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Dr. L. Manuelidis finds "infectious" nanoparticles

Kathy

Well-known member
J Cell Biochem. 2006 Oct 16;
A 25 nm virion is the likely cause of transmissible spongiform encephalopathies.

Manuelidis L., Yale Medical School, New Haven, Connecticut 06510.

The transmissible spongiform encephalopathies (TSEs) such as endemic sheep scrapie, sporadic human Creutzfeldt-Jakob disease (CJD), and epidemic bovine spongiform encephalopathy (BSE) may all be caused by a unique class of "slow" viruses. This concept remains the most parsimonious explanation of the evidence to date, and correctly predicted the spread of the BSE agent to vastly divergent species. With the popularization of the prion (infectious protein) hypothesis, substantial data pointing to a TSE virus have been largely ignored. Yet no form of prion protein (PrP) fulfills Koch's postulates for infection. Pathologic PrP is not proportional to, or necessary for infection, and recombinant and "amplified" prions have failed to produce significant infectivity. Moreover, the "wealth of data" claimed to support the existence of infectious PrP are increasingly contradicted by experimental observations, and cumbersome speculative notions, such as spontaneous PrP mutations and invisible strain-specific forms of "infectious PrP" are proposed to explain the incompatible data. The ability of many "slow" viruses to survive harsh environmental conditions and enzymatic assaults, their stealth invasion through protective host-immune defenses, and their ability to hide in the host and persist for many years, all fit nicely with the characteristics of TSE agents. Highly infectious preparations with negligible PrP contain nucleic acids of 1-5 kb, even after exhaustive nuclease digestion. Sedimentation as well as electron microscopic data also reveal spherical infectious particles of 25-35 nm in diameter. This particle size can accommodate a viral genome of 1-4 kb, sufficient to encode a protective nucleocapsid and/or an enzyme required for its replication. Host PrP acts as a cellular facilitator for infectious particles, and ultimately accrues pathological amyloid features. A most significant advance has been the development of tissue culture models that support the replication of many different strains of agent and can produce high levels of infectivity. These models provide new ways to rapidly identify intrinsic viral and strain-specific molecules so important for diagnosis, prevention, and fundamental understanding. J. Cell. Biochem. (c) 2006 Wiley-Liss, Inc.

PMID: 17044041

Dr. Laura Manuelidis is still chasing the "slow-virus" hypothesis. Could she be right? Do I agree with her?

Well, I agree that the identified "spherical" "particles of 25-35 nm in diameter" may have something to do with the malformation of the prions, and the production of reactive oxygen species.

Do these tiny round nanoparticles contain a viral genome? O,r do they consist of highly reactive metals (proteon nucleating centers - PNCs), such as insoluble uranium oxide, plutonium oxide or alloys of various metal contaminates?

She and Dr. Vitaly Vodyanoy (of Auburne Uni. Alabama) should take a closer look at these little spheres.
 

rkaiser

Well-known member
R2 writes -
There are very reputable researchers who believe that TSEs will turn out to be caused by something like a slow virus.

You do understand that a slow virus contradicts everything that you have argued thus far, don't you?

The magical theory of misfolded prions tranmistting BSE to an unfortunate host by way of digestion, the way you have argued, could be blown away by these reputable researchers.
 

don

Well-known member
it's always seemed to me the difficulty of replicating bse by feeding prion contaminated matter raised big questions as to whether prions were a cause or a symptom. the concept of a virus being the causative agent makes more sense. prions are convenient because they can be found; if the virus is harder to detect (and is in fact the cause) this might be more difficult but perhaps some headway can be made. like most other problems the symptoms are easier to identify than the real cause. could be a big problem for people hanging their hats on prion identifying tests because now there could be much more work to do.
 

flounder

Well-known member
Kathy said:
J Cell Biochem. 2006 Oct 16;
A 25 nm virion is the likely cause of transmissible spongiform encephalopathies.

Manuelidis L., Yale Medical School, New Haven, Connecticut 06510.

The transmissible spongiform encephalopathies (TSEs) such as endemic sheep scrapie, sporadic human Creutzfeldt-Jakob disease (CJD), and epidemic bovine spongiform encephalopathy (BSE) may all be caused by a unique class of "slow" viruses. This concept remains the most parsimonious explanation of the evidence to date, and correctly predicted the spread of the BSE agent to vastly divergent species. With the popularization of the prion (infectious protein) hypothesis, substantial data pointing to a TSE virus have been largely ignored. Yet no form of prion protein (PrP) fulfills Koch's postulates for infection. Pathologic PrP is not proportional to, or necessary for infection, and recombinant and "amplified" prions have failed to produce significant infectivity. Moreover, the "wealth of data" claimed to support the existence of infectious PrP are increasingly contradicted by experimental observations, and cumbersome speculative notions, such as spontaneous PrP mutations and invisible strain-specific forms of "infectious PrP" are proposed to explain the incompatible data. The ability of many "slow" viruses to survive harsh environmental conditions and enzymatic assaults, their stealth invasion through protective host-immune defenses, and their ability to hide in the host and persist for many years, all fit nicely with the characteristics of TSE agents. Highly infectious preparations with negligible PrP contain nucleic acids of 1-5 kb, even after exhaustive nuclease digestion. Sedimentation as well as electron microscopic data also reveal spherical infectious particles of 25-35 nm in diameter. This particle size can accommodate a viral genome of 1-4 kb, sufficient to encode a protective nucleocapsid and/or an enzyme required for its replication. Host PrP acts as a cellular facilitator for infectious particles, and ultimately accrues pathological amyloid features. A most significant advance has been the development of tissue culture models that support the replication of many different strains of agent and can produce high levels of infectivity. These models provide new ways to rapidly identify intrinsic viral and strain-specific molecules so important for diagnosis, prevention, and fundamental understanding. J. Cell. Biochem. (c) 2006 Wiley-Liss, Inc.

PMID: 17044041

Dr. Laura Manuelidis is still chasing the "slow-virus" hypothesis. Could she be right? Do I agree with her?


Well, I agree that the identified "spherical" "particles of 25-35 nm in diameter" may have something to do with the malformation of the prions, and the production of reactive oxygen species.

Do these tiny round nanoparticles contain a viral genome? O,r do they consist of highly reactive metals (proteon nucleating centers - PNCs), such as insoluble uranium oxide, plutonium oxide or alloys of various metal contaminates?

She and Dr. Vitaly Vodyanoy (of Auburne Uni. Alabama) should take a closer look at these little spheres.



has nothing to do with metals and op's kathy, amplification and transmission, i.e. feed ban for one. transmission studies don't lie, just the politicians and the corporate junkies that feed off lobbyist and groups that push this junk science to offset real BSE safety protocols, like the feed ban, which has been proven to be effective, which has and still is breached in the USA as we speak in 2006, that had nothing to do with metals or op's. i too have never been a great fan of the prion only theory, thus, why i have most always referenced as a human and or animal TSE. one thing for sure that is disturbing are a few other studies by Manuelidis et al, of which this too has nothing to do with metals or op's, but everything to do with BSE, sCJD and other TSE, and the fact the true numbers of infected and dead are in fact underestimated, but rising. ...TSS




SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM
1997 TO 2006. SPORADIC CJD CASES TRIPLED, with phenotype
of 'UNKNOWN' strain growing. ...


http://www.cjdsurveillance.com/resources-casereport.html





Subject: Re: Hello Dr. Manuelidis Date: Fri, 22 Dec 2000 17:47:09 -0500
From: laura manuelidis Reply-To: [email protected] Organization:
Yale Medical School To: "Terry S. Singeltary Sr."

References: <[email protected]> <[email protected]>
<[email protected]> <[email protected]>
<[email protected]> <[email protected]>
<[email protected]>


Dear Terry,

One of our papers (in Alzheimer's Disease Related Disord. 3:100-109, 1989)
in text cites 6 of 46 (13%) of clinical AD as CJD. There may be a later
paper from another lab showing the same higher than expected incidence but I
can't put my hands on it right now. We also have a lot of papers from 1985
on stating that there are likely many silent (non-clinical) CJD infections,
i.e. much greater than the "tip of the iceberg" of long standing end-stage
cases with clinical symptoms. Hope this helps.

best wishes for the new year laura manuelidis

"Terry S. Singeltary Sr." wrote: Hello again Dr. Manuelidis, could you
please help me locate the 2 studies that were done on CJD where it showed
that up to 13% of the people diagnosed as having Alzheimer's actually had
CJD. trying to find reference... thank you, > Terry S. Singeltary Sr.


4.5 MILLION DEMENTED ALZHEIMER'S PATIENTS, HOW MANY ARE CJD/TSEs ???

HOW CAN ONE-IN-A-MILLION BE ACCURATE WHEN CJD IS NOT REPORTABLE,

AND WHEN THE ELDERLY DO NOT GET AUTOPSIED??????


Transmission of Creutzfeldt-Jakob Disease from Blood and Urine Into Mice

The Lancet, November 9, 1985

Sir,--Professor Manuelidis and his colleagues (Oct 19, p896) report
transmission to animals of Creutzfeldt-Jakob disease (CJD) from the
buffy coat from two patients. We also transmitted the disease from
whole blood samples of a patient (and of mice) infected with CJD.1
Brain, Cornea, and urine from this patient were also infectious, and
the clinicopathological findings2 are summarised as follows.

A 70-year-old man was noted to have a slowing of speech and writing
and some disorientation, all of which progressed rapidly. Decorticate
rigidity, forced grasping, positive snout reflex, and myoclonus
appeared within 2 months. Electroencephalogram revealed typical
periodic synchronous discharge, and he died of pneumonia and upper
gastrointestinal haemorrhage, about 3 months after onset of the
symptoms. The Brain weighed 1290g and showed severe histological
changes diagnostic of CJD, including spongiform change, loss of
nerve cells, and diffuse proliferation of astrocytes. There were no
inflammatory cells, microglia, neurofibrillary tangles, and
amyloid plaques, although virus-like particles were detected by
electron microscopy.

Results of innoculation in Mice

Inocula NO* Incubation period (days)+
Brain 7/10 (4) 789 (+ or - 112)
Cornea 1/6 (0) 1037
Blood 2/13 (0) 1080 (+ or - 69)
Urine 5/10 (1) 880 (+ or - 55)
CSF 0/10

* Number of mice with CJD change/number examined histologically.
Number with amyloid plaques shown in parentheses.

+ means + or - SD

Samples were taken aseptically at necropsy. 10% crude homogenates
of brain and cornea in saline, whole blood (after crushing a clot),
and untreated CSF and urine were innoculated intracerebrally into
CF1 strain mice (20 ul per animal). Some mice showed emaciation,
bradykinesia, rigidity of the body and tail, and sometimes tremor
after long incubation periods. Tissues obtained after the animal
died (or was killed) were studied histologically (table). Animals
infected by various inocula showed common pathological changes,
consisting of severe spongiform changes, glial proliferation, and
a moderate loss of nerve cells. A few mice inoculated with brain
tissue or urine had the same amyloid plaques found in patients and
animals with CJD.3

In our long-term experiments, inoculating materials taken from
twenty patients with CJD or Gerstmann-Straussler-Scheinker's
disease (GSS) into rodents, positive results were obtained in
seventeen cases, including this patient. Brain tissue transmitted
the disease most frequently within the shortes incubation period,
except for one case where the lymph node was the most infectious.
Transmission through the cornea has been noted in man4 and in
guineapigs.5 Whole blood samples taken from three patients were
inoculated and a positive transmission occured only in the case
recorded here. Mouse-to-mouse transmission through blood
inoculation was successful after a mean incubation period of 365
days.1 Transmission through urine was positive in this patient
only, and negative in one other patient and in many infected animals.
Transmission through the CSF from eight patients was negative, yet
transmission via the CSF of infected rats was positive.1

As viraemia has been proved in guineapigs,6 mice,1,7 and lately
in patients with CJD, blood for transfusion or blood products for
medical use must be tested for unconventional pathogens. For this
purpose, we inoculated blood products inot rodents.8 The CJD
pathogen was not found in the products examined. However, this
approach takes too long to be of practical value. More efficient
methods must be developed to detect pathogens and to eliminate
them from blood. One proposal9 is to apply membrane filtration to
the pruification protocol of human growth hormone suspected of
being contaminated with CJD. Similar methods are needed for blood
contamination.

Department of Neuropathology,
Neurological Institute,
Faculty of Medicine,
Kyushu University,
Fukuoka812, Japan

JUN TATEISHI

1. Tateishi J, Sato Y, Kaga M. Doi H, Ohta M. Experimental transmission
of human subacute spongiform encephalopathy to small
rodents 1: Clinical and histological observations.
Acta Neuropathol (Berl) 1980; 51: 127.

2. Shibayama Y, Sakaguchi Y, Nakata K, et al, Creutzfeldt-Jakob
disease with demonstration of virus-like particles.
Acta pathol Jpn 1982;32: 695.

3. Tateishi J, Nagara H, Hikita K, Sato Y. Amyloid plaques in the
brains of mice with Creutzfeldt-Jakob disease.
Ann Neurol 1984; 15: 278.

4. Duffy P, Wolf J, Colings G, DeVoe AG, Streeten B, Cowen D.
Possible person-to-person transmission of Creutzfeldt-Jakob disease.
N Engl J Med 1974; 290: 692.

5. Manuelidis EE, Angelo JN, Gorgacz EJ, Kim JH, Manuelidis L.
Experimental Creutzfeldt-Jakob disease transmitted via the eye
with infected cornea. N Engl J Med 1977; 296: 1334.

6. Manuelidis EE, Gorgacz EJ, Manuelidis L. Viremia in experimental
Creutzfeldt-Jakob disease. Science 1978: 200: 1069.

7. Kuroda Y, Gibbs CJ Jr, Amyx HL, Gajdusek DC.
Creutzfeldt-Jakob disease in mice. Persistent viremiam and
preferential replication of virus in low-density lymphocytes.
Infect Immun 1983; 41: 154.

8. Tateishi J, Tsuji S. Unconventional pathogens causing spongiform
encephalopathis absent in blood products. J Med Virol 1985; 15: 11.

9. Tateishi J, Kitamoto T, Hiratani H. Creutzfeldt-Jakob disease
pathogen in growth hormone preparations is eliminatable.
Lancet (in press).


========================================================



PLEASE note, no metals or OPs there either kathy. ops and metals theory for cause of TSEs just do not hold water, never has, no science to date or in the past has validated any substance to this theory. ...TSS
 

rkaiser

Well-known member
Amazing how you talk of Kathy jumping all over with her common metals theory yet you R2 want to jump ship and say that this new possible theory of a slow virus is what you have been talking about all along. :roll:

You have always followed the theory of misfolded prion transmission R2. And you have to admit that that theory is flawed. Squirm all you like but you are caught on this one.

As I have said before - why bother. The goal is common. To kind a solution to the BSE problem. Bashing the metal theory only proves your own tunnel vision. And now abandoning the misfolded prion theory shows your true colors even more.
 
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