INDUCED REMISSION THERAPY - CHACHOUA SAMIR

Title:

INDUCED REMISSION THERAPY

Document Type and Number:

WIPO Patent Application WO/2004/024129

Kind Code:

Abstract:

The application relates to methods for treating a patient suffering from a disease selected from: (i) cancer; (ii) autoimmune deficiency syndrome; or (iii) heart diseasesaid treatment comprising inducement of remission by a mechanism selected from the group consisting of- G) encapsulation of a foreign biological substance, (ii) inducing metabolic immunity or elimination, (iii) tagging an undesired cell or other biological substance with an antigen different than that of said undesired cell or biological substance, (iv) inducing mutation of an undesired cell or biological substance, (v) administering an intracellular vaccine, (vi) administering cysteamine, or (vii) administering BCG.

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Inventors:

CHACHOUA SAMIR (AU)

Application Number:

PCT/IB2002/005427

Publication Date:

March 25, 2004

Filing Date:

September 10, 2002

Export Citation:

Click for automatic bibliography generation Help

Assignee:

CHACHOUA SAMIR (AU)

International Classes:

A61K31/131; A61K35/74; A61K39/00; A61P9/00; A61P31/18; A61P35/00; (IPC1-7): A61K31/131; A61K35/74; A61K39/00; A61K39/04; A61K45/00; A61P9/00; A61P31/18; A61P35/00

Domestic Patent References:

WO1997011666A2	1997-04-03
WO1997011667A2	1997-04-03
WO1997033615A2	1997-09-18
WO1993006832A1	1993-04-15

Foreign References:

AU6941196A	1997-04-17
US5756666A	1998-05-26

Other References:

MCSHANE H.: "Prime-boost immunization strategies for infectious diseases", CURRENT OPINION IN MOLECULAR THERAPEUTICS, vol. 4, no. 1, February 2002 (2002-02-01), pages 23 - 27
LETVIN N.L. ET AL.: "Prospects for vaccines to protect against AIDS, tuberculosis and malaria", JOURNAL OF AMERICAN MEDICAL ASSOCIATION, vol. 285, no. 5, February 2001 (2001-02-01), pages 606 - 611
HIROI T. ET AL.: "HIV mucosal vaccine: nasal immunization with rBCG-V3J1 induces a long term V3J1 peptide-specific neutralizing immunity in Th1- and Th2-deficient conditions", THE JOURNAL OF IMMUNOLOGY, vol. 167, 2001, pages 5862 - 5867
LEUNG N.J. ET AL.: "The kinetics of specific immune responses in rhesus monkeys inoculated with live recombinant BCG expressing SIV Gg, Pol, Env and Nef proteins", VIROLOGY, vol. 268, 2000, pages 94 - 103

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INDUCED REMISSION THERAPY EXPERIMENTAL AND THERAPEUTIC PROTOCOIS @ followire de@cribtion of mechanisms, theoires and applications are provided under strlct tlX*, t'gA'pt t J 3ltl contidentiallty to provide a guideline of information for future discussion and application. INTHODUOHON Induced Remission Therapy is a science developed by Dr. Sarnie Chachoua. The sclence t tt 4 ;, j tis ; S tN"? (. tf f>} 1 W§\< ?, { ;. s. 4i (. ; iY. lfl set i ?., í, (J t ! Ws (, ?} I eqcupsulates multiple modalitles but will focus specifically on vaccine applications in both the prevention and heatment of cancer, AIDS and heart disease. Although the mechanisms in treating all three condifions overlap, and regeneration of normal tissue is a trequent side effect, the mochanisme are best seen when discussing cancer and AIDS. So these will form the bull of our discussion. The human body is made from a conglomaration of cells types, each with delined function and purpose. However, at come time in the evolution process, many of these cells were distinct entities of independent function.We speak of immune response as being entirely composed of while blood cells, phagocytes, neutrophils, etc. However, in IRT, we recognize at least two other immune mectanism dedicated elther to a primitive function which maintain residual activity or to the survival of the organism as a whole. These two phenomena described by Dr. Chachoua are those of encapsulation and immune metabolism Other distinct entitles which also must be considered are those which maintaip genetic mtegrlly and intracellular immune response. INCAPSULATION MFCHANISMS Hssue colle are capable of encapsulating foreign invaders both singly t ! n,) s most common example would be one of abscess formation. Where while celt, and stromal cells such as fibroblasts encapsulate invading infections, to prevent both the spread and localize them for amounting immune response. Intracellular encapsulation can also be seen to occur in viral diseases such as herpes. The virus is known to dwell in nerva endings along the demtatomes. However, in the mirror reflection of conventional ways of thinking, one can see that it is possible that it is not the virus invading the nerve but nater the nerve acting as @ @@@@@@@@@@ @@@@ @@@@@@@ which drags the viras into itself and successfully encapsulates it in a specific location. Conventional immune mechanisms are clearly inept at eliminating this disease and were the nerves not to absorb it, the virus could spread throughout the body and kill its host. A subsequent infection usually triggers herpes relief, so this would indicate that healthy cells have difficulty absorbing and/or restraining more than one infection at a time. When confronted with a high voturno or invaders, tissue dtenuon and swelling may occur along with cellular hypertrophy. The most obvious of these mechanisms can be seen in fat cells. Fat cells encapsulate infections and provide an immune barrier to their spread. They even play a role in the management or cancer and other diseases. At a certain age or at a time when fat becomes saturated with a particular infectious agent or toxic condition, it becomes increasingly difficult to lose, particularly where a metabolic immune respose (see below) is absent. Fat as an immune shield can be seen to house both bacterial and cancer-related antigens in peritumor tissue and reflect its function in terminal disease stages, i.e., AIDS and cancer, where fat loss, muscle loss, and even neurologic degeneration immediately precede death. These are not as a result purely of increased calorie demande but rather represent the failure of the last lines of immune defense. ror breast function of fat as an armor immune shield can be seen in the different survival rates for breast cancer in men and women. Men with their lower breast fat content will suffer much more rapid cancer cell growth and spread. Fat cells even play an important role in antigen and disease fragment processing and expression. It is for that reason that localized fatty necrosis can result in response to the introduction of eluptious and or infectious agents. It is also for this reason that hairy tumoral fat tissue can form an excellent base with the preparation of anti-cancer vaccines. Multiple biopsies and cultures have also demonstrated the presence cf irlfecí : lous diseases such as the infect : ious diseases such as bacteria and viruses between and within fatty cells. In an otherwise healthy individual, vaccination or treatment aimed at these encapsulated agents can lead to fat loss and normalization of weight. This even holds true for circulating fat and cholesterol. These agents deposit on the inside of aged arteries where an infection has corrupted the lining, again this is an attempt to encapsulate a foreign invader. Encapsulation mechanisms and the metabolic immune response can work both together or independently, but an excess of one can relieve the demands or diminish the activity of the otter.

Metabolic Immune Response mai) rmal understanding of this is associated with hyperthermia, i.e. fever which is seen as a main component of immunity; however, in IRC metabolic immunity refers to the capacity for rapialy dividing tissue to limit and or consume a foreign invader. Metabolic immunity is activated strongly under three main parameters: 1. Overwhelming volume of invader or irritant 2. Multiple forms of infection or invader 3. Where no precise or specific immune response is present at the time of the attack Other situations necessitating metabolic immune activation where encapsulation mechanisms hall or are overly taxed, in summary encapsulation occurs where the threat is localized and either slow growing of low volume or unable to trigger, effective immune response. Encapsulation can then function to hold the disease until the standard immune mechanisms of the predator and humoral immunity can be activated, often at a sacrifice to some of the encapsulating cells. The metabolic immune response is simply explained in a car and petrol analogy where the petrol is the invader, the faster the car is run, the quicker the breakdown of the invader. Conventional immune theory falls to explain why disease breakdown occurs even from initial lecocystosis i.e. why non-specific rapid increase in the number of white blood cells should limit the growth of the virus or bacteria when none of these cells were designed for that purpose. The reason is that rapid, non-specific cellular division still provides matabolic immunity Another failure in conventional theory is that of memory cells charging to the rescue and producing protective antiserum. This process takes at least two weeks to manifest during which time an infection could easily take hold. We known, however, that there is resistance to the measles or mumps regardless of the presence of circulating antibodies. IT is possible that residual antibody levels are maintained against a few surviving microbial particles which escape the metabolic and classical onslaught only to become encapsulated. Encapsulation therefore both provides a method for restraining small numbers of possibly less virulent organisms as well as enables their antigens to maintain an antiserum and long-term immune awareness. Survival of an organism in some formats enables both immune awareness as well as a situational double jeopardy, where cells already infected can not again be infected upon second exposure. Classical examples of the above are SSPE, which is subacute sclerosing panencapilitus with measles and chicken pox, which can subsequently express as shingles. One feature of the metabolic immune response is that at least one cellular clone will overwhelm others in its growth rate and capacity and will dominate by its affinity for the characteristics and behavior of the invading agent.

Cancer Cells For over 200 years, infections have been associated with cancer. Modern scientists study the phenomena with such detail and bias that they often miss the obvious. In studying spontaneous remission, Dr. Chachoua noticed what had seemed to be a paradox, that being that patients undergoing spontaneous remission often did so in response to an acute infection, whereas often the same infection in its chronic form could be found to cause cancer. There have been reports of measles and syphilis for example in their acute form causing cancer to melt away and yet in the chronic form actually initiating the cancer. How can the same agent both cause and reverse a malignant transformation? The answer becomes clearer once we stop thinking of cancer as a mindless animal and begin thinking of it in terms of the above mentioned immune responses. If an infection is aggressive and acute it may initiate a metabolic immune response either in cancer or more likely in surviving fragments of the immune response. Once rapid cell growth consumes whatever it was that initiated the cancer, the cancer cells suicide and melt away. However, in chronic cases of infection wheter disease volume is large and progress over a long time have exhausted normal immune coping mechanisms from where cancer cells are generated to encapsulate the disease and mitigate or slow down its spread.

What is a Cancer Cell? A cancer cell has often been thought to be the result of a random mutation. This explanation fails for many reasons, most obviously random mutations should behave in a random way. However, a cancer of a particular type in thousands of people of different races, geographic locations and environmental factions will almost always behave in exactly the same way. For example, bowel cancer of a certain kind will exhibit simllar growth patterns and virtually identical areas and times of spread, regardless of particulars of the host carrying it. Cancers also tend to occur in clusters of age groups, again making the idea that they are randorn mutations scientifically silly. Cancer cells can spread through the blood-brain barrier, in characteristic only shared by white blood immune cells. Cancer cells were found to be powerful immune stimulants by Simon Roosenfelt at NCl. Cancer cells produce powerful "anticancer compounds" such as intraserum. Cancer cells carry specific information for metastases and for drug resistance. When a cancer is eliminated, another kind will often arise in its place. Cancer can be caused by so many different agents that it is again, scientifically foolish to believe that smoking, radiation, and viruses can all cause identical genetic random mutations. Cancer is not a disease, it is a preprogrammed cellular response to disease. Every cell contains this programming and it does not take advantage of a weakened immune response but rather usesits capacity for encapsulation, metabolic elimination, and disease attenuation to supplement a weakened immune response. Cancer as an evolutionary pathway With the increased incldence of cancer, there has been a gradual increase in human life expectancy. The decline in fetal bacteria and viral infections did not begin with antibiotics, vaccines, or hygiene but is the mirror image of the increase in cancer incidences. The capacity for cells to undergo malignant change eriables them to achieve a sustained, long-term metabolic immune response as well to contain and weaken more than one agent at a time. This feature of cancer has long been used to eluate or weaken aggressive viruses in the making of vaccines. Dr Chachoua isolated may agents from cancer cell extracts capable of inhibiting and destroying infections. When one thinks of the rapid rise of AIDS in accident victims and hemophiliacs needing frequent transfusions, somehow medicine missed noticing another group that required frequent tranfusions but which seemed resistant to catching AIDS, the cancer patients. If one ever had doubts that cancer can exert a protective action against rapidly fatal infection, all doubt should have disappeared with ethically questionable experiments done in the earlier half of the last century. Hundreds of cancer patients were injected with deadly and aggressive infection in an attempt to poison or kill off the cancer cells. Where these modalities often failed to cure the patient, they surprisingly also failed to kill him of their own accord. The importance of this is dramatically demonstrated when one realizes that the agents used included smallpox, tetanus, Nile encephalitis and other agents, which killed several of the doctors and nurses administering them, but failed to damage the cancer patients. Even the famous doctor Colley found it very difficult to infect cancer patients with his initial preparations. When the patients eventually succumbed to their cancer, autopsy showed that the deadly infections were housed within and perfectly encapsulated by the cancer cells and tissue and that the presence of the cancer prevented the spread to any healthy tissue. Cancer is fatal over months or years, but these infections would have been fatal in hours.

Cancer cell genetics are fluids and capable of surviving in chaos. This means that they can house several infections and toxic agents and remain alive. Under ideal circumstances, cancer cells probably only arise for a short time to hold and restrain an invader until the appropriate immune response can be generated for its elimination. In a classic experiment done by Dr. Chachoua, tetanus, injected into rats would not kill them if cancer cells were injected along side. Actually if the infection followed the cancer inoculation by up to two or three weeks, neither the cancer nor the infection resulted. However, if after a defined time period no appropriate immune response was mounted against the infection, the cancer would grow and encapsulate, otherwise it seemed to be functioning, at least in part, as an incredibly sophisticated necrophage. Cancer cells in plants clearly display this immune ability Crown- Gall Disease arises when agora bacterium tumesascines Infects a plant and donates its plasma into the plant cells and this additional genetic information brings about a malignant change which encapsulates the bacteria and stops it from spreading, unless the cancer is cut into and the bacteria spreads, the cancer then follows it and the plant dies, covered with multiple cancer nodules. Mathematics and statistics often support both illusions and delusions in medicine and inherently requires suspension of logic and common sense. For example, if a kangaroo can be taught to jump upon hearing the command "jump," and then has its legs amputated, statistics can support the conclusion that a kangaroo whith both legs amputated canot respond to the "jump" command because amputation of its legs renders it deaf. One logical consequence of cutting out the large bulk of a person's cancer is that the person should then live a significantly longer time; however, cutting into a cancer often accelerates the person's demise as well as disease spread. Again, statistics try to explain that cancer growth rate is exponential so anything less than 99,99% clearance will result in more than a week's respite. However, statistics canot explain an acceleration of the disease process. When one begins to think of cancer as an immune response (chemotherapy and radiation may sterilize the diseased area leading to destruction of cancer cause and a few cures), on can understand that destruction of the cancer shield with out obliteration of the cause of disease can result in increased disease spread with the Crown-Gall above. Another dramatic demonstration of cancer being a therapeutic response is that extraction of cancer and its preparation as an injectable extract will often extend the life span of the animal, how can injecting more cancer into an animal actually extend its life, if the cancer is not therefore by definition a therapeutic response? If one reviews old literature regarding cancer, there are clues that if we look beyond the malignaant and destructive characteristics, one can see an encapsulation phenomenon.

MORE OBSERVATIONS In the presence of other cells capable of lapid growth and therefore capable of exerting the metabolic immune response, cancer cells will often revert back to their normal cell or stem cell origins. If an acute infection stimulates rapid white cell growth or an immune response against the cancer cause, cancer often will result. Similarly if cancer is implanted next to rapidly growing tissue like the regenerating stump of a salamander's arm, or the notocords of the developing embryo, cancer will chage back into normal cellular structures. MEANING In both cancer and AIDS therefore the major pathology lies within the affected cell. Cancer cells to the outside body do not express encapsulated diseases for more than a short time window after which the bulk of cellular disruption and distinguishing features occurs in its nucleus and cytoplasm. The internal was waging within a cancer is activity to which the outside body can be completely bild. With cancer, as with AIDS, the inner cellular disturbances must be addressed for the disease to resolve. Even a powerful anti-HIV immune response has recently been shown to facilitate entry of virus into cells and to be totally ineffective against its DNA genome. In studying long term survivors, and high risk but AIDS' resistant groups, one feature which stands out is the presence of, or the capacity for, the host to develop autoimmune disease.

Autoimmune disease results from an immune response that can penetrate cells without disrupting their integrity, but attach to and destroy intracellular structures. Rather than being in itself the cause of pathology, the immune response is augmenting or at least in Dr.

Chachoua's view, correcting the cell's inability to directly deal with intracellular pathology.

Mechanisms that every healthy cell has to destroy foreign invaders seem to be lacking in autoimmune disease, and the body appears to be responding to an agent such as a retro virus, as in the case of CAEV in goats, by generating an antiserum to deal with the foreign pathogen. As in the case of malaria and thalassanemla, disease appears to confer an evolutionary advantage. Even where the trait exists, the capacity to generate an intracellular immune response, as well as a metabolic immune response (both heat and increase metabolic activity characters and other inflammation characteristics can be seen chronically in autoimmune diseases) can provide protection against infection that can bypass the ordinary lysosome, riboneucleases as well as other particules described by Dr. Chachoua and illustrated in the accompanying electron microscopy photographs representing byrosomes and proteasomes. These represent a new class of intracellular organelle or mechanisms under the broad heading of pathosomes, occasionally acting as phagosomes, but which appear to assemble in an area surrounding invading particules, as well as enzymes and other agents used in their assembly, and release a digestive mechanism which destroys the offending agent and absorbs its components. These vaculoes then appear as empty vesicles. Such structures have been seen but not fully identified in some malignant tissue as well.

OTHER CLUES As with the obvious resistance autoimmune disease seems to confer when studying statistics, there is another group of patients who show resistance to viral diseases and even prion diseases such as Mad Cow Disease. In the early 80s, when blood transfusions were not properly monitored or tested for AIDS, many hemophiliacs and car accident victims contracted and succumbed to the disease; however, there is another group of patients who regularly need blood transfusions who did not register a significant increase in AIDS infection, and that was the cancer patients. This appeared to reinforce Dr. Chachoua's earlier observations where cancer protected animals from deadly infections such as tetanus and even work in the early half of the last century where doctors attempted to infect cancer with very aggressive viral diseases including small pox without therapeutic success and abandoned the work and data as useless without noticing perhaps the most important finding in their study, that being that virtually none of the cancer patients succumbed to the deadly infection, although several of the administering medical staff did. Infections were almost always found perfectly encapsulated within the cancer mass at autopsy. We have been scientifically naive in assuming that this observation reflected the cancer's ability to be easily, passively infected, as opposed to attributing an active immune function such as that seen in the plant's model or which can be seen in certain animal models where cancer metastases toward a specific infection.

The animal model is particularly impressive when one considers that Crown Gall transformation occurs after the bacterium donates its phage to the surrounding plant cells, and the same can be found to happen in cancer cells which contain phages of both bacteria and microbe bacterial.

Pryon diseases have killed hundreds over the past few decades and the latest BSE outbreak it again is worth noting, that although one in three of the general population suffer from cancer, not one of the victims of Mad Cow Disease was reported to have cancer. Again, the recent Scientific American (July 2001) article suggests a strong relationship between Pryons and metastases.

Tying a Little Together It seems that to deal with infections and other pathogens the body can resort to intracellular mechanisms, and where they are deficient intracellular antibodies and perhaps where minimal antigen exists or targets cannot be immunologically neutralized, such as untagged pryons, or even where more than one agent can overwhelm a healthy or an autoimmune cell, a malignant cell may develop to accommodate more than one threat at the same time. Cancer can maintain both metabolic and encapsulation immune responses and can survive with genetic chaos. Where cells that are healthy and need to maintain their genetic integrity, can only deal with a limited number of insults at the one time. The liquidity needed and present in a cancer cell enables unraveling of DNA strands and activation of multlple sites that would not be possible or synonymous with survival in an ordered healthy cell. This aspect of cancer can be seen, not only with it being the cell of choice in attenuating viruses for vaccines but even historically in that it was the only cell capable of surviving HIV infection long enough to yield a positive titre in-vitro. Cancer cels can develop as last ditch defenses and they upset other immune responses that may in themselves be lethal. Researchers Molmot and Podam discovered a common leucopenia virus which they named after themselves. The M-P virus could destroy cancer cells but in the wake of it doing so, the patient would succumb to immune fluid accumulation in their lungs and other areas. It is as if a more deadly agent was released in the destruction of cancer. Interestingly, M-P pathogenicity only caused death when cancer destruction followed, or seen in another way, the presence of cancer protected the patient against an otherwise lethal infection.

Application of Theory A class of viruses similar to M-P and retro viruses, including the feline panleukopenia virus and CAEV and other retro viruses, can all interfere with HIV replication. This could be by the phenomena of viral interference or by direct competition for HIV assembly and metabolic pathways. The risk of this or any other viral therapy in the treatment of AIDS; however, is both with using a live pathogen to treat the immuno suppressed or even the more scary possible that donation of characteristics of these new agents could render HIV more aggressive or more transmittable.

HIV infected cells overwhelm the intracellular immune mechanisms of destruction at least in part by inserting into the DNA matrix and appearing to be part of the cell. The suppression of the intracellular responses against pathogens, while similar in effect to what occurs in cancer cells, renders HIV infected cells even more susceptible to Dr. Chachoua's tagging mechanisms. Tagging Therapy A cancer cell cannot be outwardly recognized by the immune response as pathologic. All of its sinister actions and mechanisms are hidden within it; however, a cancer cell that is infected with a readily recognizable agent such as measles or mumps, will express these antigens on the cell surface for a short time period, usually two to three weeks. These agents then become entrapped and enclosed within the next generation of cancer cells, and although present within the cancer cell, no longer multiply and express their antigens on the cancer cell surface. This therefore gives a limited time window for the immune response to rush in and attack the tagged cancer cell, while the invaders' antigen shine like beacons on its surface.

However, once the invader is subjugated by the cancer and antigens ceased expressing on the cancer surface, the immune system again becomes blind. Dr. Chachoua developed several ways with dealing with this limitation.

1. Optimize immune response within time window By the use of transfer factors an occasionally inactivated vaccines against the tagging agent, prior to the tagging, Dr. Chachoua can optimize and plan for optimum immune cell and antiserum levels at the time when cancer expresses the agent's antigens. If optimum immune response occurs within three or four weeks, for example, Dr. Chachoua may prime the immune system two weeks prior to insertion of the tagging agent. This would allow for optimum expression and optimum immune responses to occur simultaneously leading to a large cancer cell kill. Tagging agents, where their single DNA are in A strands or more complex fragrnents, or even whole viral or other microbial entities, will express with a gradience hundreds of times greater in cancer cells because of the lack of the cancer's ability to activate the standard intracellular immune responses.

2. Extending the Window This method of delaying maximum viral expression and maximum immune response largely relies on cortisone administration and is designed to allow large levels of viral expression to occur, but has never shown therapeutic potential in the past, and can easily overwhelm a patient and further immune suppress them. 3. Passive Immunity Administration of a ready antiserum response or even and other genetically matched white cells specifically targeted against the tagging agent can yield a large amount of disease destruction, even if the patient themselves cannot raise a sufficient response. 4. Reactivation Of the Tagging Agent Under certain situation, the tagging agents may be reactivated. In the case of a virus for example, other viruses which may not even be related can trigger their reappearance as can other infections. For example, it is common for cancer patients to suffer herpes and shingles outbreaks. These classically represent, or have been portrayed as outbreaks subsequent to immune suppression. These outbreaks, however, represent the failure of the encapsulation immune mechanism or of viral reactivation. Interestingly, the outbreaks do not occur at the point of the greatest immune suppression but rather at the time of large cancer breakdown.

Dr. Chachoua noticed that cancer patients who had recently suffered a viral infection would yield high levels of that virus upon cancer breakdown. A 40-year-old lady suffering from bowel cancer had late onset measles at age 36. When therapy commenced and cancer cells broke down, the patient had a measles relapse, four years earlier. This is significant as immune cells which would have dealt decisively with the measles virus earlier in life were probably depleted at her age, and so the encapsulation mechanism needed to be heavily relied on.

5. Use of Other Agnets Conventional agents, radiation, chemotherapy and hormonal agents may find greater results when combined with a cancer cell weakened both by tagging and by an appropriate immune response.

Mutation inhibition Despite a cancer cell's genetic fluidity, certain agents can bind in the genetic matrix and minimize a cancer cell's ability to deal with other insults, such as other modalities of thereapy.

A very applicable example is in Dr. Chachoua's patent application where prior phage infection of a bacterium can not only lead to direct bacterial destruction but upon possible synergy between phage and bacteria, the synergistic phage or that lysogensed prevents infection by another phage which may carry genetics needed for antibiotic resistance for example. Thereofre, combining phage with antibodies will severely restrict bacterial mutation to therapeutic resistance, as would insertion of microbial agents or fragments thereof into cancer cells, restrict their ability to mutate resistance to chemo or other therapy.

6. Reactivation By Tagging Agent In this scenario, the not-quite dormant initial tagging agent can be used to rebuild fragments from a secondary tagging agent. Secondary tagging is even more specific than primary tagging, as only the cancer cells which carry the first agent will be able to receive and rebuild the secondary tagging agent. These consecutive generations of tagging both allow for increases in the windows of opportunity as well as repetition for windows of opportunity, as even the primary tagging agent may be reassembled once the cell is carrying the other viruses or microbes that can reassemble it. Very precise tagging can occur particularly where more than one agent is needed to reassemble the new vaccine. Cancer cells now begin to express and can be made to express a large range of antigens, either simultaneously or in succession.

Cancer in its untagged form can even be used as a vaccine as a number of these cells will no longer reduce threshold inhibition. The use of multiple windows of opportunity also minimizes the chances of threshold inhibition of the immune response. Some cancer cells may come with their own identified viral agents which can be used to reactivate tagging mechanisms. APPLICATION TO AIDS With HIV infection, the cell lacks intracellular mechanisms of pathogen destruction, and in essence has already received its primary tagging agent. Unfortunately, the immune responses elicited by this virus are either ineffective or deficient. There have been reports that an anti- HIV antiserum may actually promote viral infection. And of course, viral mutation or dormant existence of virus can easily bypass both immune and pharmacologic mechanisms of treatment. Of the above scenarios, viral reactivation offers the best and most focused therapeutic option. The presence of HIV allows fragments from a wide range of retro viruses to be reassembled by HIV machinery. Fragements of FPLV can be reassembled and yield powerful antigens for immune destruction of HIV infected cels which attract an immune response both resistant to HIV and which can also act overwhelmingly in a rejection reaction against CAT-related antigens. An antiserum from people exposed to this virus or this vaccine can be used to optimize the windown of opportunity as referred to above. However, in the case of CAEV, is a virus that has shown itself to be innocuous in humans, as many farmers are exposed to it. Not only it their antisera high in anti retro viral activity and capable of inhibiting HIV on its own, but it can be dramatically augmented an directed when HIV infected cels are tagged with CAEV fragments. Forcing HIV to reassemble the goat virus enables not only broad spectrum rejection, but also alerts the immune response as well as directs the passive response towards cells where HIV is lurking in VHATEVER MUTATIONAL FORM AND EVEN IN STATES OF DORMANCY. Even where the virus is dormant, its assembly mechanisms will be able to reintegrate fragments of CAEV into a whole and even where the virus is dormant, HIV infected cells have their intracellular responses inactivated sufficiently to allow for preferential infection with the tagging mechanism, both in fragments and in its entirety. A system based on the above therapy would be as follows: PARAMETERS HIV infected individuals PCR greater than one million, T-cell counts greater than 200, failing conventional therapy (this protocol can be used with conventional therapy because of mutation inhibition capacity to optimize results, but for the purposes of this trial will be used as a sole agent). Agents to Be Used Fragmented CAEV / inactivated FPLV Antisera to the above Antisera to the above obtained from exposed humans general population Antisera to the above from exposed individuals with rheumatoid arthritis or other autoimmune disease Sera from general autoimmune pool The sera are IGG fragments close to Rh factor band Method Patients are injected or otherwise administered with inactivated viral fragments as above. PCR, T-cell, and electro microscopy monltoring every day. Within a two week period, upon viral reactivation, a dense body will appear in the cell nucleus or the cell cytoplasm. Any of the agents representing the passive immune responses above can then be tested with dramatic drop in viral count and increase in T-cells to be expected.

Discussion The above mechanisms can demonstrate efficacy both in-vitro and in-vivo. Design protocols for in-vitro efficacy are simple and initial in-vitro work was summarized by Dr. Duvas in her paper of 1996 over which there continues to be a legal battle with the inventor, Dr. Chachoua.

However, it is important that the risks of viral reassembly and viral interference be recognized.

USC subsequently filed a patent on this technology which betrays a lack of knowledge of mechanisms and dangers. Although Dr. Chachoua's initial patent application preceded theirs by several years, while his case has been bitterly fought in court, USC have managed to get its patent granted along with its inherent dangers. Rather than use inactive agents to be reactivated by the HIV infection, they propose to use CAEV as a living agent to prevent HIV infection. The use of any retro virus, because of its similarity to HIV, as a prevention for AIDS is folish as the same reactivation mechanisms that have been explained above can be used by a non-infective or damaged dose of HIV particle fragments to attain target infection upon reassembly by the supposedly protected vaccine.

Other Aspects of Protocol On U.S. soil, it is possible to carry out trials where specific antisera fragments are used in the treatment of AIDS infected individuals. The use of specific fragments from IGG pooled can attack external arrtigens, whereas internal antigens can be targeted by antisera fragments from autoimmune disease.

Intracellular Vaccine A modification of "subtraction vaccines," where healthy cells are disrupted with antiserum ralsed against them being used to separate out pathologic fragments from disrupted disease cells as per the Rand vaccine have usually failed in human trials, as the immune responses raised against the pathologic fragments could not penetrate the cell's structure in which they reside. The range of vaccines, both active and passive, with antisera raised in animals with autoimmune type disease can be used to target not only the disease but all enzymes and intermediate structures contained within the cell leading to a biological super-immune response In summary, defined tagging and antisera agents are available which have shown efficacy in both cancer and AIDS treatment. The above overview is suggested to initiate discussions with Harvard University for specific designing of protocols and testing under full confidentiality to be funded by and the results of which to remain the property of Dr. Samir Chachoua.

Other Agents for Testing Part of the preparation of the broad spectrum vaccine described above is the raising of human antisera against non-infected T-cells (with subsequent isolation of anti-HIV infected sera from wilpi lab arimals, infected humans, sub-sets of sera from patients with autoimmune disease and/or wit h antisera is available for speclfic and controlled suppression of transplant rejection and could facilitate transplant protocols for AIDS patients. Current modalities for immune suppression are broad spectrum and could be deadly. f :"i : l'1 (1r"/t ? ; efrt' ; jUs 1Cilts Could antibiotic preparations from cultures with tagging capacities can be easily assayed for both in-vitro and in-vivo anti-HIV and anti-cancer acitvity. As can cancer cell extracts and liquids which overlap and mimic much of the intracellular immune response, as wel as other agents that suppress cancer cell infections. Protocols Readily Empolyable to U.S.A. 1. Supplements Crude autibiotic cuiture preparations are capable of both tagging viral disease as well as providing strong antiviral activity. Although induced Remission Therapy includes multiple agents isolated from tumor cells and fluid, such agents are likely to require further definition and would be much more difficult to readily incorporate in human testing. Crude antibiotics preparation; however, can be provided with supplements as many are sourced from food type origins. Supplementation of the crude cultural extract one leaspoon three times a day have 2.. maza and formulations can be manufactured under GMT conditions and formulations can be , provided upon signing of confidentiality agreement. 2. MFA Cysteamine was first proposed by Dr. Chachoua in the treatment of AIDS because of animal trials that showed reversal of T4/T8 imbalance in animal lupus models as far back as 1982. Cysteamine can both interfere with viral replication as well as act as an immune stimulant. Cysteamine may also increase permeability and facilitate entry of antisera, in order to further inhibit additional infections which may aggravate the progress of AIDS, Dr. Chachoua recommends the addition of BHT mutilated hydroxy toluene in as high a concentration as 1% per volume of dietary intake or at least into 500 milligrams TDS. These levels are inhibitory to herpes viruses as well as other microbiological diseases. A huge range of food preservatives have had both their efficacy and safety established over many years and can be used for long- term control of both disease and opportunistic infections. Other useful agents include ethoxyquin, BHA, NDGAA, hydroxa amine hydrochloride. Preservatives and disinfectants . ; and formulations can be manufactured under GMT conditions and formulations can be provided upon isgning of confidentiality agreement. 2. MFA Cysteamine was first proposed by Dr. Chachoua in the treatment of AIDS because of auimal trials that showed reversal of T4/T8 imbalance in animal lupus models as far back as 1982. Cysteamine can both interfere with viral replication as well as act as an immune stimulant. Cysteamine may also increase permeability and facilitate entry of antisera, in order to further inhibit additional infections which may aggravate the progress of AIDS, Dr. Chachoua recommends the addition of BHT mutilated hydroxy toluene in as high a concentration as 1% per volume of dietary intake or at least into 500 milligrams TDS. These levels are inhibitory to herpes viruses as well as other microbiological diseases. A buge range of food preservatives have had both their efficacy and safety established over many years and can be used for long- term control of both disease and opportunistic infections. Other useful agents include ethoxyquin, BHA, NDGAA, hydroxa amine hydrochloride. Preservatives and disinfectants have maintained antimicrobial efficacy for many years. Combinations can be tailored for safe administration and mixtures with antisera or with biological metabolites or catalytic agents can facilitate precise targeting and safety.

3, Monoclinal Antibodies These have long been used for lagging targets and for specific delivery of therapeutic agents. f3. imitation lias always been in their ability bo bind to antigens that are often weak on the tir) e protocols is the isolation of monoclinal antibodies from autoimmunepatients and/or laboratory animals with autoimmune type immune responses. Alternatively, cells from these sources can ils immotal to produce high yields of monoclinal amibodies which can be raised against and be effective against intracellular structures. Intracellular antisera is both highly selctive in its sole of. or powerful and highly specific. If is also possible to direct them through speciflc cell junctions or receptors. Intracellular antisera mono or polyclinal represents a new generation in oit radioactive agents for direct delivery in the heart of the cells being targeted. 4. Shuctura) Therapeutics A range of antibiotic agents as referred to above and immune sera as referred to above can I ouf target antigen or organism or metabolic condition such as fiuid Ph., within the farget cell. This leads to a structural disruption and breakup of the disease cell. This crystallization and ouf physical pathways being incorporated into the one therapeutic and provides double mechanisms against which mutational resistance is unlikely to develop. off read Spectrum intra and Extra Cellular Sera Even in the absence of specific frageting, this broad spectrum antibiotic and antisera praparation (registered in latin America as Universal Antibiolic) can provide both immediate and long lenn therapeutic effexet in chronic disease treatment, inflammatory disease treatment and AIDS.

6. BCG Protocols A readily applicable tag and antisera protocol using agents available in the United States involves the use of a powerful immune stimulant.

Introduction BCG is a powerful immune stimulant, preventive against tuberculosis, anti-cancer agents in common use against bladder cancer. As tuberculosis often occurs in AIDS patients, BCG vaccination would make a logical preventative measure. The above concepts and agents in combination with this preventative measur could yield an effective therapeutic method.

Method Administration of BCG by multiple puncture in AIDS patients, T-cells 150 or above, PCR greater than 500,000. Immune stimulation by weekly punctures or other agents in the absence of active viral replication (controlled as above or by conventional means) enables an uninfected supply of T-cells to be generated. Altematives such as cross-matched T-cells transfusions protected by tagging agents or antisera can also be used but are unlikely to be as ; successful as the patient's own. Application of broad spectra antisera with intracellular components will potect the newly formed cells from infection as would many of the aforementioned tagging agents. transfusions protected by tagging agents or antisera can also be used but are unlikely to be as successful as the patient's own. Application of broad spectra antisera with intracellular components will protect the newly formed cells from infection as would many of the aforementioned lagging agents. After three weeks of initial BCG application, BCG lysates can be introduced into the body.

These will be reactivated and their antigens expressed only within HIV infected cells (as would other bacterial lysates). This would yield a strong immune resuit targeted at HIV infected cells.

Discussion Priming the immune response with BCG and subsequent targeting of desired cells with BCG lysates will give a powerful therapeutic response. A third arm to this equation could be added by providing a passive vaccine against BCG once the AIDS infected cells have been targeted. This passive vaccine would ideally contain both intra and extra cellular antisera components.

As BCG is already FDA approved and would form a reasonable part of prophylactic treatment of AIDS patients and as fragments thereof in lysates would be easy to both produce and use, and as obtaining intracellular anti-BCG antisera by BCG vaccination of patients with autoimmune disease would not be considere unethical, this protocol should be one of the easiest to initiate and evaluate.

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