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« on: March 20, 2020, 05:38:18 pm »
Of course, viral diseases are contagious... but...
Here is GCB's theory:
A NEW THEORETICAL MODEL OF VIRAL PHENOMENA
Introduction
Louis Pasteur was the first to use the term "virus" to describe the pathogenic effect of bacteria that he had discovered under a microscope. At the beginning of the century, lens with an increasingly high resolution, together with high-powered centrifugation, x-ray diffraction, and electrophoresis helped prove the existence of minute particles infective and indefinitely reproductible, though bereft of independent vitality.
More recently, the advent of molecular biology and electronic microscopes has made it possible to specify and visualize accurately the structures of very many viruses, as well as how they spread and behave on the molecular level. This has lifted the veil of mystery those infinitesimal beings were so long shrouded in, in the causation of so many aliments and diseases, and even unbearable tragedies of yore like smallpox and poliomyelitis, and, in this day and age, AIDS.
This knowledge affords us the hope of finding the right strategies, whether they be
1) preventive - that is, by working directly on the immune system through inoculation or
2) curative means, directly inhibiting viral activity within the molecules by means of viral-suppressive drugs.
However, the enduring failure of these methods in the management of HIV, in spite of the fully adequate existing technological approach, as well as the contradictions that remain between theory and practice, all this should lead us to ask a number of questions. The basis of reasoning that underlies present-day research has, in fact, been handed down from an era when man had hardly disentangled himself from superstitions connected to fear of contamination and horrendous epidemics. The manner in which past medicine depicted viruses - which were unquestioningly regarded as pathogenic, i.e. intrinsically harmful agents - is not inevitably the only possible one. Modern tendency prefers considering illness to be more of an imbalance between the host and the attacker, attributing more importance to factors liable to weaken body immunity resistance. A further step would involve studying the real meaning of viral activity, apart from strainling out any emotional bias.
There are, of course, a great many viruses in the natural world that cause no apparent harm. Even in man, a number of viral infections arise more often than not in a dubbed, asymptomatic way. Concerning poliomyelitis, for instance, serological surveys in contaminating circumstances have shown that the nervous system is only affected in a marginal number of contaminated individuals. In children, first contact with the herpes virus typically occurs latently, and in adults, sequels are rare, most individuals being silent carriers. Within the range of viral hepatitis, a great many perfectly latent forms of the virus also exist : mild forms commonly find an outlet in the full recovery of hepatocytes, and the structure of the liver cells fully returns to normal because the reticulum holds up well throughout the course of the disease. Likewise, the Epstein-Barr virus goes undetected in most cases except when blood tests and serum tests are performed. Although it occurs in the majority of African children, it only sets up Burkitt's sarcoma in one case out of 10.000 presumably aided by various co-factors. Whenever the virus causes mononucleosis, the disease normally remains minor. Rabies does evince telltale symptoms in some people though not in others. It is still not known why the disease runs a different course in each individual case.
The same obtains for animals : bird influenza occurs in domestic ducks and quails causing coughing, sneezing, and swelling around the bill - which developments bring about a fairly high death rate - whereas the flu remains benign or latent in other species both wild and domestic. Pig influenza carries a serious and possibly lethal prognosis for piglets contaminated by the sow. It occurs in pigs from different areas and it only ever remotely shows up clinically. Many epidemiologists believe that most viruses are very widespread throughout every species, including man, but only evince signs of disease occasionally, due to the effect of little understood causative factors.
In so far as the number of latent forms and silent carriers turns out to be greater than that of serious forms, there is no theoretical reason for not reassessing traditional models of reasoning. Rather than consider viral diseases to be a logical outcome of viral invasion and marvel at the virus occuring without actually causing any symptoms, it could be predicated that an asymptomatic mode of viral invasion is quite normal, whereas disease causing forms would merely be the result of random developments attributable to further pathogenic factors. Moreover, we are describing an inherently non-toxic pathway that falls within the complex laws of actual biological balance, and, so, we should be in a position to ascribe a specific, i.e. a telic (goal-oriented), assignment to the invading virus. One could stretch a point and suggest that this would be of use to the host, even though such an idea has not yet been given a hearing in classical theory.
To use a light simile to get my points across, imagine rockets being launched to put satellites into orbit. If launching fails once in every 10 attempts, a misinformed onlooker, who was more struck by the failure than by the successful launching - the latter being somewhat inconspicuous - might be forgiven for thinking that the aim of the game was to blow up the satellites and that this fell through on 9 occasions. The whole procedure, as conducted by the engineers and technicians, would be as clear to that onlooker as if he was aware of what was being attempted in spite of his feeling that many failures and pointless effort were required. Given that our onlooker is unaware of what actual intent lies behind observable facts, in other words, if he doesn't know that the satellites do have a purpose, he might think it useful to step in and blow the satellite to smithereens with basic explosives rather than try to help make the launching a success.
Viruses severely disrupt in 1 % of cases. Obviously, one can only think them awesome if their sole purpose is to cause mayhem. However, if our contention were substantiated and viral processes be endowed with purpose, not excluding a possible investigation of why and when they go wrong and turn accidentally dangerous, this would markedly alter the course of research and, hence, therapy.
As to AIDS, the virus was initially believed to be nefarious in all cases. Significantly, outstanding researchers have come to the conclusion, only 10 years after the virus was discovered, that the pathogenic impact of that retro-virus was owing more to particular co-factors than to its inherent features. Considering the dismal failure of the prevention and courses of treatment implemented and, further, considering how critical the situation has become, it is worth leaving no stone unturned.
Just as whenever a theory gets caught in deadlock or proves powerless, so, the very basis of medical reasoning must be recast in the light of new evidence and, especially, when facts are supported by fresh experiments.
That is exactly what this paper on a new theoretical model of viral phenomena by Guy-Claude Burger, a one-time mathematician and theoretical physicist, is putting forward for scruting by researchers who do not turn a deaf ear to inter-disciplinary research. In the wake of 30 years of ground-breaking experiments on man's genetic inability to handle traditional diets, he hopes to make a contribution to the all-out endeavour that has been undertaken to stamp out a looming epidemic and to further research.
Classical model of viral phenomena
Viruses are generally considered to be pathogenic agents, lacking any real life and living off the organisms they infect. The viral particte fastens on to the membrane of a cell, and sequences its DNA or RNA in order to subvert cellular genetics to viral reproduction. The new virions spread through the blood stream and lymph and contaminate other cells. The immune system of the host reacts more or less successfully by releasing antibodies that put a halt to the process. This occurs belatedly and explains the varying shades of seriousness as regards the symptoms observable in different people.
The ultimate aim of this process is to ensure that the virus replicates and endures. The virus endures at the expense of a living being, which implies that the latter must survive and does so within limits that strike a balance between the toxicity of the virus and the immunity of a species.
The nucleotide sequenes for a large number of viruses is now known as well as the structure of their capsule and the type of antigen that enable identification by the host immune system. Sizeable sections of such sequences are identical in the virus and in the infected host. This kinship, which is required for the virus to subvert cell genetics can hardly be accounted for by chance, since the likelihood of a suitable nucleotide mapping is virtually nil. Admittedly, such viruses derive from cellular DNA and subsequently, acquire features enabling them to replicate, attending toxicity notwithstanding.
Surprisingly, after a viral invasion, and in spite of defense mechanisms being marshalled, genetic viral data remains within the cell either as an inactivated viral particle or by integrating into the cell genome. Such a feature explains away the purpose of viruses as instrumental in the evolution of species.
Classical model of viral illness
Viral invasion triggers off a response from the immune system through a number of symptoms : exhaustion, high temperature, swelling, phlegm, rashes, and so on. Further, the viral process commonly co-occurs with an increment in pathogenic bacteria numbers in respiratory tract diseases. In the normal course of things, this proliferation is halted, for example in the common cold, through bacteriostasis of nasal mucus, but this balance seems broken by the action of the virus. Likewise, viral pneumonia can result in bacterial overinfection and in various complications, hence systematic recourse to antibiotherapy although nothing actually happens as regards the viral process proper. When there are no complications, viral disease spontaneously converges towards cure. In some cases, it can carry consequences (post-hepatic cirrhosis) and even result in death.
The classical methods of struggle against viral disease are prophylactics, vaccination, rest, diet, refraining from drink, vitamin therapy, and antibiotics in order to avoid bacterial complications. More recently, various molecules blocking the mechanisms of viral multiplication, or antivirals (like AZT) were used, with results that were hardly conclusive. In a general way, one can say that there is no basically satisfactery treatment against viral disease.
It is generally admitted that the spread of viral affection depends on the general state of the patient, but the factors characterizing this state have not yet been clearly established. In a sizeable number of cases, viral diseases run a latent course. Viral data can indeed remain in contaminated organisms over long periods of time, without setting up any particular symptoms. Anyone so infected will, therefore, be known, somwhat contradictorily, as a "healthy" (silent) "carrier". In respect of most viruses, that state describes the vast majority of individuals. In a substantial number of cases, viral illness occurs in a frustrated, asymptomatic way (99 % of infections through the polio virus).
Viral diseases and Burger's experience
Guy-Claude Burger is a qualified physicist, mathematician, and one-time assistant in theoretical physics at Lausanne University. He developed cancer (lymphoblastic sarcoma) in 1960 and has since been experimenting in diet by trying for a paleolithic kind of diet in an attempt to prove the possible genetic unsuitability of modern dietary patterns for human beings.
Ever since the neolithic era, a number of practices have found their way into dietary customs-namely, cooking, the selection of grain, the use of milk and manufacture of dairy, as well as various techniques used in the culinary arts at large. These techniques alter the taste of foods to enhance their palatability (which makes one prone to overeat) and also bring about changes in the biochemical structures of some nutrients : oxidation, free radicals combining with other molecules, hetrocycles caused by the heating of unsaturated fatty acids, as well as pyrolitic molecules produced by reactions between starches and proteins, etc...
As it happens, there is nothing to show that the genetic data controlling breakdown, and which were evolved in response to primitive foods, have in any way been able to keep up with new dietary factors over a timespan of a few millenia. Possible unsuitability of digestive enzymes, as well as intestinal barrier, and immune system inadequacy might well account for the onset of a good many aliments an diseases, due to molecules alien to an individual entering lymph and bloodstream (EATON, 1985), (PARKER, 1977), (COMBE, 1982), (TULLIEZ, 1986), (RUPPIN, 1980), (WALKER, 1986).
The archeological study of diseases bears out this idea and assays that most of the diseases bears out this idea and assays that most of the diseases traceable on bone remains were, at the very least, virtually non existent before agriculture and cooking came along (EATON, 1985), (GRMEK). Such evidence ought to lead one to query the nature of viral diseases : how could they indeed show up were individuals fed in accordance with their genetic programming ?
Burger's experiment has specifically been one in the observation of a large number of people fed paleolithically, that is on unprocessed and unblended organically grown ram foods barring any animal milk or dairy and on only a modicum of cereal foods and selected produce. Over periods of up to twenty years, food intake remained strictly within the taste and flavour aversion threshold, in order properly to re-enact initial dietary circumstances. Allegedly, Burger noted that in token dietary circumstances, most viral diseases developed in an either mild or asymptomatic way. Viral invasion and a swarm of viral particles appear to occur, however, in conditions not unlike typical ones. Burger does, in fact, claim having noted, in many cases, that even when the disease remained silent, contaminated individuals presented with typical symptoms only hours after the traditional meal, i.e. as soon as alien molecules which were the cause of the symptoms had entered body fluids.
A possible new theoretical model for viral phenomena
Given the pre-requisite of a paleolithic diet, in line with the genetic needs of the body, the absence or alleviation of symptoms denoting viral diseases should, by rights, warrant rethinking the very concept of viral diseases as it has so far been defined.
A preventive interpretation would be conceding quite simply that eating a natural diet is more protective against a viral onslaught. Be that as it may, one could view the problem in an entirely differetn light, and no longer consider the virus as a pathogenic agent per se, inasmuch as pathogenic symptoms ought to be investigated, rather, in some factors that prove the genetic unsuitability of unnatural food.
More to the point, it would be worth considering whether viruses, that are so common in the natural world, are not endowed with a biological assignment whose telic meaning is a closed book to contemporary medicine - at any rate, when it comes to human beings (MALTZMAN, 1981), (ZHDANOV, 1974).
In this connection, Burger notes that virtually all viral diseases present with discharges : phlegm, perspiration, rashes, diarrhea, gravid waters, over secretion of skin oils, specific body odors and so on, with the backing of such common experiential evidence, on the one hand, and current data provided put forward by enzymology, molecular biology, virology, and immunology, he propounds the following suggestion, to wit : besides coding for conditions necessary for the replication of viral particules, DNA or viral RNA also sequences protein synthesis to enable the body to clear given molecules alien to normal metabolism that might have built up within the cells.
Admittedly, retro-viruses are only endowed with a highly restricted genome and only synthesize a minute number of differing proteins whose functions have in most cases already been documented. However, a given protein may, nonetheless, evince a dual function, the first one pertaining to the replication of the virus and the second being in an as yet little understood process of serviceability to the cell. Biology has been known to have such surprises in store for us : many organs exhibit manifold functions, and some genes may be decoded by staggering a nucleotide and, thus, giving rise to two different and yet functional proteins, and so on. Not inconceivably, a viral protein could, for instance, be construed both to suppress viral replication and also to bind with a given group of alien molecules in order to ferry them out of the cell. In such a way, would viral swarm be bound up with a concentration of alien molecules, which would account for the self-regulatory process adverted bo by Burger in his clinical studies.
In the light of the foregoing, viruses, or, at any rate, some viruses would have to be viewed as complementing the immune system as traditionally described. The system ensures the synthesis of anti-bodies commissioned to clear antigens within body fluids, whereas viruses would hypothetically be agents for some kind of intracellular immune function empowering them for the upkeep of law and order inside cells.
In other words, the virus provides the cell with whatever genetic material it requires to identify and clear molecules it cannot control, through its own genetic code, and, signally, molecules alien to normal breakdown taken up by the body from various environmental sources, including foods incorporating molecules that the body is not genetically equipped to deal with. The symptoms that show up during viral development are said to express the difficulty a body has in clearing those same alien molecules, much more so than in waging a putative struggle against the actual virus.
Topic
What follows appears to agree with what is already known about viral processes and draws them together into a neat summing up.
1) Where do viruses come from ?
Admittedly, viruses have adapted to cells subsequent to a random spate of mutations subject to natural selection. Viral particles will thus have evolved the ability to fasten on to specific proteins on cell membranes, and possibly even infiltrate those membranes by way of phagocitosis, for instance, to insinuate and assert that cells evolved genetically, so as to manage the synthesis of diverse viral particles to pas on a genetic message to other cells in the organism and, thence, to other individuals in the species. Selective pressure is likely to be greater, given that the view suggest is true (on account of its being the more likely), if one accepts, like Burger, that data handed down by the virus enable the cell to get rid of nefarious molecules. This to say, that in a living species where individuals compete, those best endowed in terms of intra-cellular immunity are clearly more likely to reproduce than the rest.
2) Membrane receptors for viral particles
Given the conventional view, in the evolution of a virus the latter acquires the ability to fasten on to specific proteins on cell membranes. Conversely, we believe, that cells evolved in such a way as to endow a viral particle with proteins that could bind with given membrane proteins, which they had "taken advantage of" to provide that new function. That a cell can manage to synthesize a protein tha may alight on a receptor, however remote, is patent in the case of hormones and anti-bodies and, therefore, why should this not be so when it comes to viruses ?
As regards the bulk of data handled, it is more than likely that a cell may match up a new protein with a component it already controls the synthesis of, rather than the other way round.
In other words, it is unlikely that a virus should "manage" by more chance the synthesis of ligand proteins that would then match up with proteins that were, in fact, irrelevant to it.
3) Kinship between viral and cell membranes
Similarly, a spate of mutations hardly accounts for viral particle capability in merging its own membrane into the cell membrane, since this brings into play fairly complex molecular processes. As it happens, no natural selective process can be incepted prior to the virus being able to penetrate a cell to replicate, and further, no replication process is possible if the virus is unable even to penetrate the cell. Consequently, either the virus begs entry or it is merely born out of genetic sequencing which would have enabled it from the very outset to build up a membrane enabling it to infiltrate cell membranes. One would have a tough job rating the likelihood of such a thing happening.
Conversely, though, the merger is at once accounted for, granted that the membrane of the first virus derives from a cell membrane. This ties in neatly with the fact that some viral particles on the way out of a cell, where they thrived "borrowed" their membrane from the host's. Strictly speaking, the initial host cell uses its own membrane to "wrap up" the genetic message it circulates to other cells.
4) Affinities between DNA, viral RNA, and cell DNA
That there is definitely an identity element between a sizeable portion of the viral nucleotide sequence and that of cell DNA, as may be witnessed in retro-viruses, can hardly be put down to chance. However, this becomes clear directly one accepts that a retro-virus is merely an offshoot, further down the scale of what was a cell.
In DNA viruses, even when one isn't dealing with identical sequences, there nonetheless obtains a kinship enabling the virus to subvert cell genetics to its own end. That "opposite number" set-up could be explained away either in terms of virus genetically adapting to the cell, or of the cell adapting to an extant virus, or, further still, if viral DNA is surmised, at least partly, to derive from cell DNA.
Just as the body can control the spread of useful bacteria, in the gut, for instance, why should the body not have "learned" to control given extant viruses for its own benefit. As bacterial enzymes are called in to supplement the range of genetically sequenced host enzymes, so virus may well provide an array of proteins useful for the maintenance of intracellular cohesion.
5) Reverse transcriptase
The discovery of an enzyme that could transcribe retro-viral RNA into DNA long defied the expectations of biologists, when lo and behold, a viral type came along that could "forecast" its replication by synthesizing the enzyme it required to code for its own genetic data in cell language that was genetically relevant to the host cell. Moreover, this appeared to lay flat all that was believed about DNA not being reversibly transcribable into RNA in every living being.
Some light can be cast on that, given that on account of a possibly time-worn proces built in to their genetic background, cells have endowed the RNA of a retro-virus with the data requisite for the synthesis of an enzyme that could turn it back into DNA. On the one hand, the process enables the initial host cell to put out data through the usual polymerase - RNA channels, and, on the other hand, it would enable target-cells to take up the data thus released into its own DNA. Such reasoning becomes evolutionarily meaningful, granted that the data passed on is useful to both individual and species, as Burger would have it.
6) Contradictory replication of viroids
Apparently, viroids, which are short chains of RNA consisting of a mere few hundreds of nucleotides and, so far, investigated in the plant kingdom, replicate by means of enzymes already existent in the host cell.
However, that contention runs into difficulty if viroids are construed to originate outside cells. This would imply that the viroid can subvert enzymes with another function within the cell for its own benefit. Nevertheless, there are no loose ends if the process is considered to have been sequenced by the cell, with a purpose for both individual and species, according to Burger's theory.
In this connection, it is noteworthy that viroids only trigger off symptoms in some "sensitive" plants within a species, while they also exist harmlessly in other plants. As it is, those simple viruses already set up a concert of "silent carriers", which involves the majority of individuals infected with typical viruses. Some researchers deem viroids to be abnormal, regulating molecules, but since they're not always harmful, one should look to other factors as disease-causing. Why not say that those basic viral particles have arisen out of genetic data being transmitted down the phylum and which biology hasn't fully exposed.
7) Viral dissemination
Admittedly, viruses subvert cell genetics to their own end in order to replicate their genetic data a set number of times. This statement is based on the fact that the viruses sometimes bring cell activity to a complete standstill, with the only genes being expressed being viral genes.
Given that the expression of viral genes is purposive for body and species alike, it would be more befitting to say that some cells "zero in" on the dissemination of viral data, so as to pass it on to other cells in the body.
The normal functioning of some cells being in deadlock poses no especial threat to the body, provided the number of those cells remains within limits. Experience has shown things remain under control in the vast majority of cases.
8.) Cell lysis
Some viruses, like poliomyelitis, are known to cause the demise of infected cells. As said above, it is worth nothing that the lysis of a given number of cells scattered throughout the body is not an irretrievable condition if the percentage of them remains below a specified threshold. What is hard to determine is what factors can actually cause the threshold to be overstepped, i.e., could immune deficiency be responsible for this, or, as Burger has it, could it be an overly high concentration of alien molecules that boost the dissemination of the virus in charge of clearing them ?
Given that viral data is at all useful, there seems to be some point in the body's "letting go" a restricted number of cells so as to ensure the replication of healthy cells inasmuch as the damage is not terminal, insofar as dead cells can be replaced by functional ones. Still within the realm of poliomyelitis, the number of patients presenting with irremediable damage to their nerve cells (destruction of cell nuclei and untreatable palsies) stands around 0,25 %, which makes evidence for the virus being the direct cause of these lesions extremely scant.
Furthermore, the incubation phase, during which the virus spreads, is typically latent. According to Burger's theory, the symptoms that show up in the acute phase are of two kinds : those due to possibly irretrievable cell destruction and those due to alien molecules being cast out of the cells, as in the case of herpes viral infections, could be part of an overall sequencing that included, for instance, the growth of papules that store waste matter from cells.
9) Genetic lability
Genetic lability, common in many viruses, seems consonant with the range of alien molecule classes which they are encoded to clear. This strikes common ground with the multifariousness of antibodies lymphocytes can generate to identify various classes of antigens likely to make their way into the bloodstream or lymph. Similarly, the changeability of viruses is believed to enable intracellular immunology to face off various classes of alien molecules that could potentially stack up inside cells. Hence, a relevant question as to whether mutations occur are not actually touched off by cell genetics.
10) Viruses of flora
In the vegetable kingdom, viruses also exist that are toxic for the individual and this is due to an attempt at balancing conditions of survival within a species. This is jeopardized when the biotope gluts itself into imbalance. The purpose of this for the species appears not to accord with that purpose in an individual. This is perhaps because, in the plant kingdom, the survival of an individual is far less crucial for the survival of the species than it is in the animal kingdom, especially in higher mammals whose offspring are fewer. In this respect, it should be noted that overpopulation causes deficiencies in the topsoil that disrupt nutritional uptake. This already points to a correlation between uptake disruption and viral onslaught in the vegetable kingdom. Accordingly, it is not unreasonable to think that throughout evolution in the animal kingdom, a more elaborate process may have been at work whose purpose was to protect an individual to enhance the survival of the species.
11) The function of interferon
The secretion of interferon, during the thriving phase of a viral particle in the cells first affected, forestalls any further increment in other cells and this is meaningful, considering that the passing on of viral data to all the cells of an individual is in keeping with a genetic complementation process devised by the body.
Nevertheless, the foregoing hardly qualifies as a defense mechanism as the classical model would have it. Should such a mechanism of defense come into play against viral invasion, there seems no reason why interferon should not be secreted (before the body was weakened and less liable to fight off the attack), to avert infection, as is the case in a number of immunological patterns. Such sluggishness strikingly gainsays the laws of evolution, whereas the premise that virus and cell work together for the species, fully justifies the existence of a regulatory pattern that allows the virus to spread within suitable limits to prevent all the cells in the body from being infected. Even should a further cause of weakening delay interferon synthesis, why is it that synthesis is properly completed when both causes (a viral infection and an outside cause) conjoin and in a way that is strikingly accurate, considering the number of viral particles is not in excess of a single or, at most, a few tokens per cell ?
However, possible "cooperation" between cell and virus fully justifies such a process which can relevantly be viewed as ensuring regulation rather than defence.
12) Auto-immune mechanism
The display of given proteins by cells, as triggered off by interferon (i.e. protein p 69 displayed by pancreas cells), is presumably intended to trigger off auto-immune devices to clear ou cells beset by a glut of alien molecules. This would enable the virus to monitor the repair of cells least affected, while the immune system destroyed cells glutted beyond recovery and that want replacing. This would be borne out if it could be shown that actual display is proportional to alien molecule concentation within the cell.
13) Assembly of viral particle structures
The assembly of fully structured viral particles and their expulsion through the cell membrane also follows from a highly complex coordinated response, given the factors that come into play. The viral genome targets relevant genetic data surprisingly accurately. Since cell genome handles the bulk of relevant data, it makes better sense to credit it with targeting ability, rather than have that accounted for by selective mutations, which could only possibly begin when the virus had become replicative. Insofar as replication can only go ahead inside the cell, how could the inception of the process be explained in the first place ?
14) Viral data storage
Viral data is covertly stored in the cell and may be reactivated, if necessary. This makes sense if one accepts that we are talking about serviceable data priming the cell to discard toxic molecules when build-up becomes nefarious, due allowances being made for the process being reactivated when the build-up of alien molecules becomes harmful.
Orthodox thinking has it that a virus is merely a disease-causing factor, and this would predicate the thorough-going annihilation of viral particles and their genetic load subsequent to recovery, at any rate, in healthier individuals. As it happens, though, the recurrence of viral data is what appears to be the rule.
We are, as yet, unable to show up factors likely to initiate viral reactivation-possibly because these factors not only net in biolocial data about the virus and the cell, but also the biochemical features of molecules that have not so far been reckoned with.
15) Bacterial symbiosis
Bacterial infections often team up with viral diseases and this seems due not only to the immune system being debilitated, but also to alien molecules having been released into body fluids by the cells.
Consequently, two possibilities may be submitted :
- either alien molecules weaken the body, paving the way for bacterial invasion,
- or the swarm of particular bacteria is being coded for by viral data jointly acting with body genetics.
The second possibility is not far-fetched ; the alien molecules we assume the presence of, are known to defeat both breakdown and immune surveillance, since they have made their way right into the cells unhindered. It, therefore, follows that they can only be cleared by processes not originated by the actual body, but by bacterial enzymes, for instance, that will manage to break down unwanted molecules.
This kind of reasoning is in keeping with what is known of bacteria in the gut ; there again, the body appears to have managed to harness bacteria whose enzymes enable it to break down molecules that befuddle its own enzymes, as, for instance, in the case of sugars like cellulose.
In such a way, would the virus incept processes necessary for the upkeep of intracellular cohesion as well as enabling bacteria to proliferate that broke down waste discarded by cells. The seeming disease-causing potential (pathogenicity) of such bacteria is due not so much to the potency of given strains as to an overload of target-molecules in the blood stream and lymph.
16) Apoptosis
Apoptosis, a process involving natural cell death, as witnessed for T4 lymphocytes exposed to HIV can, in this perspective, be reads as follows : the virus sequences the suppression of lymphocytes that specifically identify strains of bacteria whose enzymes are needed to break down molecules cleared by the cells, so as to foster the swarm of the bacteria. Viral genetic data is believed to ferry alien molecules out of cells, on the one hand, and, on the other, to ensure the swarm of bacteria are likely to clear these same molecules out of body fluids.
An overload of target molecules, especially when the body is stocked up with unsuitable dietary molecules daily would explain why apoptosis runs away with itself and why the immune system apparently gives out, leaving all kinds of pathogenic particles an open field.
Auto-immune processes, such as are triggered off by dietary antigens that settle on lymphocyte membrances, moreover, could make things worse and step up the destruction of those lymphocytes.
17) Variable pathways
The varyingly serious evolution of the viral process in different individuals is bound up with the varying amounts of alien molecules that have collected in the system depending on the extent of the body's recollection of whatever molecules it has stored up.
The viral disease symptoms in humans are typical insofar as civilized diets have strayed very far from what original diets must have been and what directed our genetic evolution. It seems unlikely that over a few thousand years the human body should have genetically adapted to all the new molecules ushered in by industrial agriculture and food-processing since the neolithic period. Such an apparently dangerous virus (as SIV hardly evinces any symptoms in monkeys living in their natural habitat, nor for that matter does HIV set up symptoms in chimpanzees held captive and fed natural food. Inasmuch as a virus only thrives in the body provided there are alien molecules there, it may be accepted that an additional intake of the same molecules in traditional foods will cause viral replication to go berserk. According to Burger, when some people suffering from infection eat particular foods during the incubation period, this causes subsequent symptoms to worsen, as, for instance, in the case of viral hepatitis. In that light, it becomes obvious why clear diets one part of standard medical prescription against head-colds, hepatitis, a.s.o., has been effective enough to endure in the medical tradition.
18) Childhood diseases
Popular wisdom, which once believed viral infantile diseases to have their purpose is now being vindicated, considering that once the body is provided with whatever genetic accretions it gets from viruses, it is better armed against toxic molecules likely to beset its cells throughout its existence. This in turn challenges the usefulness of vaccinations : the purpose of those diseases remains to defeat viral infections such as can spell disaster against a conventional dietary background. Conversely, if Burger was right, one could fear that the lack of genetic additions afforded by common viruses would leave individuals out in the cold when it came to ensuring cell cohesiveness as well as stepping up morbid degenerative changes and jeopardizing vital bodily functions.
19) Modification of the biotope
The advent of some viral diseases in wild animals may be attributed to environmental changes involving the cultivation of grain or other mutated plants with attending increments of new proteins in their natural dietary environment (to wit, proteins generated by mutations engineered in wheat and their build-up in the bodies of rodents, thus activating rabies, which was previously extant yet without entailing further change).Molecules from industrial waste and pollution need also be reckoned with.
20) Anti-viral molecules
The comparative failure of antiviral molecules is due to great difficulty in averting genetically encoded vital processes. Interactions between viral and cell genome actually occur within cell nuclei and are accurately coded for, so much so that they are very hard to inhibit without attending damage to the cell. These presumably resort to self-regulatory and substitution techniques to secure changes that will defy therapy unless, and until, their biological purpose is explained.
21) Oncogene viruses
Oncogenes viruses are a race apart : they are perhaps always harmful. Yet, the replication of cells can be useful to various ends, if only to make up for cell destruction due to one reason or another. Conceivably, therefore, those viruses provide the body with useful data, although they may wreak havoc in the presence of given co-factors. The Epstein-Barr virus only shows up as a sarcoma in a minute proportion of children contamined, and only in Africa, at that. Over and above genetic propensity, Burger's theory advocates seeking out the existence of a particularly high concentration of alien molecules, presumably due to the dietary habits of African children.
22) AIDS
As for HIV, virtually anyone contaminated was thought to have a present with serious symptoms. Facts have so far shown that, besides a very few exceptions, being seropositive carried a death-sentence. These facts seemed to gainsay previous arguments. In recent years, the same or similar retro-viruses, however, have been discovered in many wild animals that did not appear sick in any way.
Top researchers ended up thinking that the virus was not actually disease-causing, but rather that as yet unknown "co-factors" were at work.
In Burger's view, those co-factors could well be the molecules that the virus is commissioned to clear that may have built up much more in human beings than in wild animals : the latter do indeed feed on natural foods that their genetics has fully adapted to from time immemorial, whereas people regularly eat traditional foods that were not part of man's primitive background, and which human genetics has simply not had time to keep up with.
There is, therefore, some concern that alien molecules may have had a chance to stack up in human cells to levels unrivaled in the history of mankind. Consequently, the viral processes devised to sequence the clearance of those molecules in an initially silent way, are now being overrun : the surfeit of target molecules is believed to disrupt that regulatory processes that ensured its proper functioning and, most notably, bring out "adventitious infections" that are dangerous on account of the over-expansion in the numbers of bacteria relevant to the clearing of the same molecules.
Why, therefore, should it be that the HIV retro-virus, which may have been part of man's low profile genetic legacy - as is the case for animals - why indeed should it have reared its head out of cell nuclei to trigger off a serious epidemic ? Indisputably, the causes instrumental in this include sweeping dietary changes over the last few decades, especially in Third World countries where Western dietary habits have spread like wildfire, as have fresh causes of contamination. Having been sparked off, viral replication could not but exel itself : the most highly contagious viral particles and those that most affect mucous membranes are the fastest spreading. What is more, organisms that no longer harbored the virus or in whom it had been thoroughly mothballed have had ample time to clock up a signally high amount of target molecules. This accounts for the uncanny aggressiveness of the viral process, further magnified by the daily intake of foods that are vectors for molecules from the same groups.
Theoretical and in situ cross-checking
A new theoretical model in so complex and emotionally charged a field as disease and contamination, can only be borne out with the hindsight derived from being grounded in sound initial reasoning and especially from the observation of facts.
Unfortunately, getting new ideas published prior to their endorsement by the medical powers-that-be is no easy task, even though one's sole ambition may be to put them before the critical judgment of experts. Burger is, therefore, most anxious that researchers interested should assess the model put forward in the light of their theoretical knowledge, and that practitioners rate whether the correlations between the diet of patients and the evolution of viral diseases is in keeping with possible predictions. Burger would be most grateful to be informed of either significant contradictions to, or, alternatively, correlations with the model, by such researchers as would be willing to let him know of their findings.
If Burger's viral model does prove conclusive, it may well pave the way for new avenues of research, not least, into AIDS. This would not merely boil down to devising a vaccine or evolving anti-viral molecules to step into the breach, but would also make it possible to typify the dietary molecules that are possibly instrumental in disrupting the viral process. Preventative dietary strategies might possibly improve survival prospects for present-day seropositive victims. The daily intake of alien molecules is also likely to bear on the regulation of viral processes. This being so, a change in diet could improve the condition of individuals already contaminated and perhaps rein in symptoms even once they had set in.
Unfortunately, no epidemiological survey has so far been conducted to show the possible link between the irrelevant immune response of seropositive victims and the daily diet of AIDS victims, and how serious their symptoms are.
Further, pinning down dietary life-unfriendly factors could be serviceable in helping gain an understanding into various metabolic or other dysfunctions involving biochemical processes - like impulse transmission, DNA replication, and so on. Some wheat gluten proteins (i.e. gliadines), are known to worsen the symptoms of schizophrenia ; also, a number of pyrolitic molecules have proved mutagenic and, no doubt, there are quite a few pathogenic factors to be unearthed in the field.
In a similar connection, Burger's heuristics would warrant a more systematic investigation of dietary antigens involved in auto-immune diseases. Such a procedure has enabled the recent discovery of a peptide in cow's milk that causes the immune system to turn against pancreas Beta cells that are a carrier for a protein with a similar site, thus coding for juvenile diabetes, and has confirmed experiments on rheumatoid arthritis with 80 % of cases experiencing relief for patients eating a dairy- and wheat free diet.
Synopsis
Burger et Al. are putting forward a model for viral processes that incorporates current genetic, immunological, virological, and dietary findings, stringing them together into a sensible theory.
The viruses and bacteria involved in the genesis of most so-called infectious diseases are regarded as vectors and partners in genetically encoded symbiotic processes, so as to help the body clear molecules alien to organic function inside actual cells. These processes show up as disease-causing when an overload of alien molecules occurs in body fluids - this being bound up with inadequate dietary habits - since the workings of human metabolism are unable to handle changes in such culinary practices as have been with us since the neolithic era.
It may be suggested that the grand-scale use of antibiotic courses of treatment and inoculations - inasmuch as they have inhibited the processes described above - may have prompted the advent of degenerative and auto-immune diseases - as well as carcinomatosis - subsequent to the build-up of alien molecules, whether antigenic or life-unfriendly, inside the body, that are likely to disrupt immunological and biological functions such as are required for the maintenance of health.
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