
  1. Dr Afzal (email:mafzal{at}nibsc.ac.uk).
  1. E ARMITAGE,
  2. S GHOSH
  1. Division of Virology
  2. National Institute for Biological Standards and Control
  3. South Mimms, Potters Bar
  4. Hertfordshire EN6 3QG, UK
  5. Gastrointestinal Unit
  6. Department of Medicine
  7. University of Edinburgh
  8. Western General Hospital
  9. Edinburgh, Scotland, UK
  1. Dr Afzal (email:mafzal{at}nibsc.ac.uk).

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Editor,—We read with interest the view of Professor ter Meulen (Gut1998;43:733–4) regarding the possible association of measles virus and Crohn’s disease. We are in complete agreement with the author that current data available in the literature, mostly derived from serological, epidemiological and case control studies, are controversial and need to be investigated further. Professor ter Meulen proposes that the definitive answer to the problem of the involvement of measles virus in inflammatory bowel disease (IBD) would come from amplification of measles virus genome from IBD tissues by polymerase chain reaction (PCR) and then characterisation of the amplified DNA fragment by nucleotide sequencing. We would like to draw attention to published studies from several groups including ourselves and the IBD study group, who formulated the original measles hypothesis, which have tackled this issue using PCR but have not been mentioned by Professor ter Meulen in his article. These papers report highly sensitive measles specific RT-PCR systems that have been used to examine both colonic biopsy specimens (from both newly diagnosed and treated patients with Crohn’s disease) and resection specimens, and have targeted different regions of the measles virus gene using primers corresponding to the N, F and H gene regions.1-5 All have produced negative results.

Professor ter Meulen also suggests that lack of detection of measles virus in diseased tissues may be a result of low copy number of viral genes in infected cells. The sensitivity limits of the detection systems established by the groups mentioned earlier varied considerably. One group reported amplification of the target sequence from a single copy of the measles virus genome.5 We successfully amplified RNA templates extracted from virus particles corresponding to about 10−3 pfu (plaque forming units) and applied approaches which potentially improved the sensitivity of the detection system by examining the amplified DNA products by Southern blotting or digoxigenin antibody assay.2 Others also used different approaches to improve the assay sensitivity including enriching the measles virus RNA templates by oligonucleotide capturing from IBD specimens.3 In our laboratory we were able to amplify measles virus RNA from a nucleic acid mixture extracted from control tissues including material from SSPE brain, colonoscopic biopsy samples spiked with measles virus, and from virus infected tissue culture fluid.2

This evidence supports the view that measles virus does not persist in IBD tissues and therefore probably is not involved in the aetiology or pathogenesis of Crohn’s disease. In addition we suggest that lack of detection of measles virus sequence is not due to low copy numbers of viral genes but perhaps their complete absence.

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