The true nature of Viruses

18. The true nature of viruses

In many ways, we are still at the beginning of scientific research – for we still do not have a full understanding of even what is happening inside us. The more we know of this, the more we realise just how much more there is to understand. For example, most western biologists are still left bewildered by the success of ancient Eastern medical practices such as acupressure and acupuncture.
After several years investigating the work of the “virus-hunters” I have come to the conclusion that Western medicine is being handicapped by long entrenched paradigms – in particular by the focus on understanding disease rather than health, and by the concepts that viruses are fundamentally dangerous to our survival, that they are extremely “cunning foes” (despite being “dead”) and essentially invasive.
The particles we normally label as viruses are only seen as tiny grey dots dwarfed by cells, like ants next to buffalo, even in the most powerful of electron microscopes. To get such photographs, ultra-thin slices have to be made of filtered cell cultures, the content fixed, dehydrated, stained and embedded into plastic. The resulting particles could be anything – but we then try to select out those that resemble ones that in the cell cultures appear to multiply. These we call viruses.
Why these dots cannot be seen in regular microscopes is that they are shorter than light waves. We now know they seem to be everywhere. They range in size enormously. But, they were given their “disease-causing” role in biology before they were seen. It was even seen as their defining role. They were even given a symmetrical shape in advance of it being seen; by Crick and Wilson in 1956 on the theoretical basis that anything this small must be constructed simply.
It could be that there are larger viruses. Recently giant ‘mimiviruses’ have been reported with over 1,000 genes. However, I think the definition of them as viruses could be mistaken. I would argue that a virus is a messenger vesicle, and that these are clearly more like cells.
Virology has long defined viruses also as “dead,” on the basis that they cannot reproduce – and because they could be reduced into the forms of crystals and then reactivated.
In the decades preceding the invention of the electron microscope, biologists had theorised that there were tiny germs that could pass through filters, thinking of these as mini-bacteria. When the microscope found small dots that seemed able to enter and leave cells at will, and even to change the DNA of cells, it was immediately decided these were the enemy, the “filterable viruses” that had been long sought.
But new techniques such as NMR spectroscopy and especially X-ray crystallography are now starting to show us the minute world in which they exist as living, pulsating with energy, colour and movement – and, with this new vision, very different views of viruses are emerging. We have so focussed on seeming viruses as invaders, that we seem to have forgotten that cells create viruses. Thus, we should get a better understanding of them if we look to see why cells make them..
On my own journey into this science, I have found inspiration in the work of several great woman of biology who transformed our knowledge of cells. First among these is Dr Barbara McClintock who, after being practically ignored and belittled most of her life, was finally in her old age, was awarded a Nobel Prize in 1983for her discoveries in biology.
She achieved a totally different vision of the living cell from most of her peers. In her Nobel Lecture of 8th December 1983 she spoke of cells as making “wise decisions” and as highly sophisticated in their responses to the environment. “A genome may reorganize itself when faced with a difficulty for which it is unprepared.” “Cells are able to sense the presence in their nuclei of ruptured ends of chromosomes, and then to activate a mechanism that will bring together and then unite these ends, one with another. …[This] is a particularly revealing example of the sensitivity of cells to all that is going on within them. They make wise decisions and act upon them.”

McClintock continued: “Cells must be prepared to respond to many sources of stress. Mishaps that affect the operation of a cell must be occurring continuously. Sensing these and instigating repair systems are essential. … It is becoming increasingly apparent that we know little of the potentials of a genome. Nevertheless, much evidence tells us that it must be vast.”

As for the virologists that presume cell and viral genomes stay the same in their vaccine cultures: “The establishment of a successful tissue culture from animal cells, such as those of rat or mouse, is accompanied by readily observed genomic restructuring.”

She concluded: “In the future attention undoubtedly will be centered on the genome, and with greater appreciation of its significance as a highly sensitive organ of the cell, monitoring genomic activities and correcting common errors, sensing the unusual and unexpected events, and responding to them, often by restructuring the genome. We know about the components of genomes … [but] we know nothing, about how the cell senses danger and instigates responses to it that often are truly remarkable.”

This was very far from the mechanistic molecular studies that still dominate virology, in which the cell is often seen as the passive invaded victim of the cunning hijacking germ. I loved her vision.
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Another great woman of science is Dr Lynn Margulis who was also belittled and marginalised for many years. She theorised that our cells evolved and were constructed by “germ” bacteria that had learnt to live together. She predicted that their genetic codes would be discovered within the calls, and they were. Today she is credited for revealing that the powerhouses of our cells, our mitochondria, were once separately existing bacteria, as were also the other organelles, or “small organs”, within the cells.

No talk here of a race between selfish particles, of cells as fiercely independent individuals. Rather the more female vision of advance through compromise, symbiosis and cooperation.

The third biologist who has taught me much is Dr Mae-Wan Ho, the founder of the Institute of Science in Society (ISIS), at the UK’s Open University. She took the ideas that Barbara McClintock first put forward and ran with them. What emerges from her work is a picture of cells as centres of dynamic fields of energy, as fluid crystals, electric, magnetic, coherent and quantum. In one of her papers she shares the vision that drives her. “I see all nature developing and evolving, with every organism participating, constantly creating and recreating itself anew.”

Then there is the work of a man – of Professor James A. Shapiro. He has shown how our cells use massive amounts of information with enormous computational skills. He wrote: “The expectation of its pioneers was that molecular biology would confirm the reductionist, mechanical view of life. However, the actual result of molecular studies of heredity, cell biology and multicellular development has been to reveal a realm of sensitivity, communication, computation and indescribable complexity.”

In 2006 Drs. Andrew Z. Fire and Craig C. Mello jointly won the Nobel Prize for Medicine for describing how our cells control the making of proteins ‘involved in all processes of life, for instance as enzymes digesting our food, receptors receiving signals in the brain, and as antibodies defending us against bacteria.’

They showed how our cells delicately control this process through sending instructions by “messenger RNA (mRNA)” These particles are alike to retroviruses in carrying double-stranded RNA. They are somehow directed to control and regulate our genes – and to also monitor the arrival of new information. When viruses arrive at the cell, the code they contribute is immediately assessed, and may then be silenced by these same mRNAs (by a process known as “RNA interference”).

DNA, genetic codes, are simply information. By using a base of four to encode this information (the four nucleotides), rather than the base of two used by computers, our cells pack into tiny particles an incredible amount of information. “The bases are spaced every 0.35 nm [billionths of a metre] along the DNA molecule, giving DNA a data density of over one-half million gigabits per square centimetre.”

Our cells are a hive of activity. Information is more vital to our bodies than it is for a high-tech factory. This includes the constant dispatch of precise encoded information in tiny particles. Every day each cell makes and utilizes thousands of transport particles of varying sizes; with some, like retroviruses, capable of moving a few thousand “base-pairs” of code at a time, even cellular genes, while others, smaller than messenger RNA, are known as “microRNAs” since they carry only 20 or so base pairs of code. Every part of the cell thus talks to every other part.

“Exosome” is another name given by scientists to such “cargo-loaded small vesicles released into extra-cellular space”. In different papers exosomes are varying described as round particles of “up to 120nm”, “from 40 to 100nm”, from “60 to 90nm”. They are thus the same size as, or a bit smaller than, the typical retrovirus. Like retroviruses they are produced when cells are subjected to radiation damage. It is sometimes difficult to tell exosomes and retroviruses apart. It seems the distinction between them may hark back to the older concept of retroviruses as essentially pathogenic.

Exosomes are the subject of many a recent scientific paper. They are produced by many different types of cells, including T-Cells, and can be found in and around tumour cells where they produce a strong anti –tumour reaction. They stimulate the immune system, are T-cell stimulants, and have been found to fight both streptococcus pneumonia bacteria and diphtheria. They may be loaded with antigens against illnesses. It seems every year we are learning more of how such cellular mobile elements serve to protect us.

Even the p53 protein that we came across earlier as a possible target of a the SV40 virus, has now been found to play an important role in regulating the production of exosomes. Cells produce it as a reaction to damaging radiation exposure. It is now said to fight DNA damage.

Such particles, no matter how small, are not static pages of code, but are created as a vibrant part of a complex living cell, and thus may communicate by movement, through electrical currents , photons or magnetic fields as well as through moving genetic codes. Even the cellular water in which these particles float plays a major role in communications. Rich in salts, they preserve information, and as they flow within the cell they generate the electric currents that power the signals our nerves send.

Over the past few years cellular biology has become so important a field of research that in 2006, not only the Nobel Prize for Medicine was awarded for increasing our understanding of the cell, but also the Chemistry Nobel award. This was given to Roger D. Kornberg; “for his fundamental studies on how the information stored in the genes is copied and transferred to the parts of the cells that produce proteins.”

In his Nobel speech he emphasised that if this communication: “is interrupted the organism will soon die, since all protein production in the cells ceases.” He added: “Many illnesses – like cancer, heart disease, and different kinds of inflammation are linked to disturbances in the transcription process.”

So – how does all this relate the principle purpose of this chapter – the real nature of viruses, including the one we know of as HIV?

Well, HIV specialists today hold that HIV is assembled by the very same membranes within our cells where are made the above mentioned vital transport vesicles. They reported: “human immunodeficiency virus type 1 (HIV-1) is generally thought to assemble at the [cellular] plasma membrane.” Dr Gallo himself referred in 2007 to how HIV is created on the membranes within the cell.

The proof they produce of this is interesting. They say HIV must be present, as they have found several proteins in this location that are known to make up HIV; particularly the protein p24 that was first identified by Dr. Robert Gallo as a vital constituent of HIV,

But, cellular biologists have revealed that the p24 protein is in the location where HIV is reportedly assembled, because this is where it normally does its work, playing a major role in the production of the normal healthy non-HIV retroviruses and vesicles. P24 is thus a normal part of every cell – not specific to HIV at all.

HIV scientists also reported: “Our data indicate that most of the infectious HIV produced by primary macrophages is assembled on late endocytic membranes [as are other healthy vesicles] and acquires antigens characteristic of this compartment.” They are thus saying it is close to being a normal human retrovirus or vesicle as it utilizes some of the “antigens’ (proteins) that make up them.

Dr Chris Kaiser recently described how our cells create and use an intricate transport system to deliver to the correct locations the proteins and information needed. In the cell’s Golgi apparatus are made transport vehicles, or vesicles, of every size, from healthy retroviruses carrying genetic codes with thousands of base-pairs down to the smallest mini-vesicles carrying 20 or so base-pairs of DNA.

There is a protein that plays a very major role in the process. It is known as the p24. Kaiser said of these; “Because of their abundance [in this part of our cells], their conservation through evolution, and the fact that they shuttle from the ER [membrane] to the Golgi compartments in transport vesicles, the p24 proteins are thought to be fundamental constituents of vesicles.”

The p24s also play a major role in creating all our healthy retroviruses. They serve as the central Gag protein – and, as such, help form the basic structures. “The Gag protein is the precursor to the internal structural protein of all retroviruses. …The internal structural proteins of retroviruses are derived from a single polypeptide.”

But, could this part of our cells also contain a different form of p24, one that is specific to HIV? I have searched the literature for proof of an `HIV specific p24’ and have not found it. The only thing near to this was a claim made by Gallo and Popovic in 1985 that the p24 in their AIDS virus HTLVIII could be distinguished from that found in HTLVI and HTLVII by the Western Blot test – but the data they produced was inconclusive. No proof was produced of these antibodies or antigens being unique to any of these viruses. This paper was apparently produced to substantiate Gallo’s claim that he, not the French, had found the AIDS virus and it was part of his HTLV viral family.

But I did find that p24 is regarded as a very stable molecule. Dr. Kaiser stated it is a “conserved” molecule – suggesting that it appeared early in evolution and still plays a vital role, thus ensuring it is protected from variations by the cell. Nobel Laureate Leland Hartwell stated in his 2001 Nobel Lecture: “The genetic control of cell division provided two important lessons that have been repeated over and over in molecular, cellular and developmental biology. The first is the conservation of proteins and their functions throughout evolution. This was not a surprising conclusion because all living organisms share a common ancestor.”

If there is thus no such thing as an HIV-specific p24, this would also explain why anti-p24 “responses are minimal or absent in many HIV-infected individuals.”

As far as I could see, the methods these HIV scientists used for this 2003 experiment were scarcely more advanced than those used by Popovic and Gallo in the early 1980s. The experimenters reported that they measured the amount of released HIV “by measuring levels of p24, or reverse transcriptase activity” –not by measuring HIV, or anything unique to HIV. In particular, they did not describe how they distinguished this p24 from that naturally in our cells.

Dr. Kaiser had no doubts about the importance of cellular p24. He stated: “The challenge is to explain the following: p24 proteins are abundant constituents of the vesicle membrane, and their cytosolic tails interact with and powerfully nucleate assembly of both COPI and COPII vesicle coats.”

Thus p24 helps make both the vital COPI vesicles that carry proteins to the membranes, and the COPII vesicles that carry proteins from the membranes back to the assembly factories. So – at the very sites were HIV is supposed to be replicated – the p24s are very busily at work doing entirely healthy normal things.

Professor Elizabeth Dax, in her testimony during the 2007 Australian Court Case, mentioned that HIV deviously manages to coat itself with normal human proteins, thus hiding itself from the immune system.

Again this is said to happen in the same compartments within the cell where are made our normal healthy vesicles. Is she right in thinking this a super-viral act of deception – or is what she is observing really the creation of normal endogenous retroviruses out of normal human proteins?

All retroviruses are assembled by the cellular membranes, in the same place where are made the smaller transport vesicles. HIV is said to be made here also– yet seemingly this assertion is not backed by any attempt to distinguish the healthy retrovirus production from that of HIV. .
Each of our cells is constantly prepared to evolve and adapt its DNA in response to environmental challenges. Each has within it particles known as ‘transposons’, molecular-sized engineers that experiment, so to speak, with our DNA, swapping tiny bits of it around, as if looking for ways to resolve problems. To date they have reshaped at least 45% of our genome.

It is the identical process to that used by the “hospital super-bug”. These modify their DNA to protect themselves from antiseptics or antibiotics in exactly the same way as our cells seek protection from toxins.

But we are more than single cells. An adult human contains approximately 100 000 billion cells. Cellular organisms thus simply have to communicate and co-operate. Our cells “talk” to other cells. Part of this may involve sharing potentially useful genetic code variations with other cells.

We have evolved a way to do this. Our cells produce a vesicle capable of passing from one cell to another. Into this they put the genetic code that is to be shared with other cells. Around this is wrapped a coat of proteins to protect it on its voyage. Such a particle is called a retrovirus,

Like the smaller transport vesicles used within the cells, it is assembled with the help of the Golgi apparatus. It is then budded out. On arrival at another cell, it places its cargo of genetic code within that cell and the protective retrovirus shell is thrown away. The cell then reads the new code, and may then incorporate this into its own DNA or possibly inactivate it.

In virology a division has been made between ‘exogenous’ retroviruses that travel between cells and ‘endogenous’ that we make ourselves, but, reportedly with “no absolute biochemical or functional distinction between them.” I believe they are essentially the same, with some tailoring for specific functions. The evidence is that our cells make them to meet toxic challenges, to repair and to protect the organism.

Thus, although, “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 “ , Rous himself admitted that the cause of the malignancy might have been a chemical toxin in his filtrate. Could this toxin have stimulated cells to produce retroviruses?

Then 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 the Sloan-Kettering Institute for Cancer Research reported in January 1963 that viruses in general seemed to multiply after cells were exposed to “x-ray, ultraviolet light or certain mutagenic chemicals” and that this seemed to “alter the benign relationship” that otherwise existed between cells and bacteria.

Then in the 1980s Gallo found that he had to add toxins to cell cultures if he wanted them to produce retroviruses. He called these toxins his viral “growth factor.” But – if cells produce retroviruses when they encounter toxins – this suggests that cells make them for protection.

Retroviruses are also produced when there is a lack in methylation of cellular genetic codes – meaning that these codes are inadequately protected from oxidation, perhaps because supplies of the vital antioxidant glutathione are exhausted. Are the retroviruses produced to protect these codes?

Within our cells, there is a similar response to stress events. It is reported: “Unusually high activity or unexpected appearance of retroelements” [retroviruses without protective envelopes] within cells is often found in connection with stress events.”

In all these cases, cells produce viruses in response to toxins or other stresses. It has been suggested that retroviruses may serve by replacing damaged DNA (perhaps a reason why they have been found near cancer cells.)

White reported that: “Many retrotransposons carry enhancer sequences responsive to host gene regulatory systems so that they are capable of rewiring the regulation of adjacent genes—perhaps another example of “genomic altruism.” Such retrotransposons may be useful to their hosts in allowing rapid adaptation to a new environment or changes in a developmental pathway. There may therefore be a selection for retention of such retrotransposons as handy intragenomic mutator systems. Recent studies of plant genes, associated with sequences suspiciously similar to those of LTR retrotransposons, support this idea.

Professor James A. Shapiro noted; “molecular analysis has confirmed the generality of Barbara McClintock’s revolutionary discoveries of internal systems for genome repair and genome restructuring.”8 but I would add, such repair systems do not stop at the borders of the cell – they must extend to the whole of the organism.

It seems there is strong evidence for our retroviruses playing a very valuable role during human pregnancy. Several types of human retrovirus are produced in great numbers in the placenta. It is believed they serve to protect the fetus. It has also been reported that two retroviral genes play a critical role in the development of the placenta.

Shapiro acknowledged, in the light of recent discoveries, our notions “require a profound re-evaluation. All aspects of cellular biology are subject to computational regulation. So we can no longer make the simplifying assumption of randomness.” A wonderful example of non-randomness, he says, is how the caterpillar transforms into the butterfly. This involves its genome being “fragmented into hundreds of thousands of segments which are then processed and correctly reassembled.”

In 2007 it was discovered that cells seemingly spin a fine thread between themselves to guide the emerging retrovirus particles to their destination. Each retrovirus can carry some 5,000 base pairs of genetic code including, in addition to the genes it needs itself, “long terminal repeats” and sometimes extra “open reading frames,” perhaps to guide the production of other proteins.

We need an information genetic highway, and we have it – the world of retroviruses is entirely made by cells –and so too is the world of viruses.

It took me an embarrassingly long time to realize it, but it is not just retroviruses but all viruses that are the products of cells – and thus share the life of cells. If our cells make retroviruses for a reason, they presumably can make viruses for a reason. It may thus well be more appropriate to call viruses ‘cellular mobile elements’ (CME) rather than use a word for them that comes from the Latin for poison.

The cells of our world have been very busy. We now know that they have filled the atmosphere, waters and soils of our planet with countless numbers of virus transports carrying milliards of genetic codes. We live submerged in a sea of them. They enter us by the million with every breath. Given their numbers they are extremely rarely associated with illnesses – and we are assembled out of them.

Cells thus invest an enormous amount of energy in creating viruses. Within the cells this means that energy-producing mitochondria cluster around the transport-creating Golgi apparatus. Sometimes this process may go wrong – as in viremia – but I would argue that cells would not normally invest so much in this if it did not serve to both protect them and aid them by driving forward information exchange between organisms and, with it, evolution.

James Lovelock took this one step further by saying: “Living organisms and their natural environment are tightly coupled. The coupled system is a superorganism.”

Lynn Margulis strongly disagreed with him on this, saying calling Gaia a single organism was a step too far, but nevertheless, we now know, thanks to her and others, that our cells evolved out of germs that learnt to live together – and that viruses transported to us a large part of our very DNA. We once called such codes “Junk DNA” but we now know that they regulate our genes, guided our evolution – and that they, rather than our genes, make up the main difference between us and chimps. Our cells have thus a vast encoded library, assembled over eons. Today, evolutionary biologists are constructing a map of evolution going back over 300 million years by tracing this assembly.

Our DNA is thus not fixed but fluid. Some 45% of our 3,000 million base-pair genome is made up by moveable (“transposable”) elements. “The genome-integrated retrotransposons [retroviral-like particles] have been recognized as a major evolutionary force” and may have started to evolve some 3.5 billion years ago – at the same time that DNA first appeared. “It is probable that the cross-species transfer of sequences, either as DNA or RNA” has played a major role in evolution.

We are now inside the world of the virus, the centre of our study. What I have learnt of the cells that create every virus has shifted the paradigm with which I started this work. My first teachers of biology told me that viruses were dead, but nonetheless devious, invaders and hijackers. But, since all viruses are made by the sensitive and highly organized cells described above, I now see them as primarily mobile elements created to travel between cells, carrying and sharing genetic codes. This is the task our cells give them. They are thus not individualistic selfish particles with no need for their parents. Instead they carry with them the life and knowledge of the cell.

Unfortunately there is an unspoken theory underlying much of virology. It is that viruses are always invaders, and that they possess a survival instinct identical to that of a bacteria or cell. But I would question this. Their genetic codes are tiny. They are not designed to reproduce themselves or to live independently of cells – or to scheme to force cells to do work for them. I would suggest that it has never been proven that they are capable of having such motives. I would posit that they are essentially nothing else than cellular transport vesicles incapable of any guile or wish to survive apart from the cell.

I am not thereby presuming none of them can damage us. Every living particle can malfunction. Encounters with unknown genetic codes might have created havoc among Aborigines when Europeans first went to Australia – but the cells of Aboriginal people would have swiftly worked to adapt. A healthy immune system has many ways of protecting us by destroying or neutralising such strange or dangerous viral genetic codes. But that does not mean that viruses are primarily made to infiltrate and hijack organic life.

To date it has proved extremely difficult to kill or inactivate viruses. I would suggest that our “viral” illnesses could be more successfully treated if we regarded them instead as “cellular” illnesses – for it is the cell that produces our viruses. A cell can be poisoned and it can be starved. The flow of energy and communications on which its health depends can be disrupted and presumably it can be misinformed.

The ability of our cells to absorb genetic information from outside, from endogenous viruses and others is basic to our defences. This ability may also be a path whereby occasionally a dangerous code or toxin, gains entry, but it is a path formed by our bodies because of the vital need they have to absorb new genetic information.

Why else should cells evolve the receptors they possess for viruses? Surely, not to facilitate invasion? It is more logical to posit that the receptors are there because the cells need to take in what the transporting virus brings them.

The International Committee on Viral Taxonomy describes a virus as “an elementary biosystem that possesses some of the properties of living systems such as having a genome and being able to adapt to changing environments. However, viruses cannot capture and store free energy and they are not functionally active outside their host cells.” But this description fails to give them any function or to explain why a cell would make them. It omits entirely their ability to move genetic codes from cell to cell.

When we look down an electron microscope for viruses, what do we see? Very small rounded grey particles, with perhaps a dark core of varying shapes. Sometimes they appear to be budding out of the side of a cell. It seems they place in cells their cargo of genetic code. The protein container for the code is then simply thrown away, as far as we can judge.

But, sometimes cells are observed to die shortly after the particle enters them. On the face of it, this seems like aggression, like “typical virus behaviour” – but, it is reported that this process may well not be pathogenic, but part of the natural process of cell replacement by which our bodies stay healthy.

Our cells are known carefully regulate all such processes by instituting systems of control. Dr L. Huber reported that natural cellular death, or apoptosis, involves intracellular communication. Tiny “microparticles” or “vesicles are released from the membranes within the cell during activation or cell death.” They leave the cell to travel to other cells where seemingly they have work to do. “These particles can serve as mediators of intercellular cross-talk and induce a variety of cellular responses.”

For example, on arrival at macrophages, or immune cells, they may enter and tell these cells that it is time to die. Huber stated: “Previous studies have shown that macrophages undergo apoptosis after phagocytosing microparticles.” Apoptosis is normal programmed cell-death. He added that, in their experiments, the “microparticle-induced apoptosis” seemed to be caused by the particles’ “cross-talk” perturbing biolipids, or the fat content, of the macrophages.

But, these normal particles thus do what viruses are supposed to do. They enter, “infect” cells and bring about their deaths. Yet, our bodies stay healthy. What these “infectious” vesicles are doing is entirely natural and healthy.

But Huber suggest that in certain circumstances, when our bodies are under severe stress, such as in “clinical situations with excessive cell death due to malignancies, autoimmune diseases and following chemotherapy, high levels of circulating microparticles” might be produced that might suppress ‘the immune response due to loss of macrophages.” This, Professor Umber suggests, could be mistaken for the action of HIV.

Although, as pointed out earlier, AIDS-related illnesses do not always correlate with having low numbers of CD4 immune cells, it seems possible that such low numbers may thus be caused by the normal process of programmed cell death going askew under cellular stress.

Dr. Steven Lanka, a virologist, has reported that he cannot find evidence for the complete isolation of any medically relevant virus – and given the extreme physical difficulties of doing this, this is not too surprising. He interprets the electron photographs of “viruses” published to date as showing parts of the normal “intra- and intercellular transport” system. He calls viruses simply “cell components.” These insightful statements fit with the research reviewed above.

Jean Claverie of the Structural & Genomic Information Laboratory summarized: “Viruses have come a long way from being unbecoming to the Tree of Life, to be given a central role in all major evolutionary transitions” in “a spectacular renaissance in the field of viral evolution.” He argues that “viruses are the dominant life form on earth” – but if so, I would add that it is only in unity with cellular life.

On this journey I have thus found I was wrong in thinking of viruses as alien foreign creatures, as rivals in the battle of life; and have learnt that we should not be so scared of them for we evolved from them, make them and live within a sea of them.

Effectively, for our own bodies, we are Gaia. We rule over bodies that are the natural home for vast herds of bacteria of many kinds and a milliard flights of viruses, As long as they exist in harmony, we basically stay healthy. They serve us and do not hurt us. Nearly all the so-called dangerous germs, such as TB bacteria, are simply ordinary parts of us, our inseparable and harmless companions.

In 2006 a study of mine was published on TB among diamond mineworkers. What I had learnt during research in South Africa was that TB bacteria live contentedly in every healthy adult – and, in the case of these workers, it was when their lungs were cut to pieces by the silica dust and asbestos ore fibres plentiful and scandalously uncontrolled in major De Beers diamond mines, that the bacteria started to grow in the wounds in their lungs. One mineworker told me; ‘the diamonds are sitting in asbestos”. Another, a driller who had had part of his lungs removed by surgery, said he thought the mine owners wanted the mine to be very dusty “to hide the diamonds from us.” From all reports, the company unfortunately blamed the TB on AIDS rather than put in normal ‘wet-drilling” dust-suppression measures.

It is always easier to blame germs. If the cause is toxins, someone might be able to be sued.

As for AIDS, my conclusion is that we need to revise our concept of this illness. The fight against HIV has been misconceived and an incredible waste of money. But our immune systems can get damaged, our cells’ energy systems can go down – and when they do, they can create a chaos in which our minute inhabitants can hurt us - and this is really what AIDS is – a generic condition common to many illlnesses.

What can take our systems down? A major cause is poor diet and water, lack of certain vital minerals such as selenium, used by our cells to protect themselves from toxins, and high degrees of environmental or inside-body pollution. Look around us. Is it surprising that birds in China started to fall ill with “Bird Flu” when they were flying through ever-increasing vast clouds of industrial pollution? Their cells must have found it incredibly hard to cope. No wonder many died.

Why spend billions on chasing tiny bits of genetic code in dead migrant birds, looking for an unidentifiable part of a not-yet found mutant flu virus when we put scarcely anything into stopping this mutant-causing pollution?

Look again at the “Great Flu Epidemic of 1918.” Was it surprising that it broke out on the Western Front of the Great War, after five years of carnage and chemical warfare? We would need another war like this to reproduce those horrific polluting cell-damaging circumstances. Why do virologists now scare us with predictions that a similar epidemic is certain to strike soon?

It is as if the virus is essentially a nano-terrorist sent to us from an alien plant, equipped with a brain capable of out-witting our cells, a fearsome hijacking infiltrating enemy that deserves to have a multi-billion dollar “war on terror” waged against it – to the great benefit of the pharmaceutical industry.

A side consequence of this – is, as it was at the birth of the AIDS epidemic, that we are distracted away from the far greater and important tasks of dealing with environmental toxins, lifestyle issues, poverty issues.

In fact, it is even worse. Not only are we distracted from these tasks, the priority we give to the fight against viruses has resulted in far greater and more dangerous pollution. We spray organophosphate and organochlorine toxins to kill them, we administer toxic chemotherapy drugs to dissuade our cells from making them – despite making them being an entirely natural process.

It thus could well be argued that the war on terror waged by virologists has been more dangerous to us than the war on terror waged internationally.


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