'Fear of the Invisible'


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Home Why Poisoned Cells make Viruses
Poisoned cells make Viruses PDF Print E-mail
Written by Janine Roberts   
Friday, 22 August 2008 23:05

from the final chapter of Fear of the invisible..


The Nature of Viruses


There are some basic facts about viruses all biologists agree on.

Viruses have no metabolism so they cannot produce energy or eat. They have no nervous system, no sensory system, no intelligence that can facilitate any kind of invasion or hi-jacking of a cell a billion times larger.

But, the conventional theory of viral hijacking is that, after the short genetic code of a virus has been absorbed by a cell, the ‘viral genes' absorbed start to ‘direct the production of proteins by the host cellular machinery.' It is assumed they are able to force the host cell to do this, It is said they force the cell to assemble proteins into a shell or ‘capsid,' to insert into this a clone of the original viral genetic code and then to launch it out of the cell by using the same machinery that the cell uses to harmlessly produce its own exosomes and other extra-cellular particles or vesicles.

But I had to ask, would cells give such minute and ‘dead' messenger vesicle the extraordinary ability to pirate vastly larger and intelligent cells - including cells of the same organism?  This is the quandary we are left with if we agree that viruses are not alive and thus incapable of having a survival instinct.

But what if cells create viruses as weapons - against other cells?  If they do, then this would be remarkably suicidal as viruses usually pass from cell to cell within the same organism.

Such thoughts have left me deeply puzzled about the many pathogenic viruses reported to exist. I have severe doubts about some of these, particularly the poliovirus and HIV. I would have to look again at the evidence on other viruses.




Viruses are commonly blamed for illnesses that seem easily passed from one person to another. Bacteria may cause many of these  - but viruses are often blamed.  Our only medical weapons against them are said to be vaccination and powerful chemotherapy-type antiviral medicines designed to stop the cell from making viruses, rather than to attack the virus itself, for apparently it has proved too elusive a target.

But, why do cells make pathogenic viruses? Surely the reason for this has been established in numerous laboratory experiments? It is a doctrine in virology that cells make malignant viruses only after a disease virus arrives and infects them.

I had long presumed this must be so, but when I tried to analyse it, I had problems.  I found myself asking, since a virus cannot make a virus, surely the first viruses to cause an illness must have been made by an uninfected cell? 

I had earlier learnt how viruses did their damage. I had been told that they burst forth from infected cells, ‘exploding' them. I was now surprised to discover that this is not so; that viruses are far too small, at one-billionth of the mass of a cell, to have this effect. 

Current courses on Medical Microbiology now teach, as mentioned briefly above,  that viruses kill or damage cells indirectly, by triggering cellular processes that do this damage. Professor Tritz blames allergic reactions.  ‘With animal viruses, cell lyses [death] is usually the result of one of four types of allergic reactions' and  ‘allergy to viruses usually results in a very localized anaphylactic reaction.' Alternatively, he suggests that the immune system sees the virus-producing cell as foreign and kills it. 

He also suggests that some illnesses are due to ‘toxic substances' produced by cells because they are infected. ‘Virus-infected cells, at times, will produce compounds coded for by the host DNA, but which are not normally produced by the host. These are often cytotoxic at relatively high concentrations.'  Finally, some viruses might cause ‘structural alterations in the host cell', affecting the chromosomes, moving the nucleus or creating bubble-like spaces, but so far I have been unable to locate experiments that prove viruses operating in isolation can cause such effects.

Another university course teaches, ‘virus infected cells may be recognized by the immune system, which leads to the destruction of the virus infected cells.'

From what they say, cell deaths are not directly due to viral infection. This perhaps makes sense. The virus is so minute compared to the cell - and our protective systems will destroy a very sick cell that does not self-destruct. Our cells often seem altruistically to decide to die when not needed, poisoned or otherwise diseased.

But on reflection, how can we prove cell's illness is caused by the small viral genetic code it's absorbed?  How can we be sure that a damaged cell is so solely because it is infected?  It may be naturally dying or poisoned.  It may even produce viral-like particles for waste disposal, or to attempt a cure or help protect other cells.

Also, if cell deaths in viral illnesses are mostly caused by our immune system, why do we have such deaths when the immune system is down, as surely it often is in such circumstances?

But nevertheless, viruses are encoded information, and since cells can make errors, I must conclude that they may sometimes wrongly encode the viruses they send out.  These in theory could misinform other cells, perhaps sometimes encouraging them to take courses of action that they would not take otherwise.  But as to how often the codes thus transported could lead to such effects, I had no idea.

I went to consult a standard textbook, ‘Introduction to Modern Virology' by N. Dimmock and S. Primrose, published by Blackwell Scientific Publications.

On page 230 I found it surprisingly reported that, although people have presumed that flu is spread by coughing, ‘transmission experiments from people infected with a rhinovirus to susceptibles sitting opposite at a table proved singularly unsuccessful. Equally unsuccessful was the transmission of influenza from a naturally infected husband/wife to his/her spouse.'

Also on the same page it reported:  ‘it has been shown that recently bereaved people are susceptible to infectious diseases. Thus one's resistance is influenced by one's state of mind.' It then went on to discuss winter life styles; such as living crowded in unventilated and over-heated rooms, all things it says might make us produce the symptoms of illness - and all things that make cells ill without any need of help from viruses.
It then concluded on page 212: ‘Evidently viruses do not kill cells by any one simple process and we are far from understanding the complex mechanisms involved ...[it] seem more akin to death by slow starvation than acute poisoning. Lastly it is by no means clear what advantage accrues to the virus in killing its host cell. This situation may represent a poorly evolved virus-cell relationship or virus in the ‘wrong' host cell.'

It thus seems that cells may be sick, poisoned, stressed or malnourished in some way before they show the symptoms of ‘viral infection.' There is a considerable body of research that indicates cellular illness or malnourishment often precedes the production of viruses, rather than the converse. For example:  it is reported that deficiency in selenium, a metal our cells use as an antioxidant, can precede the symptoms of colds, flu and even AIDS. (There is also a strong co-relation between selenium levels in soils in African countries and the prevalence of AIDS symptoms. )

Dr Melinda Beck reported that selenium-deficient mouse cells show symptoms of illness and emit viruses.  She and her co-authors deduced from this that a lack of selenium made viruses dangerous - and consequently that these viruses made the cells ill. But was this deduction soundly based?   Selenium is a component of glutathione peroxidase (GPX), an enzyme that protects cells from oxidative stress. Selenium-deficiency thus makes cells ill with oxidative stress without any need for a viral illness.  They consequently could produce viral-like particles as waste or for repair purposes.

Another research paper reported that, when cells are suffering from ‘oxidative DNA damage' (such as from chemotherapy), then they are more likely to get hepatitis due to HCV viral infections. Again, what comes first?  The authors presume the virus must cause the illness - but surely the illness started with the earlier oxidative stress.

The first observation of retroviruses is credited to Peyton Rous. ‘It is generally accepted that Peyton Rous discovered retroviruses in 1911 when he induced malignancy in chickens by injections of cell-free filtrates obtained from a muscle tumour.' But, when I went back to his records, I found that he also suggested that the cause of his chickens' illness might be a chemical toxin in his filtrate! If retroviruses were indeed also present, might they have appeared as a defence against this toxin?

In earlier chapters we found that toxins, rather than viruses, are likely to be the primary causes of polio and AIDS - but what then about measles, mumps, flu and colds? 

I had long presumed the evidence for these illnesses being due solely to viral infection must be overwhelming - but I have found to my surprise that scientists have long known that the guaranteed way to make cells produce viruses in the laboratory, including flu and measles virus, is not primarily by getting them infected, but by exposing them to stress and toxins!

In 1928 the President of the Royal Society of Medicine's Pathology Section, A. E. Boycott, in a report on the ‘nature of filterable viruses,' stated that with toxins ‘we can with a considerable degree of certainty stimulate normal tissues to produce viruses.'

Then in 1963 the famous Sloan-Kettering Institute for Cancer Research reported that viruses multiplied after cells were exposed to ‘x-ray, ultraviolet light or certain mutagenic chemicals' and that this exposure seemed to ‘alter the benign relationship' that otherwise existed between cells and bacteria.

Then in the 1980s Robert Gallo reported that, when he added certain chemicals to cell cultures, these cells produced retroviruses. Gallo thus named these chemicals his viral ‘growth factor' - and Montagnier at the Institut Pasteur used the same. If retroviruses were indeed thus produced, then surely this can be explained as a cellular response to stress from toxins?

In 2007 Dr Dominic Dwyer, a Senior Medical Virologist, formerly of the Institut Pasteur in Paris, testified that to persuade blood cells to produced HIV retroviruses, ‘we stimulate them with compounds such as PHA.'   He added; if we want to persuade cells to produce the flu virus ‘we use other things like tryspin.' - thus that they expose cells to different chemicals to make them produce different viruses!  (Tryspin is destructive to proteins, and Phytohemagglutinin (PHA) is mitogenic. ) This surely suggests that virus production can be a cell's response to being stressed and poisoned  - and that there might thus be no need for it to be infected beforehand?

Dr David Gordon, the Chair of the Clinical Drug Trials Committee at Finders University in Australia, testified, at the 2007 Parenzee trial in Australia, that there is no need to ‘purify a virus in order to identify it'.  He repeated emphatically: ‘No need to purify' then rhetorically questioned: ‘Has any virus ever been purified?'  He explained: ‘The issues are exactly the same with any virus.' He doubted if any virus was ever isolated from sick cells.  It seemed that a cellular illness was all the proof he needed to conclude that unseen viruses were present - no matter how artificial the laboratory circumstances or what chemicals were added.


So - viruses may not be the primary causes of illnesses - they might instead be caused by a cell being poisoned. Why  do our cells make them?  Could they be possibly a protective reacition ?


more on this in the book

Medical Microbiology Fall 2000.  Tritz  Professor/Chairman Department Microbiology & Immunology http://www.kcom.edu/faculty/chamberlain/Website/Lects/MECHANIS.HTM


  Burcher, Sam.  Selenium conquers AIDSInstitute of Science in Society. http://www.i-sis.org.uk/AidsandSelenium.php

Melinda A. Beck Antioxidants and Viral Infections: Host Immune Response and Viral Pathogenicity. Departments of Pediatrics and Nutrition, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina. April 27 2000 or 1999 issue of the FASEB Journal, a scientific journal published by the Federation of American Societies for Experimental Biology.

  Fabio Farinati et al. Oxidative DNA damage in circulating leukocytes occurse as an early event in chronic HCV infection.  Free Radical Biology and Medicine, December 1999. Pages 1284-1291.

J. Exp. Med. vol. 13, no. 4, pp. 397-411 (April, 1911).


Boycott AE. The transition form life to death; the nature of filterable viruses. Proc. Royal Soc. Med. 1928;22:55-69.

Sloane-Kettering Institute for Cancer Research, Progress Report XV, Viruses and Cancer. January 1963

Nucleic Acids Res. 1977 August; 4(8): 2713-2723.

Nucleic Acids Res. 1977 August; 4(8): 2713-2723.