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AFTER THE BSE INQUIRY
Dr Harash Narang's Comments
Following the publication in October 2000 of the UK Government's Inquiry into BSE and CJD Dr Harash Narang, previously employed at the Government's Public Health Laboratory Service as a virologist send us these comments:
I gave written and oral evidence to THE BSE INQUIRY: Summary
Dr Harash K Narang. (Tel 0191 281 6622)
Some of the points contained in my 1990 memorandum to the House of Commons were as follows: -
1. BSE in cattle appeared due to the addition of cattle remains to cattle feed containing the scrapie agent from both sheep and cattle (cannibalism).
2. BSE is different to the scrapie agent in that the incubation period in mice is consistently shorter (approximately half)
3. There is a simple test for BSE
4. Affected ewes mated with affected rams, produce offspring, which nearly always become affected. If this were true of cattle, by keeping calves from sick animals, UK would never be free from BSE.
5. There was an urgent need to use the diagnostic test I had developed
6. A study was needed to examine human brains from all suspect cases along with other neurological diseases using the sensitive test I had developed.
7. There were grounds for postulating that humans might possibly acquire SE through ingestion of contaminated tissue. It would be unwise to add potentially contaminated foods into the human food chain.
At the start of the BSE epidemic the following main issues needed to be answered.
1. The nature of the agent.
2. Origin of BSE
3. Origin and Classification of CJD cases
4. Eradication of BSE
5. Vertical transmission of BSE
6. BSE in other animals.
Those scientists who gave evidence to the BSE inquiry, none of them could give a definite answer to any of the above question. Does MAFF know the answer to these questions, obviously, not.
Here are the answers: I would like to emphasise many scientists who gave evidence, although it may appear that they were giving facts, it was only their opinion. Prusiner acting as a magician has engraved the prion hypothesis in people's
minds, like the Hans Christian Anderson story, The Emperors New Clothes. Prusiner has now admitted three of my main findings:
1. That "X" protein other than prion is required for modification. I published this work in 1992 in Research in Virology. Vol.143 Page, 381-386)
2. Sheep contains two types of prions, scrapie and BSE prion (Prusiner, year 2000). (Narang HK. Origin and Implications of Bovine Spongiform Encephalopathy. Proc Soc Exp Biol Med 211:306-322, 1996).
3. When both prions are present, scrapie prion is dominant and prevents BSE prion from infecting humans and cattle (Prusiner, year 2000). Narang Research in Virology. Vol.144 Page, 375-387, 1993; Narang HK. The Link. Creutzfeldt-Jakob disease: Bovine spongiform encephalopathy. Scrapie. From Sheep to Cow to Man. HH Publisher, Newcastle UK 1997.
The nature of the agent
I have published a large number of papers supporting the hypothesis that the BSE/CJD agent is a virus. The sequence of single stranded DNA (ssDNA) has revealed a simple multi-palindromic repeat uniform symmetrical sequence. Furthermore, has a self-priming property for self-repair and replication of the ssDNA.
I transmitted the disease using isolated single ssDNA - and demonstrated Kock's postulate - that a ssDNA genome is the viral genome which is the agent that causes BSE and CJD (Narang, Res Virol 149:375-382, 1998).
My research has confirmed that the infective agent is a virus and function is controlled by ssDNA.
Origin of BSE
In my evidence to the BSE Inquiry, Based on clinical signs, I had given account of the existence of two main strains of scrapie known since 1961.
Type I Scrapie: This type causes sheep to lose their wool and is the common type.
Type II Scrapie: The rarer form of scrapie. It shows up in sheep as trembling ataxia. Clinically it is the same in its major symptoms as BSE and a typical CJD cases.
Prusiner now also believes as he told a scientific meeting in Birmingham, in June 2000 that his colleague Mike Scott now believes that sheep carry two strains of the agent, the scrapie prion and the BSE prion while MAFF have not got a clue where BSE came from.
This brings Prusiner's group closer to Narang's research findings that the agent is a virus.
Origin and Classification of CJD cases
After 15 years of research and spending millions of pounds, so far MAFF and other government funded scientists are unable to give a definite answer to the origin of BSE.
As to the answer to the origin of CJD, it would be a guesswork. However, in my evidence to the BSE Inquiry I made it clear, all CJD cases are caused my infection.
Based on clinical signs, like scrapie there are two types of CJD.
Type I has been described as classic sporadic CJD and is caused by accidental inoculation with type one scrapie. Not all humans will develop CJD and can be distinguished by three main features from Type II:
a) The classical CJD starts with dementia.
b) Confluent spongiform changes are very unusual in the cerebellum in classic CJD.
c) PrP plaques are rarely observed in classic CJD.
Type II CJD has been termed "new variant" (nvCJD) and is caused by eating the BSE strain of the agent. I have to stress here that this is not new strain, it originated from the Type II scrapie sheep with trembling and ataxia. Therefore the name "new variant" CJD is misleading.
Three main points distinguishing them:
a) Starts with leading clinical features, such as difficulty in balancing and ataxia.
b) Confluent spongiform changes are seen in the cerebellum
c) The other main distinguishing feature of "nvCJD" is the distribution of PrP plaques, which are unique, and different from those traditionally observed in classic CJD.
Since the first appearance of BSE, CJD has been identified in young patients however, based on three main distinguishing features described above and review of literature has revealed that patients of all age groups have died of CJD but not recorded having died after being infected with the BSE agent.
Increase in the number of CJD cases
Report in The Lancet (Vol. 356, p481) shows 15 deaths a four-fold increase in this year compared with 18 for the whole of 1998. BSE is a notifiable disease while CJD is not. Comparative deaths due to CJD in the Years:
| 1970 | 1971 | 1972 | 1973 | 1974 | 1975 | 1976 | 1977 | 1978 | 1979 |
| 11 | 13 | 9 | 16 | 18 | 9 | 16 | 20 | 21 | 18 |
| 1990 | 1991 | 1992 | 1993 | 1994 | 1995 | 1996 | 1997 | 1998 | 1999 |
| 33 | 36 | 51 | 46 | 59 | 47 | 60 | 80 | 88 | 83 |
I should point out here that no all cases of CJD are referred to the CJD Surveillance Unit. Further more post-mortem is not done on all suspect cases of CJD.
Vertical transmission of BSE
MAFF now admit that even after taking ultra-precautions the had a case of BSE. However, up to June 1999, there are 39,384 BSE cases confirmed in cattle born after the feed ban.
Eradication of BSE
There are two ways to eradicate BSE
1 Test animals
2 Vaccine against BSE
Tests
There are three methods to confirm that animal or human is suffering with TSE.
1. To find spongiform changes in the brain: Brain tissue is required.
2. Demonstrate presences of PrP: Can be applied on brain or body fluids
3. Demonstrate presence of SAF/Nemavirus: Can be applied on brain or body fluids
Since it has been know that BSE is passed down by vertical transmission, for breeding it is important not to use cattle those incubating the disease, therefore we need a test which can be used on live animals.
Before BSE was identified, a simple grid-touch negative-staining method. Full details of the work were published in 1987 (Narang, Asher and Gajdusek: Proc Natl. Acad. Sci. USA-8 4:7730-7734, 1987). Subsequently many more papers were published describing in detail the simple technique using CJD human brains. I was invited to AFRC and MRC NeuropathogenesisUnit, Edinburgh in September 1987 to demonstrate the test. Preparation and examination was carried out on six randomised scrapie and normal brains and correct results were recorded on all six brains within two and a half hours from start to finish. MAFF were aware of this test because I presented the test to the 74th Meeting of the British Neuropathological Society on the14th and 15th January 1988.
On many occasions in 1988 and subsequently I proposed at least random postmortem testing of cattle but random BSE testing was then judged to be of low priority because MAFF considered that a visual examination of animals, noting the overt symptoms of clinical cases before slaughter, was adequate.
If random testing had been started when I suggested it we would have been able to discover the true extent of the disease and it could have been eradicated. In a study undertaken for "World in Action" in 1995 obtained 30 cattle heads from abattoirs in the Midlands. I tested 28 brains and established that 8 of the cattle tested which must have appeared healthy at slaughter, actually had BSE. This BSE would be detected by my test even though they were sub-clinical, symptom free cases. To date, MAFF has no such test of its own.
Urine Test
Mice inoculation studies have revealed that CJD blood has 1,000 units of infectivity per ml. I have used this CJD urine test on a number of live subjects who have subsequently died and were confirmed to have had CJD by the Surveillance Unit in Edinburgh.
Shortly after I was asked by the parents of victim 12 to carry out a urine test Dr Duke of MRC contacted the victim's relatives in October 1995. Dr Duke told the relatives that the test had not been approved and suggested to the relatives that they could take a legal action against me. They did not agree with this suggestion and I duly carried out the test.
I used the urine test on Peter Hall. His parents approached me after doctors had told them repeatedly that he was too young to be suffering from CJD and that his symptoms were not those of CJD. In January 1996 the urine test confirmed that he had CJD. Following this his mother insisted upon the post mortem, which her doctors were advising was not necessary because they were unlikely to learn anything. Five weeks after Peter's death the post mortem confirmed CJD. In the light of this experience it must be expected that other young individuals who have died of CJD have not been subject to a post mortem and are therefore not included in the definite statistics.
Western Blotting
I have developed an alternative method to electron microscopy, western blotting to detect PrP in human CJD urine. The science involved in this technique is well understood. This method is more user friendly and is also cheaper. Hundreds of specimens can be tested within one working day and this process would be very useful for the purpose of testing blood donors. Since March 1997 I have been funded by MRC to carry out work using EM techniques. Initially they told me at a meeting with MAFF that they would also purchase western blotting equipment to develop the urine test.
However, they are now very reluctant to allow me to develop western blotting at the same time and I never got the go ahead with the test.
Vaccine against BSE
In evidence to the BSE inquiry I said: There are some 20 different strains of the scrapie agents. Infection with one strain blocks the others (Ref 24: Narang, Res.Virol.1993,144:375-387) and comparative experiments show a promise of vaccine. I approached MAFF on a number of occasions, to produce and test vaccine against BSE: and as usual there was no response.
Now Prusiner has also openly admitted the phenomena of interference between the two strains of the agent. He believes that the scrapie strain is somewhat dominant, preventing the BSE strain from infecting cattle and people when both are present. In other words the scrapie strain acts as a vaccine against the BSE strain.
The type I strain of scrapie acts as vaccine against BSE, many people have eaten this strain unknown to themselves and therefore will have a natural protection. This is the point Prusiner is making at the meeting.
It is the effect of vaccine that prevents humans being infected with the BSE strain of the agent and not genetic variation as many scientists have been suggesting.
This suggests that the BSE agent could not be a protein after all. It must be a virus.
BSE in other animals.
To the BSE Inquiry gave I evidence of BSE in sheep and chickens. MAFF denied it, now as it has been made out "new research" admits yes BSE has crossed many animals species.
Now Mr Nick Brown has announced a 3-year study to examine a possible link between milk and CJD. What has he got in mind? - just read page 38 of my Book "The Link".
Blood Donors
Similarly, I had been warning about the use of blood and blood products in blood transfusions, which might produce a devastating effect (as in the case of growth hormone treatment) in the next few years. Finally, therefore, I would like to utilise this inquiry for the purpose of a plea that all future blood donors should be tested utilising my urine test to prevent further transmission from blood products.
By Dr Harash Narang (Oct. 2000)
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