A new theoretical model of the viral phenomenon

The following is a booklet published in Mars 1993 by Guy-Claude Burger, introducing a ground-breaking new understanding of the viral phenomena as a purely positive natural mechanism only seldom causing harm because of our unnatural diet.

I hasn’t hasn’t age at all, since medicine hasn’t in the slightest in its understanding of the viral phenomena, or human biology for the matter. Ergo, everything written still stands as strong and time could only add more exemples from molecular and genetic studies.
Pasteur was the first to use the term “virus” to designate the pathogenic action of bacteria that he had discovered in the field of the microscope. At the beginning of the century, increasingly sophisticated filters, followed by ultracentrifugation, X-ray diffraction and electrophoresis techniques, made it possible to establish the existence of very small particles, which carry an indefinitely reproducible infectious power, although they lack autonomous vital functions.

More recently, molecular biology and the electron microscope have made it possible to determine and visualize the exact structures of a large number of viruses, as well as the mechanisms of their multiplication and their action on a molecular scale. Thus, the mystery of these infinitesimal beings which had remained hypothetical for so long, associated with so many illnesses and diseases, and even unbearable tragedies such as smallpox or polio in the past, and AIDS today, seems solved.

This knowledge gives us hope to find ways to fight either preventively by acting on the immune system with vaccines, or curatively by directly inhibiting viral activity by molecular means with antivirals. However, the prolonged failure of these techniques in the case of HIV, despite the importance of the technological apparatus implemented, as well as the contradictions that remain between theory and facts, should prompt us to ask ourselves a number of questions.

The basis of the reasoning behind current research is in fact the legacy of an era when the superstitions attached to the fear of contagion and major epidemics were barely overcome. The image that the medicine of that time gave us of the virus, considered a priori as a pathogenic agent, harmful by definition, is not necessarily the only one possible. The current trend is to consider the disease more as an imbalance between the host and the aggressor, giving more importance to the factors likely to decrease the resistance of the organism. A further step would be to look for the meaning of the viral phenomenon in itself, without any emotional connotation.

There are many viruses in the natural world that do not manifest themselves as a nuisance. Even in humans, many viral diseases occur mostly in a frugal or asymptomatic form. In the case of poliomyelitis, for example, serological studies in epidemic settings have shown that nervous system involvement occurs in only a very small percentage of infected persons.

In children, primary infection with herpes virus usually occurs inapparently, and in adults, complications are exceptional, with the majority of individuals being healthy carriers. In the different classes of viral hepatitis, there are also a large number of completely latent forms; the benign forms usually end with complete regeneration of the hepatocytes, with restoration of a normal architecture thanks to a remarkable conservation of the reticulum during the course of the disease.

Similarly, the Epstein-Barr virus is detectable in most cases only by hematological and serological examinations, and is found in the majority of African children, whereas it causes Burkitt’s sarcoma in only one case in ten thousand, probably in cooperation with various cofactors; when it triggers mononucleosis, this is usually not serious. The rabies virus itself develops the classic symptoms in some people and not in others, and the reasons for these differences are still unknown.

The situation is similar in animals: avian influenza manifests itself in domestic ducks and quails in the form of coughing, sneezing, and swelling around the beak, leading to significant mortality, whereas it remains mild or inapparent in other wild or domestic species. The swine influenza virus, considered dangerous, even fatal for young pigs infected by their mothers, is found in pigs from different regions where it is only sporadically accompanied by clinical manifestations.

Many epidemiologists are of the opinion that most viruses are widely distributed in all living species, including humans, but only occasionally manifest themselves by pathological symptoms, under the effect of triggering factors still not well known.

Insofar as the number of inapparent forms and healthy carriers turns out to be greater than that of the serious forms, there is nothing to prevent, at least from a theoretical point of view, a reversing of the classical model of reasoning. Rather than considering the viral disease as the natural outcome of the invasion by the virus and being surprised that the virus can be present when nothing is happening, one could postulate that the asymptomatic form of the viral invasion is the normal form of a natural phenomenon, the pathological forms being only the result of an accidental evolution due to certain other pathogenic factors.

Moreover, if it is a phenomenon not harmful in itself and belonging to the complex equilibrium mechanisms characterizing biological reality, it should be possible to attribute to it a precise function (a teleological meaning), at the very least a function that is useful to the host, even if this possibility does not yet seem to have been envisaged in the classical conceptions.

To illustrate this in a somewhat trivial way, let us take the case of the rockets used to put satellites into orbit: if the launch fails in one case out of ten, an uninformed observer, struck more by the accidents than by the successes, much less impressive, could think the purpose of the operation is to destroy the satellite and that this purpose is missed in the nine other cases; all the operations conducted by the engineers and technicians would be explained for this observer as well as if he knew their real purpose, apart from the impression of a great quantity of failures and useless efforts; without knowing the real intentions behind the facts he can observe, that is to say, without knowing the satellites can have any usefulness, such an observer would believe it useful to intervene by destroying the satellite with simple explosives rather than to join in the work that represents its launching.

Viruses cause significant problems in about one in a hundred cases. They remain frightening if they have no other meaning than to cause disease. On the other hand, if our postulate were confirmed and if we could attribute a useful function to the viral process on the one hand, while identifying on the other hand the causes of dysfunction causing the accidental danger, a very different direction of research, even therapeutic action, would unveil.

“In the case of AIDS, it seemed a priori that the virus had a harmful effect in 100% of cases. It is significant that the best-placed researchers have come to believe, some ten years after its discovery, that the pathogenic activity of this retrovirus is due more to certain co-factors than to its intrinsic characteristics.

Faced with the general failure of the prophylactic and therapeutic means implemented, and faced with the urgency of the situation, all paths certainly deserve to be explored: the very basis of the reasoning on which medical action is founded, as each time a theory leads to failures or contradictions, must be reconsidered in the light of the knowledge acquired in the meantime and, above all, in the light of the facts that can be brought to light by new experiences.

This is precisely another theoretical model of the viral phenomenon Guy-Claude Burger, a former mathematician and theoretical physicist, proposes here for the consideration of researchers open to a multidisciplinary reflection. After thirty years of unprecedented experience on genetic maladjustment to traditional food, he hopes to make a modest contribution to the general effort to curb the threatening epidemic and to advance knowledge.

Classical model of the viral phenomenon

Viruses are generally considered as pathogenic agents, devoid of life of their own and subsisting at the expense of the organisms they infect. The virion (viral particle) attaches itself to the membrane of a cell, introduces its DNA or RNA and hijacks the cell’s genetic machinery in order to reproduce itself.

The new virions spread into the circulating masses and infect other cells. The host’s immune system reacts with varying degrees of success by creating antibodies to stop the process. This is done with a certain delay or falure rate which explain the variable importance of symptoms observed in different subjects.

This process has no other teleological significance than the virus’ multiplication and perpetuation. It is carried out at the expense of a living species that must not, out of necessity, succumb, a fact within limits accounting for a certain balance between the harmfulness of the virus and the resistance of the species.

We know today the sequences of nucleotides of a great number of viruses and retroviruses, as well as the structure of their envelope and the nature of the antigens which allow the immune system to recognize them.

Classical model of viral disease.

Viral invasion triggers an immune system reaction that results in various symptoms: asthenia, hyperthermia, inflammation of the mucous membranes, catarrh, rashes, etc. In addition, in association with the viral process, especially in diseases of the respiratory tract, the multiplication of pathogenic bacteria is often observed.

Normally, this proliferation is slowed down, for example in the case of coryza, by the bacteriostatic action of the nasal mucus, but this balance seems to be broken by the action of the virus. Similarly, viral pneumonia can lead to bacterial superinfection and various complications, hence the systematic use of antibiotic therapy, although this has no effect on the viral process itself.

In the absence of complications, the viral disease converges spontaneously towards recovery. In some cases, it may leave sequelae (e.g., post-liver cirrhosis) or even lead to death.

The classical means of fighting viral diseases are prophylaxis, vaccination, rest, diet, abstention from alcohol, vitamin therapy, and antibiotics to avoid bacterial complications. More recently, various molecules blocking the mechanisms of viral multiplication, or antivirals (such as AZT), have been used, but with inconclusive results. It can be said in general that there is no satisfactory background treatment for viral diseases.

It is accepted that the evolution of a viral disease depends on the general condition of the patient, but the factors characterizing this condition are not yet clearly established. In a significant number of cases, viral diseases develop in a frugal or asymptomatic form. Since the viral information can remain present in infected organisms for a long time without causing any particular symptoms, the a priori contradictory concept of “healthy carrier” requires definition. This state concerns, for most viruses, the majority of individuals.

Viral diseases and Burger’s experiment.

Guy-Claude Burger, a physicist and mathematician, former assistant in theoretical physics at the University of Lausanne, was diagnosed with cancer (lymphoblastic sarcoma of the pharynx) in 1960. For about thirty years, he pursued a dietary experiment consisting of reconstituting a Paleolithic type of diet, in order to demonstrate the influence of a possible genetic maladjustment of the human organism to the data of modern nutrition.

Since the Neolithic period, many artifices have been introduced into food habits, such as cooking, the selection of cereals, the use of animal milk and the manufacture of dairy products, as well as the various processes used in the culinary arts in general. These processes modify the organoleptic qualities of foods so as to increase their palatability (which tends to increase their consumption) and also lead to transformations in the biochemical structures of certain nutrients (oxidation, free radicals attaching themselves to other molecules, heterocycles by heating unsaturated fatty acids, Maillard molecules resulting from the reactions between carbohydrates and protids, etc.)

However, there is no evidence that the genetic data of assimilation, first constituted in contact with primitive foods, could have been adapted in a few millennia to these new food factors. A possible maladjustment of digestive enzymes, of the intestinal barrier, and of the immune system could explain the appearance of numerous disorders and diseases, as a result of the penetration into the circulating masses of molecules foreign to the functioning of the organism.

Paleopathology corroborates this hypothesis by demonstrating that most of the diseases whose traces we know how to recognize on the bones, did not exist or were very rare before the agricultural and culinary era. These few elements may lead us to wonder about the nature of viral diseases: how would they manifest themselves if organisms were fed according to their genetic programming?

Burger’s experiment consisted precisely in observing, over periods of up to twenty years, a large number of subjects fed according to the Paleolithic model, i.e. exclusively with raw food, organically grown, neither prepared nor mixed, excluding all animal milk and all dairy products, and with a minimum of cereals and selected products. The food intake was regulated by a strict observation of the alliesthetic mechanisms (variations of the olfactory and gustatory sensations) so as to reproduce as much as possible the primitive conditions of food.

Burger would have noted, under these particular feeding conditions, that most viral diseases systematically present themselves in a frugal or asymptomatic form. The viral invasion and multiplication of virions, however, seem to occur as under classical conditions. Indeed, Burger claims to have observed in many cases that infected subjects, even though the disease remained inapparent, developed classical symptoms within hours of ingesting traditional foods, i.e. as soon as the foreign molecules of which they could be the vectors had passed into the circulating masses.

Proposal of a new theoretical model of the viral phenomenon

If, within the framework of a Paleolithic type of diet, in principle in conformity with the genetic data of the organism, the absence or the reduction of the disorders associated with the viral affections were to be confirmed in a systematic way, the very notion of viral disease would have to be called into question.

A first interpretation would be to say simply that a natural diet confers a better resistance to viral aggression. However, it would also be possible to turn the problem around and stop considering the virus as a pathogenic agent in se, the pathogenicity of the phenomenon being sought rather in certain factors of genetic maladjustment to the unnatural diet.

More fundamentally, one should ask whether the viral phenomenon, which is widespread in the natural world, does not possess a biological function whose teleological significance is still poorly discerned by contemporary medicine, at least when it comes to the human being.

Burger points out in this connection that practically all viral diseases are accompanied by “effluents”: catarrh, perspiration, rashes, diarrhea, heavy urine, seborrhea, particular body odors, etc. Basing himself on these facts of current observation, on the other hand on the current data provided by enzymology, molecular biology, virology and immunology, he proposes the following hypothesis: the viral DNA or RNA would program, in addition to the mechanisms necessary to the multiplication of virions, the synthesis of proteins ensuring the evacuation of certain molecules foreign to the normal metabolism which would have accumulated in the intracellular medium.

It is true that retroviruses have a very restricted genome and that they produce only a small number of different proteins whose functions are already known in most cases. However, it is not excluded that a given protein has two functions, one belonging to the reproduction of the virus, the other to a process useful to the cell, still unknown. Biology has already provided more than one such surprise: many organs have multiple functions, some genes can be read with a shift of one nucleotide and give rise to two different yet functional proteins, etc.

It is no more unreasonable to consider, for example, the hypothesis that a viral protein can, on the one hand, exert a suppressive action on viral replication and, on the other hand, bind to foreign molecules of a given class, in order to ensure their transport outside the cell: viral multiplication would thus be linked to the concentration of foreign molecules, which would explain a self-regulation of the phenomenon such as seems to be apparent from Burger’s clinical observations.

From this point of view, viruses, or at least certain viruses, should be seen as a kind of complement to the traditional immunological system: the latter ensures the synthesis of antibodies responsible for eliminating the antigens present in the circulating masses, whereas viruses would be the agents of a kind of intracellular immunology responsible for maintaining order inside the cells.

In other words, the virus would provide the cell with the necessary genetic complement to recognize and eliminate the molecules that it is not able to control by its own genetics, in particular the molecules that are foreign to the normal mechanisms of assimilation, introduced into the organism by the effect of different environmental factors, in particular as a result of the absorption of food containing molecules that are foreign to the genetic data of metabolism.

The symptoms which appear during the viral process would then reflect the difficulties encountered by the organism to get rid of these foreign molecules, more than a fight against the virus itself.


This hypothesis seems to be in agreement with the data already known about the viral process, which it allows us to include in a coherent synthesis.

Origin of the virus.

It is generally admitted that the virus has adapted to the cell by a series of mutations obeying the laws of chance and natural selection. The virion would thus have become capable of attaching itself to certain proteins present on the cell membrane, or even of integrating into this membrane by using, for example, the mechanisms of phagocytosis to surreptitiously penetrate the plasma, and then of hijacking the cell’s genetic machinery to its advantage.

It is also possible to reverse the reasoning and postulate that the cell has evolved genetically in such a way as to proceed to the synthesis of various viral particles, allowing it to transmit a genetic message to the other cells of the organism and to other individuals of the species.

The selection pressure is probably stronger in this second hypothesis (which would thus appear more probable), if we admit, as Burger does, that the information transmitted by the virus allows the cell to eliminate harmful molecules: in a living species whose representatives are in competition, the individuals best equipped in terms of intracellular immunology obviously have more chances of reproducing than the others.

Membrane receptors

In the first hypothesis, the virus would have acquired during its evolution the ability to bind to certain proteins present on the cell membrane.

In the second hypothesis, the cell would have evolved to endow the virion with proteins capable of adhering to certain membrane proteins, which it would have taken advantage of to ensure this new function.

The ability of a cell to synthesize a protein capable of binding to a receptor, even a distant one, appears for example in the case of hormones or antibodies, and there is nothing to prevent us from presupposing an analogous phenomenon in the case of the virus.

From the point of view of the quantity of information, it seems more likely that a cell can match a new protein to an element whose synthesis it has already mastered, than the reverse, i.e. that a virus can “succeed” by chance alone in synthesizing binding proteins corresponding to proteins which would be in no way related to it.

Viral membrane and cell membrane.

Similarly, a series of mutations hardly explains the ability of the virion to integrate its own membrane with that of the cell, which requires rather complex molecular mechanisms. Indeed, no process of natural selection can begin before the virus is able to enter a cell to multiply, and no process of multiplication is possible if the virus is not already able to enter a cell. It is difficult to estimate the probability of such an arrangement occurring, but it is certainly very low.

However, this integration phenomenon is immediately explained if we admit that the membrane of the first virus is derived from a cell membrane. This is also perfectly consistent with some virions leaving the cell where their multiplication took place “borrow” their membrane from that of their host, or rather: that the multiplying cell uses its own membrane to “package” the genetic message that it sends to its fellow cells.

Similarity between viral DNA or RNA and cellular DNA.

The remarkable identity between an important portion of the viral nucleotide sequence and that of the cellular DNA, as it is observed in retroviruses, seems difficult to attribute to chance. On the other hand, it is immediately explained if one admits that the retrovirus, in a more or less distant past, originated from the cell.

In DNA viruses, even if we are not dealing with identical sequences, there is nevertheless a relationship that allows the virus to hijack the cellular genetics to its advantage. This “homology” can be explained either by a genetic adaptation of the virus to the cell, or by an adaptation of the cell to an existing virus, or by assuming that the viral DNA is derived, at least in part, from cellular DNA.

Just as the organism knows how to control the multiplication of useful bacteria, for example in the intestinal flora, it is conceivable that it could have “learned” to control certain existing viruses in order to take advantage of them: just as intestinal bacteria are useful to it by their enzymes which complete the range of enzymes provided for in the genetic make-up, viruses were able to provide an assortment of proteins useful for maintaining the integrity of the intracellular environment.

Reverse transcriptase.

The discovery of an enzyme capable of transcribing retrovirus RNA into DNA defied all predictions of biologists at the time. This viral type suddenly proved to be able to “predict” its copy by synthesizing itself the enzyme necessary to the transcription of its genetic information in the language proper to cellular genetics. Moreover, this fact seemed to contradict everything we knew about the irreversibility of the transcription of DNA into RNA in all living beings.

Such a phenomenon can be better explained if we postulate that the cell, by virtue of a perhaps very old mechanism inscribed in its genetic heritage, has endowed the RNA of the retrovirus with the information necessary for the synthesis of an enzyme capable of retranscribing it into DNA. This allows, on the one hand, the transmitting cell to export information by passing through the classic way of the RNA-polymerase, and on the other hand, the receiving cell to integrate the transmitted information at the level of its own DNA. This reasoning is only meaningful in terms of evolution if one postulates that the transmitted information is useful to the individual and to the species, in accordance with Burger’s hypothesis.

Replication of viroids.

It seems that viroids, short chains of RNA consisting of only a few hundred nucleotides, studied so far in plants, reproduce thanks to the action of enzymes already present in the host cell.

This fact is difficult to explain if one admits that the viroid is of external origin to the cell: it implies that the viroid is able to divert enzymes in charge of other functions in the cell for its own multiplication. On the other hand, they fit perfectly into the logic of an action programmed by the cell, useful to the individual and the species according to the Burger hypothesis.

In this respect, it should be noted that viroids only cause symptoms in certain “sensitive” plants of a species, whereas they are also present in others without causing any harmful effects: the problem of the “healthy carrier”, which concerns the majority of individuals infected by classical viruses, is already present in these simplified viruses. Some researchers consider viroids to be “abnormal” regulatory molecules: since their action is not systematically harmful, there is reason to look for other factors responsible for triggering a pathology.

Nothing to prevent us from thinking that these rudimentary viral particles are the result of archaic mechanisms of transmission of genetic information, the secrets of which biology has yet to reveal.

Viral multiplication

It is generally considered that the virus “hijacks the cell’s genetic machinery for its own benefit” in order to reproduce its own genetic information a certain number of times. This statement is based on the fact that the virus induces in some cases a complete blockage of the cellular machinery, the only genes expressed being then the viral genes.

If one accepts that the expression of viral genes is useful to the organism and the species, one should rather say that certain cells “concentrate their activity on the multiplication of viral information, in order to retransmit it to the other cells of the body”. 3

The blocking of the normal activities of certain cells does not pose any particular problem for the organism if their number remains limited. Experience shows that such a limitation is indeed assured in the vast majority of cases.

Cellular lysis

Some viruses, such as the poliomyelitis virus, are known to cause the destruction of infected cells. As in the previous paragraph, it should be noted that the lysis of a certain number of cells dispersed in the organism does not represent an irreversible lesion if their percentage remains below a certain threshold.

The problem is rather to know which factors can cause this threshold to be exceeded: for example, a deficiency in the immune system, or, in accordance with Burger’s hypothesis, an exaggerated concentration of foreign molecules stimulating the multiplication of the virus responsible for their elimination.

If the viral information is supposed to be useful, it does not appear unfavorable in itself that the organism “sacrifices” a limited number of cells in order to ensure their multiplication, as long as the phenomenon remains reversible, i.e. the dead cells can be replaced by operational cells. Still in the example of poliomyelitis, the number of patients presenting irreversible lesions of the neurons (alteration of the nucleus of the cells and irreversible paralysis) is about 0.25%, which is obviously insufficient to be able to consider these lesions as a consequence directly linked to the action of the virus.

It should also be noted that the incubation phase, during which the virus multiplies, is generally silent. In Burger’s hypothesis, the symptoms which appear during the state period should be divided into two classes: those which result from possibly irreversible cellular destruction, and those which are caused by foreign molecules released by the cells into the circulating masses. y

In addition, the destruction of certain cells, as in the case of infections by the herpes virus, could be part of a general programming of the phenomenon including, for example, the formation of papules useful for the elimination of substances rejected by the cells.

Genetic variability

The genetic variability observed in many viruses can be accounted for by the diversity of the classes of foreign molecules whose elimination they are responsible for programming. There would be a certain analogy with the multiplicity of the different antibodies that lymphocytes know how to elaborate to recognize the different classes of antigens likely to penetrate the circulating masses. Similarly, the variability of viruses would allow intracellular immunology to cope with the various classes of foreign molecules capable of accumulating inside the cells. It is therefore questionable whether the mutations we observe are not induced by cellular genetics.

Plant viruses

The existence of viruses that are obviously harmful to the individual in the plant world can be explained by a kind of homeostasis at the level of the species: the survival of the species is indeed endangered if the biotope becomes unbalanced due to overpopulation. The usefulness for the species seems here to go against the usefulness for the individual. This is undoubtedly due to the fact that the survival of the individual, in the plant world, is much less important for the maintenance of the species than in the animal world, especially in the higher animals where the litters are few.

In this regard, it can be noted that overpopulation causes deficiencies in the humus, which in turn leads to nutritional disorders in plants. Thus, there is already a relationship between nutritional disorders and virosis in the plant kingdom. It is therefore not absurd to think that this same phenomenon could have taken, through the evolution undergone by the animal kingdom, a more elaborate form whose strategy consists in preserving the individual to favor the survival of the species.

The role of interferon

The production of interferon during the multiplication of the virion in the first cells, avoiding further multiplication in the other cells, is meaningful if we admit that transmission of the viral information to all the cells of the individual responds to a process of genetic complementation “foreseen” by the organism.

On the other hand, it is difficult to explain in terms of a defense mechanism as the classical model would have it: if such a defense mechanism is possible at the time of viral invasion, it is not clear why interferon would not be synthesized early enough (at a time when the organism is not yet weakened and would therefore be in a better position to defend itself), as is the case for many immunological mechanisms. Such slowness seems to contradict the laws of evolution, whereas the hypothesis of a collaboration between the virus and the cell, useful for the species, justifies perfectly the presence of a regulation mechanism allowing the virus to multiply within the adequate limits so as to avoid that all the cells of the body are infected.

Even if one accepts that another cause of impairment causes the delay in interferon production, it is still troubling that this production can be completed correctly when the two causes are superimposed (viral infection and external cause), in a manner precise enough to keep the number of virions limited to one or a few copies per cell. On the other hand, the hypothesis of a “collaboration” between the cell and the virus fully justifies the presence of such a mechanism, which then appears as a regulatory system rather than a defense system.

Autoimmune mechanisms

The display of certain proteins by cells, which occurs under the influence of interferon (e.g. the p69 protein displayed by pancreatic cells), could have the function of triggering auto-immune mechanisms designed to eliminate cells invaded by excessive quantities of foreign molecules. Thus, letting the virus program the return to integrity of the least affected cells, the immune system would take charge of eliminating the cells that are too severely encumbered and should be replaced. This hypothesis would be confirmed if it could be demonstrated that the display in question is proportional to the concentration of foreign molecules in the cell.

Perfection of virion structures

The construction of perfectly structured virions and their expulsion through the cell membrane is the result of a coordinated action, which is very complex if we consider the mechanisms involved. This action is programmed by the viral genome in a surprisingly targeted manner. It seems less risky to attribute its origin to the cellular genome, which has the necessary mass of information, than to a mutation-selection process at the level of the viral particle. This process can only start when the virus is already able to reproduce itself. Insofar as this reproduction can only take place in the cell, it is difficult to see how the phenomenon could have been initiated.

Conservation of viral information

The fact that the viral information is stored in the cell and hidden, with the possibility of being reactivated, seems more logical if one postulates that it is useful information, allowing the cell to ensure the evacuation of certain harmful molecules, even if it means reactivating the process at the moment when their accumulation becomes detrimental.

The classical view of the virus as a simple pathogen would suggest that virions and their genetic content are totally destroyed after recovery, at least in the most resistant individuals. However, the persistence of viral information actually is the rule.

If it has not yet been possible to identify the factors likely to trigger the reactivation of the viral process, it is perhaps precisely because they involve not only the biological data of the virus and the cell, but also the biochemical properties of molecules whose existence has not been taken into consideration until now.

Bacterial Symbiosis

The bacterial infections that we often see associated with viral diseases could be explained not only by a weakening of the immune system, but by the presence in the circulating masses of foreign molecules rejected by the cells.

Two hypotheses are therefore possible: either these foreign molecules weaken the organism and open the way to bacterial invasion. Or the multiplication of certain bacteria would also be programmed by the viral information in interaction with the genetics of the organism.

This second explanation is not absurd: the foreign molecules whose presence we postulate escape by definition from the mechanisms of assimilation as well as from the vigilance of the immune system, since they have been able to reach the interior of the cells without ambiguity; their elimination thus requires mechanisms which do not belong to the organism itself, for example bacterial enzymes able to degrade the undesirable molecules.

This model of reasoning is in agreement with what we know about the bacterial flora: there too, the organism seems to have been able to “domesticate” bacteria whose enzymes allow it to degrade molecules that escape its own enzymes, for example carbohydrate chains like cellulose.

Thus, the virus would induce not only the processes necessary to maintain intracellular integrity, but also the multiplication of bacteria capable of degrading the waste products rejected by the cells. The apparent pathogenicity of these bacteria could be attributed less to the virulence of particular strains than to an excessive level of target molecules in the circulating masses.


Apoptosis, the process of natural cell death observed, for example, in T4 lymphocytes in the presence of HIV, would have the following meaning in this conception: the virus would program the suppression of lymphocytes in charge of recognizing classes of bacteria, whose enzymes are required to degrade the molecules rejected by the cells, so as to favor the multiplication of these bacteria. The viral genetic information would thus program the transport of foreign molecules out of the cells while bacteries multipliply likely to rid the circulating masses of them on the other.

Under the effect of an exaggerated concentration of target molecules, especially when molecules of the same type are brought in daily by unsuitable food, it would make sense in this hypothesis that apoptosis exceeds the correct limits, and the immune system enters a state of apparent deficiency, letting all sorts of pathogenic elements develop freely.

Autoimmune mechanisms, triggered by the presence of food-borne antigens also bind to lymphocyte membranes, could complicate the phenomenon and aggravate the destruction of these cells.

Difference in evolution

The more or less severe evolution of the viral process in different individuals can be explained by a more or less important accumulation of foreign molecules, according to the different food anamnesis.

The symptomatic form that it takes more regularly in the human species would be due to the fact that the food proper to the civilization has considerably moved away from the primitive food which could have determined the evolution of our genetics, and it is unlikely that in a few thousand years the human organism could have adapted genetically to all the new molecules brought by the agricultural and culinary artifices established since the Neolithic.

A virus as dangerous as SIV hardly causes any symptoms in monkeys living in their natural environment, nor even HIV in captive chimpanzees fed in a natural way. Since the regulation of viral multiplication depends on the presence of foreign molecules in the body, it is to be expected that additional intake of the same molecules through conventional foods would disrupt the process.
According to Burger, the consumption of certain foods by infected subjects during the incubation period would cause an aggravation of the subsequent symptoms, for example in viral hepatitis. From this point of view, it is understandable that the diet prescribed regularly by family doctors to patients with influenza, coryza, hepatitis, etc., has had enough effect to be maintained in the medical tradition.

childhood diseases

The popular wisdom which attributed a utility to the diseases of children, for the majority of viral etiology, is paradoxically justified: the organism equipped with the complements of genetic program brought by the various viruses is better armed against the harmful molecules likely to invade its cells during the existence. This calls into question the fundamental meaning of vaccinations: their usefulness would be to avoid viral invasions that could have serious consequences in the classical food conditions.
On the other hand, if Burger’s hypothesis were to be confirmed, there would be reason to fear that the absence of the genetic complements provided by common viruses would deprive individuals of the mechanisms provided to ensure the maintenance of the integrity of the cellular environment, with the risk of aggravating degenerative processes and compromising various functions of vital importance.

Changes in the biotope

The expansion of certain viral diseases in wild animals can be explained by changes in the environment, the cultivation of cereals or other mutated plants introducing appreciable quantities of new molecules into the natural food environment (proteins produced following mutations in wheat, for example, accumulating in the body of rodents, then in that of the fox, causing the activation of the rabies virus, which was already present before without causing any particular problems). To this could be added the influence of molecules introduced by industrial waste and pollution.


The relative failure of so-called antiviral molecules can be explained by the difficulty of counteracting vital processes programmed by genetic means. The interactions between the viral genome and the cellular genome take place in the cell nucleus and respond to precise mechanisms, so that it is very difficult to inhibit them without harming the cell at the same time. Such processes probably include self-regulatory or substitution mechanisms intended to guarantee their action, the rebellious nature of which may seem paradoxical as long as their biological purpose cannot be defined.

Oncogenic viruses

The case of oncogenic viruses occupies a special place; they may always be harmful. However, the multiplication of cells can be useful for various purposes, if only to compensate for cellular destruction due to some cause. It would therefore also be possible to envisage that these viruses provide useful information to the organism, even if this means that they can lead to disastrous results under the effect of certain co-factors.
The Epstein-Barr virus only manifests itself as a sarcoma in a very small proportion of infected children, and only in Africa. In addition to genetic predisposition, it would be appropriate to investigate, on the basis of Burger’s hypothesis, the presence of certain foreign molecules reaching a particularly high concentration, resulting for example from the dietary habits of young Africans.


As far as HIV is concerned, it has been admitted that almost all infected persons should develop severe symptoms. Indeed, the evidence so far has confirmed that, with very few exceptions, HIV-positive status will result in a fatal outcome. These facts seem to contradict the previous points. However, the same or similar retroviruses have been found in recent years in many wild animals, which do not seem to show any particular symptoms.

The best researchers have come to believe that the pathogenicity of this virus is due rather to some as yet unknown “co-factors” than to the nature of the virus itself.

In Burger’s hypothesis, these co-factors could be the molecules that the virus would be responsible for programming the elimination of, present in much greater numbers in human organisms than in wild animals: the latter feed mainly on natural foodstuffs to which their genetics have been able to adapt since time immemorial, whereas humans regularly absorb traditional foodstuffs that did not exist in the primitive environment, and to which human genetics have hardly had time to readjust.

It is therefore to be feared that certain foreign molecules will have the opportunity to accumulate in human cells at concentrations that have never been reached in the history of the species. The viral processes in charge of programming their elimination, in a primitively silent way, would thus be confronted with an unforeseen situation: the abundance of target molecules would disorganize regulatory mechanisms that ensure their proper functioning and would lead to the appearance of dangerous “opportunistic infections” as a result of an exaggerated multiplication of the associated bacteria.

It remains then to explain why this retrovirus, which was perhaps part of the genetic heritage of humanity without signalling itself, as it is the case in animals, would be suddenly out of the shadow of the cellular nuclei to cause a serious epidemic. Among the reasons to be considered are the changes in eating habits, which have been considerable in the last decades, especially in the Third World countries, where Western eating habits spread quite suddenly, as well as new causes of contagion. Once viral multiplication has been triggered, the virus could only improve its “performance”: the most contagious virions and those causing the most mucous lesions are the ones that multiply preferentially.
In addition, organisms no longer in possession of the virus or in which it was more deeply inactivated, had the time to accumulate a particularly high quantity of target molecules. This would explain the particular violence of the viral process, further increased by the daily intake of foodstuffs carrying molecules of the same classes.

Theoretical and empirical verification.

A new theoretical model, in a field as complex and charged with emotional factors as disease and contagion, can only be verified with sufficient hindsight, through the coherence of the reasoning to which it provides the starting point, and above all through the facts.

Unfortunately, it is not easy to obtain the publication of new ideas not yet endorsed by the scientific corpus, even if it is only a matter of submitting them to the criticism of specialists. Burger therefore invites all interested researchers to criticize his proposed model in the light of their theoretical knowledge, and all practitioners to observe whether the presumed relationships between patients’ diets and the evolution of classical viral diseases correspond to possible predictions. He would be glad if those who observe either significant contradictions or concordances could take the trouble to communicate them to him.

If Burger’s viral model proves successful, it could open up a new avenue of research, especially in the field of AIDS. It would not only be a matter of looking for a vaccine or developing antiviral molecules to deal with the most urgent problems, but also of identifying the molecules of food origin potentially responsible for disrupting the viral process.

Dietary measures applied as a preventive measure could consequently improve the future prospects of current seropositive people. The daily intake of foreign molecules may also play a role in the regulation of the viral process. A correction of the food hygiene could, in this hypothesis, improve the fate of the persons already contaminated, and perhaps limit the evolution of the symptoms even after their appearance.

It is regrettable that no epidemiological research has been done so far to establish the possible existence of a relationship between the dietary history of HIV-positive persons or the daily diet of AIDS patients and the severity of symptoms.

Furthermore, the identification of food-borne xenobiotics could lead to a better understanding of the cause of many dysfunctions affecting metabolism or other functions involving biochemical mechanisms, such as the transmission of nerve impulses, DNA replication, etc. Certain proteins contained in wheat gluten (gliadins) seem to aggravate the symptoms of schizophrenia, various Maillard molecules have been shown to be mutagenic, and there are certainly many pathogenic factors still to be discovered in this field.

In the same perspective, the heuristic proposed by Burger would lead to a more systematic search for food-borne antigens involved in the genesis of autoimmune diseases. The recent discovery of a peptide in cow’s milk, apparently responsible for the reversal of the immune system against the B cells of the pancreas, and opening the way to juvenile diabetes, as well as various experiments on rheumatoid arthritis, improved in some 80% of cases by a diet excluding cow’s milk, wheat and their derivatives, go in the same direction.


Burger et al. propose a model of the viral process that integrates current data from genetics, immunology, virology and dietetics and attempts to bring them together in a coherent theory.

The viruses and bacteria involved in most of the so-called infectious diseases are considered as vectors and partners of genetically programmed symbiotic processes, intended to carry out the elimination of molecules foreign to the functioning of the organism, accumulated in particular in the cells.

The pathological aspect of these processes would come from an excessive concentration of foreign molecules in cells and in circulating masses, mainly linked to an inappropriate food hygiene and the inadaptation of metabolic data to the modifications in eating habits since the Neolithic period.

The systematization of antibiotics and vaccinations, by inhibiting these processes, could contribute to the development of degenerative, auto-immune and cancerous diseases as a result of the accumulation of foreign molecules, antigens or xenobiotics, which could disrupt the biological and immunological functions necessary to maintain health.