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
Howewer, 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 medecine 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 satelittes 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 satelittes 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 inhability 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.
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 symtoms 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 notwitstanding.
Suprisingly, after a viral invasion, and in spite of defence
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.
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).
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 : oxydation, free radicals
combining with other molecules, hetrocycles caused by the heating
of unsatured 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.
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 medecine - at any rate, when it comes to humain
beings (MALTZMAN, 1981), (ZHDANOV, 1974).
In this connection, Burger notes that virtually all viral
diseases present with discharges : phlegm, perspiration, rashes,
diarrheoa, gravid waters, over secretion of skin oils, specific
body odours 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 differeing
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 comissioned 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 incorpating 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.
What follows appears to agree with what is already known about viral processes and draws them together into a neat summing up.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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 isjeopardized 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.
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 defence mechanism
as the classical model would have it. Should such a mechanism
of defence 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.
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.
The assembly of fully strutured 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 ?
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.
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, paaving the way for bacterial
invasion,
- or the swarm of particular bacteria is beiing 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.
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.
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
headcolds, hepatitis, a.s.o., has been effective enough to endure
in the medical tradition.
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.
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.
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 substition techniques to secure changes that will defy therapy unless, and until, their biological purpose is explained.
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.
As for HIV, virtually anyone contamined 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 unrivalled 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 overexpansion
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 contries
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, oganisms that no longer harboured
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.
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 contamined
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 disfunctions 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, ther 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 rhumatoid arthritis with 80 % of cases experiencing
relief for patients eating a dairy- and wheat free diet.
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 molecuules, 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.