Dr Harash
Narang and His Scientific Views Dr Harash
Narang and His Scientific Views
I joined the Medical Research Council as a research scientist after receiving
my PhD from Newcastle upon Tyne University in 1969. I have devoted over 30 years
of my professional career to the study of group of animal and human diseases
classified as Spongiform Encephalopathies ("SE's"). I was the only
SE expert working for the PHLS when I was made redundant.
I have been doing research on these diseases since 1970, when I first examined
a brain from a CJD victim. I have published many research papers in scientific
journals describing the origin, their transmission pathogenesis and also the
nature of the infective agent, which causes the disease and why does it take
so long to show up the clinical signs. To obtain copies of these publications,
please: Email Harash@cjdfoundation.com
My hypothesis is that the infective agent is a virus - not a protein - with a single stranded DNA (ssDNA). This is the basis and theme of all my present and past papers and is fundamentally different from the prion hypothesis (See details).
Hypotheses are being misquoted and stressed as facts. Since the public and the media have joined in the debate, the issue has become very complicated. Therefore it is important to distinguish between a hypothesis and a fact.
Like all other common infections, over twenty different strains of the scrapie agent has been identified from sheep. A search of the literature indicates two distinct clinical syndromes in sheep, both of which have been called scrapie.
I have designated these, Type I (the common type), which exhibit itchiness and lose their wool, and Type II, which exhibit trembling and ataxia.
Comparative studies have demonstrated that, no clinical disease has so far been shown to develop in cattle or mink by feeding them with Type I infected sheep brains. However, feeding with the Type II, 100% of calves and mink develop the clinical disease.
These clinical signs observed in Type II scrapie, trembling and ataxia, are
similar in BSE, recent cases of CJD, and Kuru. Sheep inoculated or fed with
brain tissues from BSE cows also develop trembling and ataxia. Brain pathology
of Type II scrapie, BSE, Kuru and recent CJD, show similar damage (see details).
This suggests that Type II is the cause of BSE, and recent CJD and Kuru.
Like scrapie in sheep, based on clinical symptoms, CJD cases can be divided
into two groups.
Group I include the classic sporadic CJD cases and is caused by accidental inoculation with Type 1 scrapie. The classical CJD in older patients starts with dementia.
BSE is an infectious disease and has been transmitted orally to many other animals
including humans. There is clear evidence of maternal transmission.
Why the disease has appeared in 1980’s
For a number of years, phenomenon of interference between the two strains of
the agent has been known. Based on this phenomenon I proposed that the Type
I strain of scrapie acts as vaccine against BSE, Type II scrapie. I believe
that the scrapie strain Type I was dominant before meat and bone meal was fed
to cows and this prevented the BSE strain from infecting cattle and people.
In other words the scrapie strain acts as a vaccine against the BSE strain.
Many people have eaten Type I strain unknown to them and therefore will have
a natural protection. Now Dr Stanley Prusiner has openly admitted the phenomena
of interference between the two strains of the agent. The phenomena of interference
will only be effective if the agent causing the disease to be a virus.
The details are described in History of Events 1977-2005 and other sections
will follow.
