Published Date: 2001-05-15 23:50:00
Subject: PRO/AH> CJD (new var.), second wave of cases possible - UK
Archive Number: 20010515.0948

CJD (NEW VAR.), SECOND WAVE OF CASES POSSIBLE - UK
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See Also

CJD or CJD (new var.), uncertain diagnosis - UK 20010502.0850
CJD (new var.), more clusters suspected - UK 20010514.0936
2000
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CJD (new var.), children - UK 20001016.1772
CJD (new var.), death of elderly man - UK 20001102.1912
CJD (new var.), onset, death data - UK 20000403.0492
CJD (new var.), revised mortality prediction - UK 20000811.1335
CJD (new var.), young adults - UK 20000330.0468
CJD (new var.) - UK: apparent rise in incidence 20000804.1302
CJD (new var.) - UK: under-reporting risk 20001208.2146
CJD (new var.): is rise in cases real? - UK 20000117.0062
1999
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CJD (new var.), case rate - UK 19990327.0482
CJD (new var.), case rate - UK (03) 19990907.1575
CJD (new var.), youngest human case - UK 19991124.2080
CJD (new var.) - UK: forecast 19990801.1314
CJD (new var.) transmission 19990220.0222
Date: Tue 15 May, 2001
From: ProMED-mail <promedm@promedmail.org>
Source: BBC News Online, Tue 15 May, 2001, 05:27 GMT 06:27 UK [edited
<http://news.bbc.co.uk/hi/english/sci/tech/newsid_1330000/1330251.stm>

Mouse Experiments Suggest Emergence of a Second Wave of vCJD Cases is Possible
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Scientists are warning that the predicted size of the variant
Creutzfeldt-Jakob disease (vCJD or CJD new var.) epidemic may have been
underestimated. Research in mice suggests that only people with the
shortest incubation periods for the disease are showing symptoms of vCJD,
the human form of BSE. If confirmed, the findings would mean that the
current cases are just the tip of the iceberg and that a "second wave" of
cases will emerge. Projections of the scale of the epidemic are based on
the theory that some people are unlikely to contract CJD from infected meat
because of their genetic make-up. This idea is now contradicted by research
reported in the scientific journal Proceedings of the National Academy of
Sciences of the USA
[vide; Identification of multiple quantitative trait loci linked to prion
disease incubation period in mice. Sarah E. Lloyd, Obia N. Onwuazor,
Jonathan A. Beck, Gary Mallinson, Martin Farrall, Paul Targonski, John
Collinge, and Elizabeth M. C. Fisher, PNAS, published 15 May 2001, 10.1073
<http://www.pnas.org/cgi/content/abstract/101130398v1> - Mod.CP
"Those patients that we have seen so far with vCJD may be those genetically
disposed to have the shortest incubation periods," said John Collinge,
Director of the Medical Research Council Prion Unit in London. Following
infection, there is a very long incubation period before symptoms of the
disease occur. According to the latest figures from the Department of
Health, 99 cases of vCJD have been recorded to date in humans. But it
remains unclear how many other people have been exposed to BSE and what
proportion of these will eventually develop the human form of the disease.
One clue is our genes. As with conditions like cancer and heart disease,
genetic factors are thought to be involved in determining an individual's
risk of developing CJD, after exposure to the infective agent. All patients
identified so far have a particular variation in their genetic make-up
(MM), shared by about 40% of white Britons. Two other [genotypes (VV and
MV) are seen. The current estimates assume that only people with the MM
genetic make-up will contract the disease if they come into contact with
the infective agent, for example by eating contaminated meat.
However, Professor Collinge, who led the team that carried out the new
research, warns that such predictions may be "overly optimistic." "This
study reminds us that we cannot be complacent about the potential risks to
public health posed by BSE," says Professor Collinge. "We cannot rule out
an epidemic that evolves over decades."
The new work confirms that in mice at least, a number of genes are involved
in susceptibility to prion diseases. And although it may take longer for
symptoms to appear in some animals because of their genetic make-up, that
does not mean they will not eventually succumb to the disease. As the mouse
and human genomes are so similar, corresponding genes are almost certain to
be found in humans.
[Byline: Helen Briggs
--
ProMED-mail
<promed@promedmail.org>
[The PNAS paper abstract states the following: "Polymorphisms in the prion
protein gene are known to affect prion disease incubation times and
susceptibility in humans and mice. However, studies with inbred lines of
mice show that large differences in incubation times occur even with the
same amino acid sequence of the prion protein, suggesting that other genes
may contribute to the observed variation. To identify these loci 1009
animals were analysed from an F2 intercross between 2 strains of mice,
CAST/Ei and NZW/OlaHSd, with significantly different incubation periods
when challenged with RML scrapie prions. Interval mapping identified 3
highly significantly linked regions on chromosomes 2, 11, and 12; composite
interval mapping suggests that each of these regions includes multiple
linked quantitative trait loci. Suggestive evidence for linkage was
obtained on chromosomes 6 and 7.
The sequence conservation between the mouse and human genome suggests that
identification of mouse prion susceptibility alleles may have direct
relevance to understanding human susceptibility to bovine spongiform
encephalopathy (BSE) infection, as well as identifying key factors in the
molecular pathways of prion pathogenesis. However, the demonstration of
other major genetic effects on incubation period suggests the need for
extreme caution in interpreting estimates of vCJD epidemic size utilizing
existing epidemiological models." - Mod.CP
..................cp/pg/es
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