Antigen Quotes

The mind likes a strange idea as little as the body likes a strange protein and resists it with similar energy. It would not perhaps be too fanciful to say that a new idea is the most quickly acting antigen known to science. If we watch ourselves honestly we shall often find that we have begun to argue against a new idea even before it has been completely stated.

An antigen is a piece of an enemy that your immune system can recognize.

Neural stem cells are not the only type of living cell therapy being used to treat brain cancer. I’m part of the team developing a kind of anti-tumor immune therapy using what’s called chimeric antigen receptor (CAR)–engineered T-cells.

new influenza virus emerges, it is highly competitive, even cannibalistic. It usually drives older types into extinction. This happens because infection stimulates the body’s immune system to generate all its defenses against all influenza viruses to which the body has ever been exposed. When older viruses attempt to infect someone, they cannot gain a foothold. They cease replicating. They die out. So, unlike practically every other known virus, only one type—one swarm or quasi species—of influenza virus dominates at any given time. This itself helps prepare the way for a new pandemic, since the more time passes, the fewer people’s immune systems will recognize other antigens.

because bureaucracy moves at the speed of an elderly slug.

Chlamydia, today´s most common cause of venereal disease, does the equivalent of hiding in the police station. Schistosomes of the mansoni type go a step further and essentially steal police uniforms. These parasites, a serious cause of liver disease in Asia, pick up blood-group antigens so that they may look to the immune system like our own normal blood cells.

99.4% communicability, he thought. It played insanely over and over in his mind. And that meant 99.4% excess mortality, because the human body couldn’t produce the antibodies necessary to stop a constantly shifting antigen virus. Every time the body did produce the right antibody, the virus simply shifted to a slightly new form. For the same reason a vaccine was going to be almost impossible to create.

99.4% communicability, he thought. It played insanely over and over in his mind. And that meant 99.4% excess mortality, because the human body couldn’t produce the antibodies necessary to stop a constantly shifting antigen virus. Every time the body did produce the right antibody, the virus simply shifted to a slightly new form. For the same reason a vaccine was going to be almost impossible to create. 99.4%.

The CRISPR-based tests developed by Mammoth and Sherlock are cheaper and faster than conventional PCR tests. They also have an advantage over antigen tests, such as the one developed by Abbott Labs that was approved in August of the plague year. The CRISPR-based tests can detect the presence of the RNA of a virus as soon as a person has been infected. But the antigen tests, which detect the presence of proteins that exist on the surface of the virus, are most accurate only after a patient has become highly infectious to others.

Herd immunity may never be achieved because high vaccination rates encourage the evolution of more severe disease-causing organisms “A partially effective immune response — enough to exert selective pressure but not effective enough to suppress escape viral mutants — is the most effective driving force of antigenic variation.” Rodpothong P, Auewarakul P. Viral evolution and transmission effectiveness. World J Virol 2012 Oct 12; 1(5): 131-34. In theory, if enough people are vaccinated, herd immunity will be achieved and chains of infection will be disrupted. In reality, a true herd immunity threshold may never be reached within normal heterogenous populations. If a true herd immunity threshold level is achieved, it will create a strong selective pressure that encourages the emergence of mutant viral strains.

Perhaps it is in this respect that language differs most sharply from other biologic systems for communication. Ambiguity seems to be an essential, indispensable element for the transfer of information from one place to another by words, where matters of real importance are concerned. It is often necessary, for meaning to come through, that there be an almost vague sense of strangeness and askewness. Speechless animals and cells cannot do this. The specifically locked-on antigen at the surface of a lymphocyte does not send the cell off in search of something totally different; when a bee is tracking sugar by polarized light, observing the sun as though consulting his watch, he does not veer away to discover an unimaginable marvel of a flower. Only the human mind is designed to work in this way, programmed to drift away in the presence of locked-on information, straying from each point in a hunt for a better, different point. If it were not for the capacity for ambiguity, for the sensing of strangeness, the words in all languages provide, we would have no way of recognizing the layers of counterpoint in meaning, and we might be spending all our time sitting on stone fences, staring into the sun. To be sure, we would always have had some everyday use to make of the alphabet, and we might have reached the same capacity for small talk, but it is unlikely that we would have been able to evolve from words to Bach. The great thing about human language is that it prevents us from sticking to the matter at hand.

Autoimmune Disease—the “Leak” in Your Gut Autoimmune diseases are a disaster and there are no good medicines available (steroids work, but the treatment is worse than the disease). They’ve been around for centuries, but there’s been a clear uptick in the last fifty years. Why? Two hypotheses have been proffered to explain it: the barrier hypothesis (our skin or lungs are letting in antigens) and the hygiene hypothesis (we don’t eat dirt and are too hygienic). But in fact, in the gut, they’re the same thing; because the gut is the dirtiest place in the world—one hundred trillion bacteria to have to fend off at all times—you don’t need an intestine, you need a fortress. We’ve known for a while that leaky gut is akin to chinks in the walls of that fortress. Antigens, like enemy soldiers, escape through those chinks into the bloodstream, where T cells and antibodies react against them. But in a case of mistaken identity, these immune cells then accidentally identify parts of your body as foreign invaders and generate an immune response to kill them off, a process termed molecular mimicry. Then there are two new twists. First, it appears that one autoimmune disease, called ankylosing spondylitis, produces antibodies to a gut bacterium called Klebsiella pneumoniae. Conversely, a different autoimmune disease called rheumatoid arthritis produces antibodies to a second gut bacterium called Proteus mirabilis. Now, this might not seem that earth-shattering, but recent work has shown that the refined carbohydrates in processed food feed those two bacteria in particular, and that carbohydrate restriction improves both of these diseases. Indeed, a low-sugar, high-fiber Mediterranean diet has been shown to be efficacious at prevention and treatment of rheumatoid arthritis. Furthermore, introduction of fiber to the diet appears to improve asthma (frequently an autoimmune disease), likely by improving gut function and reducing inflammation.

Inflammation, which you know by now is the cornerstone of many brain disorders, can be initiated when the immune system reacts to a substance in a person’s body. When antibodies of the immune system come into contact with a protein or antigen to which a person is allergic, the inflammatory cascade is provoked, releasing a whole host of damaging chemicals known as cytokines. Gluten sensitivity in particular is caused by elevated levels of antibodies against the gliadin component of gluten. When the antibody combines with this protein (creating an anti-gliadin antibody), specific genes are turned on in a special type of immune cell in the body. Once these genes are activated, inflammatory cytokine chemicals collect and can attack the brain. Cytokines are highly antagonistic to the brain, damaging tissue and leaving the brain vulnerable to dysfunction and disease — especially if the assault continues.

Indications of spermatic firepower are evident in the differences between a man’s first spurts and his last. A human ejaculation typically consists of anywhere from three to nine spurts. Researchers who somehow managed to capture “split ejaculates” for analysis found that the first spurts contain chemicals that protect against various kinds of chemical attack. What sort of chemical attack? Aside from leucocytes and antigens present in a woman’s reproductive tract (more on that later), they protect the sperm from the chemicals in the latter spurts of other men’s ejaculate. These final spurts contain a spermicidal substance that slows the advance of any latecomers. In other words, competing sperm from other men seems to be anticipated in the chemistry of men’s semen, both in the early spurts (protective) and in the later spurts (attacking).

Part One—The Lipid Panel. Used to evaluate heart health, this panel comprises of four biological markers representing the four types of fat found in the blood—triglycerides, total cholesterol, high-density lipoprotein (HDL), and low-density lipoprotein (LDL). Two additional measures of cardiovascular health, homocysteine and c-reactive protein (CRP), may also be measured as part of a more comprehensive profile. These two labs are discussed in Part Six, “Optional Tests” (see page 8). •  Part Two—The Basic Metabolic Panel. The labs used to evaluate metabolism measure blood sugar regulation, electrolyte and fluid balance, and kidney function. Biomarkers included in this panel are glucose, calcium, sodium, potassium, blood urea nitrogen (BUN), and creatinine. •  Part Three—The Hepatic Function Panel. This panel determines how well your liver is functioning by measuring levels of different proteins produced and processed by the liver, like albumin and globulin, as well as liver enzymes. •  Part Four—The Complete Blood Count (CBC) Panel. The lab values measured in the complete blood count (CBC) panel include red blood cells, white blood cells, platelets, and hemoglobin. Maintaining healthy levels of these biomarkers affect your vitality and energy, immune system, and cardiovascular health. •  Part Five—Hormones. Although they are not always included in a routine blood test, hormones should be periodically tested, especially in aging adults. Hormones such as estrogen, testosterone, progesterone, DHEA, and prostate specific antigen (PSA) play an integral role in reproductive wellness and affect other aspects of health. Maintaining balanced levels can slow down the aging process, for instance. Hormones involved in metabolism, like the thyroid hormones and the stress hormone cortisol, are also discussed in this section. •  Part Six—Optional Tests. This final part of the book highlights four tests—homocysteine, c-reactive protein (CRP), vitamin D, and magnesium—that are not typically measured unless requested, or if a standard blood test shows an abnormality that requires a more in-depth analysis. These tests can provide a more complete picture of heart health, immunity, calcium absorption, blood sugar regulation, and a number of other vital processes.

REFERENCE RANGES FOR PROSTATE-SPECIFIC ANTIGEN Total PSA (ng/mL) Category 4.0 to 10.0 High 0.0 to 4.0 Normal

The body uses a code system called the HLA (human leukocyte antigen) system, which works in a similar fashion. It gives a code to all surfaces. Immune cells basically identify surfaces. Everything has a surface, whether it is your own cells, a microorganism, or a piece of food. When your immune system scans the interior surfaces of your body, it compares each to a list of approved codes, the ones it classifies as “self.

After the antivaxxers’ claims that the MMR vaccine caused autism were debunked, they argued that the thimerosal in vaccines caused autism. After this was debunked, new claims surfaced that the cause was the vaccines being given too close together and too early, somehow shocking a child’s immune system and resulting in autism. This, too, was debunked. Science shows that even though the number of shots has risen over time, the actual load on the immune system has decreased because today’s vaccines are better engineered. Before 1991, the whooping-cough vaccine had three thousand different antigens. Today’s whooping-cough vaccine has no more than five particles—just as effective, but much easier on the immune system. After the “too many, too soon” myth was debunked, antivaxxers began claiming that the MMR vaccine was “triggering” autism in children who were somehow genetically predisposed to it. That, too, was debunked.

ERV envelope genes possess unique properties that make them suitable for use in forming the placenta: they are fusogenic proteins and they have immunosuppresive properties. Eutherian (placental) mammals distinguish themselves from nonplacental animals in the ability of the female to nurture the fertilized ovum and growing embryo within the body. The placenta is a transient tissue of embryonic origin whose evolution made it unnecessary to partition the embryo into a protective egg, which matured outside the mother's body. It serves two purposes for the maturing embryo: it is a conduit for respiratory gasses and nourishment supplied by the mother, and it provides an environment of immune tolerance. The fetus is necessarily half-foreign tissue, an allograft within the mother. It draws half of its genetic, and hence antigenic, identity from maternal and half from paternal genes. If the fetus is to mature within the mother, it must be isolated from the maternal immune system such that a graft-versus-host response does not reject it. The placenta forms early after implantation of the embryo. Syncytins mediate the formation of a continuous fused layer of cells around the embryo, isolating it from the mother, yet allowing essential nutrients to traverse from the mother's system. Although the observations on human syncytin-1 and -2 were compelling, it was left to scientists to definitively link syncytins to placental formation by studying mice. Here two syncytins (dubbed A and B) from murine ERVs were implicated, and genetic experiments with mice defective in these genes confirmed that their dysfunction disrupted placental formation. Notably, however, syncytin-A and -B were not syntenic with the human syncytins. That is, the human and mouse genes are not descended fron common ancestral syncytins; they have arisen by separate ERV gene capture events from different families of ERV in human and mouse ancestors.

The basis for the potential of all virolytic therapeutics resides in the exquisite selectivity they exhibit for infecting and killing cancer cells. The very nature of cancer cells makes them extremely susceptible to virus infection: they divide in an uncontrolled fashion and are metabolically hyperactive, thus they exhibit greatly diminished capacity for apoptosis and innate immune defense against virus infection. While normal cells reduce metabolic activity, activate apoptotic signaling pathways, and block cell cycle progression in response to virus infection, cancer cells remain oblivious. These are perfect conditions for the growth of viruses, particularly those that are attenuated for growth in normal cells. Consequently, oncolytic viruses are specific reagents that target cancer cells and spread from cell to cell within tumors. It has become apparent that the direct lytic effects of viruses on cancer cells is just one element of their therapeutic effects, the cytolisis of infected cells releases viral and cellular antigens that can provoke anti-tumor immune responses, and some cancer therapeutic viruses are engineered to deliver additional genes such as immune activators to augment these effects.

There’s a curious correlation between these sunspot peaks and flu epidemics. In the twentieth century, six of the nine sunspot peaks occurred in tandem with massive flu outbreaks. In fact, the worst outbreaks of the century, killing millions in 1918 and 1919, followed a sunspot peak in 1917. This might just be coincidence, of course. Or it might not. Outbreaks and pandemics are thought to be caused by antigenic drift, when a mutation occurs in the DNA of a virus, or antigenic shift, when a virus acquires new genes from a related strain. When the antigenic drift or shift in a virus is significant enough, our bodies don’t recognize it and have no antibodies to fight it—and that spells trouble. It’s like a criminal on the run taking on a whole new identity so his pursuers can’t recognize him. What causes antigenic drift? Mutations, which can be caused by radiation. Which is what the sun spews forth in significantly greater than normal amounts every eleven years.

Two methods of testing for a leaky gut include the lactulose-mannitol test, and the Intestinal Antigenic Permeability Screen by Cyrex Labs.

When an antigen is to blame for stimulating an autoimmune attack, an immune panel of tests may show both the TH-1 and TH-2 cytokines are high and T-suppressor cells are low. This indicates the body is currently in a heated battle against something the immune system recognizes as an enemy, which is stoking the autoimmune mechanism. Another essential immune panel measures the ratio of T-helper cells to T-suppressor cells. This is the CD4/CD8 test (CD4 measures T-helper cells and CD8 measures T-suppressor cells). Typically when an autoimmune disease such as Hashimoto’s is being driven by an antigen response, the CD4/CD8 ratio is above 2. If follow-up tests of the CD4/CD8 ratio show it lowering, then you know the approach you’re using is having an effect.

Monitoring and Supporting Hashimoto’s ​• ​After Hashimoto’s is assessed with a positive TPO and/or TGB serum antibody test, establish TH-1 or TH-2 dominance with an immunological serum test. Look at the percentage values, not the total. ​• ​A TH-1 serum profile includes interferon, IL-2, IL-12, interferon-gamma, and TNF alpha. ​• ​A TH-2 serum profile includes IL-4, IL-13 and IL-10. ​• ​If the TH-1 cytokines are high, then modulate the autoimmune condition by supporting the TH-2 pathway with TH-2 stimulators. ​• ​If the TH-2 cytokines are high, then support the TH-1 pathway with TH-1 stimulators. ​• ​A CD4/CD8 (T-suppressor cell/T-helper cell) ratio of 2 or higher is an indication that an active antigen is driving the autoimmune response. This test is also a baseline from which to monitor overall progress. ​• ​If an active antigen or hapten is at work, then stimulate the dominant TH pathway to eradicate the antigen or drive it into remission. ​• ​If both TH-1 and TH-2 stimulators make you feel worse, a hapten may be driving the autoimmune condition. In that case, restore the immune barriers. ​• ​In all instances, modulate immune T-helper cell response with therapeutic doses of emulsified vitamin D plus cofactors, fish oil, and liposomal glutathione and superoxide dismutase cream. Have a licensed healthcare practitioner qualified to work with vitamin D therapy prescribe the appropriate dose. ​• ​Add in nutritional compounds individually every three days to monitor response. ​• ​Remove gluten and possibly dairy from the diet and support other systems, organs, and functions in the body.  (Managing blood sugar, digestive function, and adrenal health using functional medicine principles is explained in later chapters.) ​• ​Monitor whether support is effective with follow-up TSH, CD4/CD8, and TH-1 and TH-2 cytokine tests.

an algebraic expression. [GEOLOGY] denoting the uppermost soil horizon, especially the topsoil. the human blood type (in the ABO system) containing the A antigen and lacking the B. (with numeral) denoting a series of international standard paper sizes each twice the area of the next, as A0, A1, A2, A3, A4, etc., A4 being 210 × 297 mm. 2 a shape like that of a capital A: [in combination] an A-shape. 3 [MUSIC] the sixth note of the diatonic scale of C major. The A above middle C is usually used as the basis for tuning and in modern music has a standard frequency of 440 Hz. a key based on a scale with A as its keynote.

The word 'vaccination' comes from vacca, the Latin word for 'cow'. This is a poignant recapitulation of the history of vaccines. The first vaccine properly so called had, as its active ingredient, the cowpox virus, a close relative of smallpox that however was much less likely to cause severe, disfiguring or lethal disease. Edward Jenner observed that milkmaids, who were often exposed to cowpox, suffered a relatively mild disease, but would be immune to the much more serious smallpox. In an experiment that would unlikely pass muster in the modern world, he infected James Phipps, then an 8-year-old, with cowpox. He suffered a mild and transient illness, but when he was later exposed to scabs from a smallpox patient, he proved immune. Unlike the earlier practice of variolation, which has been practised in late Song dynasty China that sought to induce the cutaneous form of smallpox, variola minor, to protect against the more severe forms of smallpox (variola major), Jenner's vaccination used a less pathogenic virus. He relied on what would later be called 'antigenic similarity', but which was at the time hardly understood.

In the traditional approach to making a vaccine, the antigens are cleaved off the virus that you’re targeting, a tactic that requires scientists to isolate proteins on the surface of the virus.

Influenza was a terrible, yet fascinating foe. It was one thing the first time you met it, and something completely different the next. It liked to mutate, was almost designed to do so. Every time it replicated in a cell, there was a slight mutation in the antigens on the surface of the virion. But it was bizarre for the virus to have changed so radically in so short a time. It was almost as if a new strain of the flu had been introduced—from where, though, could it have come? Steve

The carriers of the altered genes must have come into contact with an antigen that triggered the production of a virus, until that moment dormant in their DNA. Even now, now that she had all the pieces, Carmen could still hardly believe it. It was too terrible, too cruel. It made no difference to the children's suffering〰they would have succumbed immediately, passing the virus on to the others before they died. Holly was the one who was going to suffer. She would see it as her fault: the direct consequence of her desire for healthy offspring. All that terrible suffering, all that black putrification and agony, flowing from her loins.

When antigenic shift occurs, strains crop up bearing a totally new hemagglutinin spike, and sometimes also a new neuraminidase molecule, that most people have never encountered. As a result the virus may evade the antibody repertoire carried by all populations around the globe and trigger a pandemic. In today’s jet-linked world, people can spread a dangerous new virus from one part of the earth to another in a day. Such a drastic metamorphosis cannot occur through simple genetic mutation. The best-studied process leading to antigenic shift involves the mixing of two viral strains in one host cell, so that the genes packaged in new viral particles (and their corresponding proteins) come partly from one strain and partly from the other. This reassortment can take place because the genome, or genetic complement, of the influenza virus consists of eight discrete strands of RNA (each of which codes for one or two proteins). These strands are easily mixed and matched when new influenza A particles form in a dually infected cell. For instance, some influenza viruses infect both people and pigs. If a pig were somehow invaded by a human virus and by a strain that typically infected only birds, the pig might end up producing a hybrid strain that was like the human virus in every way except for displaying, say, a hemagglutinin molecule from the bird virus.

What specially excited him when his graduate student Daniel Linzer, who did the original experiments, showed him his results was that the rogue protein occurred in large quantities in the SV40-infected cells, suggesting it must be doing something important, and that it was interacting specifically with the viral oncogene, large T antigen. What’s more, his team had found exactly the same protein also in uninfected fetal cells.

Somatic hypermutation gives rise to B cells bearing mutant immunoglobulin molecules on their surface. Some of these mutant immunoglobulins have substitutions in the antigen-binding site that increase its affinity for the antigen. B cells bearing these mutant high-affinity immunoglobulin receptors compete most effectively for binding to antigen and are preferentially selected to mature into antibody-secreting plasma cells. The mutant antibodies that emerge from the selection do not have a random distribution of amino-acid substitutions. The changes are concentrated at positions in the heavy-chain and light-chain CDR loops that form the antigen-binding site and directly contact antigen. As the adaptive immune response to infection proceeds, antibodies of progressively higher affinity for the infecting pathogen are produced – a phenomenon called affinity maturation. Affinity maturation is a process of evolution in which variant immunoglobulins generated in a random manner are subjected to selection for improved binding to a pathogen. It achieves in a few days what would require thousands, if not millions, of years of classical Darwinian evolution in a conventional gene. This capacity for extraordinarily rapid evolution in pathogen-binding immunoglobulins is a major factor in allowing the human immune system to keep up with the generally faster-evolving pathogens.

Fasting followed by a vegetarian diet has a favorable influence on disease activity in some patients with rheumatoid arthritis. This effect cannot be explained entirely by psychobiologic factors, immunosuppression secondary to energy deprivation, changes in the plasma concentration of eicosanoid precursors, or changes in antibody activity against dietary antigens. Changes in disease activity were found to be associated with concurrent alterations in the fecal microflora and in the antibody activity against P. mirabilis. These findings may indicate that the beneficial effect of dietary treatment is caused by alterations in the microflora secondary to changes in the diet.

Every result converged on the same conclusion: the transforming principle was composed of DNA. The discussion section of the article outlined the genetic context of their findings, using similar terms to their Rockefeller Institute report from earlier in the year: The inducing substance has been likened to a gene, and the capsular antigen which is produced in response to it has been regarded as a gene product.

suffer from rheumatoid arthritis and find that fasting so effectively removes the antigen/antibody complexes from your body's tissues that you may he pain-free, possibly for the first time in

The RAG [(Recombination-Activating Gene)] genes [which assist in the facilitation of V(D)J recombination] lack the introns that characterize eukaryotic genes. In this unusual feature they resemble the transposase gene of a transposon, a type of genetic element that can make and move copies of itself to different chromosomal locations. The essential components of a transposon are a transposase—an enzyme that cuts double-stranded DNA—and regions of repetitive DNA, called the terminal repeat sequences, that are recognized by the transposase. These two features allow the transposon to be excised from one location and inserted into another. The similarity of the RAG recombinase to a transposase has led to the hypothesis that the mechanism now used to rearrange immunoglobulin and T-cell receptor gene segments originated in a vertebrate ancestor with the insertion of a transposon into a gene encoding a receptor of innate immunity. The inserted transposase genes evolved to encode RAG proteins, and the terminal repeat sequences evolved to become the recombination signal sequences for the first rearranging gene segments. During this evolution, the transposase gene and the long terminal repeats of the transposon were separated and became components of different genes, both expressed specifically in lymphocytes. Today, the human RAG genes are on chromosome 11[,] and on four other chromosomes are the much-expanded sets of rearranging antigen-receptor genes.

The majority of genes in the [MHC (Mean Histocompatibility Complex)] class I region are not involved in the immune system; neither do the class I genes form as a compact cluster as the class II genes. Whereas genes encoding class II molecules are only present in the class II region of the HLA [(Human Leukocyte Antigen) complex], genes encoding class I molecules and related class I-like molecules are found on several different chromosomes. A further difference is that HLA class II molecules are dedicated components of adaptive immunity that serve only to present antigen to T cells, whereas HLA class I and class I-like molecules encompass a broader range of functions, including uptake of IgG in the gut, regulation of iron metabolism, and regulation of NK [(Natural Killer)]-cell function in the innate immune response. Together, these genetic and functional differences show that MCH class I is the older form of MHC molecule and that MHC class II evolved more recently from MHC class I. Consistent with this proposition, MHC class II is not always essential for a vertebrate immune system, unlike class I. The Atlantic cod manages very well with only MHC class I genes.

The tests fit the production code like an antibody fits an antigen.

Viral capsid antigen (VCA)-IgM. The presence of these IgM antibodies indicates a recent infection with EBV. VCA-IgG. The presence of these IgG antibodies indicates a past infection. Epstein-Barr nuclear antigen (EBNA). These antibodies will develop 6 to 8 weeks after being infected initially with EBV, and will remain detectable for life.

The elderly tend to get fewer colds than kids, even though they have a weakened immune system. This happens because our systems develop defenses against antigens; we acquire antibodies to the germs we’ve defeated in the past (stored in plasma cells in your bone marrow, as mentioned earlier in Chapter 6), and destroy those antigens and viruses before they can multiply and cause that illness.

Censoring Measuring response rate and progression offers more problems than measurement error. We may not be considering the right denominator of patients. In 2017, the FDA approved the first cellular cancer therapy, called tisagenlecleucel (Kymriah, Novartis), or CAR-T, for short. A CAR-T is a chimeric antigen receptor T-cell, basically a genetically modified cell taken from a patient that is trained to attack cancer cells and then placed back in the patient. In the data submitted to the FDA, 88 patients had the cells removed, but 18% (16/88) did not receive the cells because some patients died and some patients’ cells could not be manufactured.17 Unfortunately, the FDA excluded these patients from the denominator and assessed response only in patients who got the cells. This violates a principle called intention to treat, that is, you should judge a drug based on all patients allocated to get it, irrespective of whether or not they received it. Why? Because therapies that take a long time to give (this CAR-T took approximately 22 days to make) may exclude the sickest patients who die while waiting, thus distorting their benefit. In fact, if I have a patient in my office and we decide to treat with tisagenlecleucel, the response rate from the package overestimates her chances of success, as I am unsure she will live long enough to receive the cells.

Dr. Bill Hamilton, among others, has contributed to research showing that the nitrogen bubbles are treated as invaders by the body’s immune system, which mounts a complex and not fully understood systemic defense. Part of the immune defense involves the creation of nitrogen-specific and helium-specific antigens—antigens are the marker cells that attach themselves to invading viruses and bacteria, targeting the invading cells for destruction. Even after a person recovers from the bends, specific inert-gas antigens lurk vigilant in the body against a future bubble attack.

RNA viruses mutate relatively quickly, and many, like influenza, are able to undergo a process known as antigenic drift, by which the virus is able to alter the surface antigens that are the targets of our antibodies—thus evading our existing immunity. Some viruses, like measles, cannot change their genomic sequence in ways that substantially alter enough of their surface proteins, so measles remains susceptible to our vaccines or the immunity that we get from prior infection. However, for viruses like influenza, as their surface proteins undergo change, the virus is able to dodge the protective antibodies that we’ve developed from past infection or vaccination

Antigenic shift generated the deadly 1918 influenza virus and the swine flu outbreak of 2009.

By 2021, lateral flow tests, also known as rapid antigen tests (RAT) started replacing the PCR as a purported SARS-CoV-2 detection tool. As explained by Dr Mark Bailey, these tests had no more capability than the PCR to detect an imagined virus or diagnose

What accounts for this great diversity running through our veins? The struggle for survival entails not only the competition for resources and mates but also the battle against pathogens. In this immunological arms race, the blood group antigens of human populations have coevolved with a microscopic world of enemies (as well as allies and neutral parties). Natural selection shapes the human immune system by favoring the configurations best adapted to a population's environment.

In 1922, a fourteen-year-old boy with type 1 diabetes was resuscitated from a coma—born anew, as it were—by the infusion of insulin extracted from the pancreatic cells of a dog. In 2010, when Emily Whitehead received her infusion of CAR (chimeric antigen receptor) T cells, or twelve years later, when the first patients with sickle cell anemia are surviving, disease-free, with gene-modified blood stem cells, we are transitioning from the century of the gene to a contiguous, overlapping century of the cell.

isoantigens—antigens within the same species.

process called cytokine storm. It’s when the body’s immune system senses the virus antigens and then goes berserk, releasing a bevy of extraordinarily damaging hormonelike proteins.

After it defeats an infection, specialized white cells (called “memory T cells”) and antibodies that bind to the antigen remain in the body. If any invader carrying the same antigen attacks again, the immune system responds far more quickly than the first time. When the immune system can respond so quickly that a new infection will not even cause symptoms, people become immune to the disease.

Pandemics generally develop only when a radical change in the hemagglutinin, or the neuraminidase, or both, occurs. When an entirely new gene coding for one or both replaces the old one, the shape of the new antigen bears little resemblance to the old one. This is called “antigen shift.

The Spanish Flu pandemic of 1918 was a myxovirus. It killed twenty million people. Viruses mutate every few months. The antigens on their surface change so that they’re unrecognizable to the immune system. That’s why seasonals are necessary.

But the virus, even as it lost some of its virulence, was not yet finished. Only weeks after the disease seemed to have dissipated, when town after town had congratulated itself on surviving it—and in some places where people had had the hubris to believe they had defeated it—after health boards and emergency councils had canceled orders to close theaters, schools, and churches and to wear masks, a third wave broke over the earth. The virus had mutated again. It had not become radically different. People who had gotten sick in the second wave had a fair amount of immunity to another attack, just as people sickened in the first wave had fared better than others in the second wave. But it mutated enough, its antigens drifted enough, to rekindle the epidemic. Some places were not touched by the third wave at all. But many—in fact most—were.

As I wrote in my original report, “we have learned the immune system is not static, it changes with age according to environmental toxins, infections, and vaccinations. Vaccines are immunotherapy. That is, they are designed to alter the immune response to an antigen/infection. We have long recognized that the reasons some individuals react badly to immunotherapies, including vaccines, while the majority of people who are treated/vaccinated do not, has much to do with the recipient’s genetics and the status of the recipient’s health and immune system at the time of administration of the immunotherapy/vaccination.”12

Vaccines also lower the diversity of the microbiome and contain ingredients (see appendix B), such as glyphosate, that make the gut lining more porous. They also shift the immune response to a predominant antibody-producing mode. Once the gut microbiome is altered and the gut lining becomes porous, large macromolecules that should never have access to the bloodstream begin to show up in the blood. This antigen exposure provokes an antibody response from the person, shifting them even further into a dominant antibody- producing mode. At that point, we have an imbalanced immune system prone to creating excessive inflammatory reactions directed against its own tissues.

Una Palabra Acerca de los Exámenes de la Próstata (PSA) El Dr. Thomas Stanley, profesor de urología en la Escuela de Medicina de la Universidad de Stanford desarrolló la prueba de sangre del Antígeno Específico de la Próstata (Prostate Specific Antigen, PSA, por sus siglas en inglés) en los años ´80s. Recientemente, en una conferencia médica, él hizo el siguiente anuncio: "Necesitamos reconocer que el PSA no es ya más un marcador para cáncer de próstata. Originalmente pensamos que estábamos haciendo lo correcto, pero ahora estamos intentando descubrir cómo nos equivocamos".

Yet from 1975 to 2007, breast cancer rates increased by one-third and prostate cancer rates soared by 50 percent. Widespread screening with mammography and the prostate-specific antigen (PSA) test played a significant role in detecting these cases, making direct comparisons difficult. Still, we clearly have a problem. Almost 1.6 million people were diagnosed with cancer in 2011.12 When have Americans ever waged such a long, drawn-out, and costly war, with no end in sight?

Second, there are vaccines which contain killed micro-organisms. These vaccines may contain an intact (but dead) organism or a sample pack of specific antigens.

Beyond the towers of Antigen Bay, the other floating cities of the Moveable Feast mingled in sunset glamor.

Antigen drift can create epidemics. One study found nineteen discrete, identifiable epidemics in the United States in a thirty-three-year period—more than one every other year. Each one caused between ten thousand and forty thousand “excess deaths” in the United States alone—an excess over and above the death toll usually caused by the disease. As a result influenza kills more people in the United States than any other infectious disease, including AIDS.

Instead of injecting an antigen & adjuvant as with traditional vaccines, Moderna plugs a small piece of coronavirus genetic code into human cells, altering DNA throughout the human body and reprograming our cells to produce antibodies to fight the virus. MRNA vaccines are a form

pandemics are lethal. Antigen shift guarantees that the new virus will infect huge numbers of people, but it does not guarantee that it will kill large numbers. The twentieth century saw three pandemics. The most recent new virus attacked in 1968, when the H3N2 “Hong Kong flu” spread worldwide with high morbidity but very low mortality—that is, it made many sick, but killed few. The “Asian flu,” an H2N2 virus, came in 1957; while nothing like 1918, this was still a violent pandemic. Then of course there

In addition to antigenic drift, there is a larger change that the flu virus can undergo, antigenic shift, and that’s how we get our flu pandemics. During this shift, viral proteins assume an entirely new structure, and the virus is said to be “novel.” These novel viruses—which most often arise when animal and human viruses share and swap their genes—are like entirely new criminals, not old ones in disguise. This makes them sneakier, more prolific, and perhaps more deadly. Antigenic shift generated the deadly 1918 influenza virus and the swine flu outbreak of 2009.

One more thing makes influenza unusual. When a new influenza virus emerges, it is highly competitive, even cannibalistic. It usually drives older types into extinction. This happens because infection stimulates the body’s immune system to generate all its defenses against all influenza viruses to which the body has ever been exposed. When older viruses attempt to infect someone, they cannot gain a foothold. They cease replicating. They die out. So, unlike practically every other known virus, only one type—one swarm or quasi species—of influenza virus dominates at any given time. This itself helps prepare the way for a new pandemic, since the more time passes, the fewer people’s immune systems will recognize other antigens.

One way to conceptualize antigen drift is to think of a football player wearing a uniform with white pants, a green shirt, and a white helmet with a green V emblazoned on it. The immune system can recognize this uniform instantly and attack it. If the uniform changes slightly—if, for example, a green stripe is added to the white pants while everything else remains the same—the immune system will continue to recognize the virus with little difficulty. But if the uniform goes from green shirt and white pants to white shirt with green pants, the immune system may not recognize the virus so easily.

Exposure to stress can also be a form of strength building, which is what chemists call hormesis.32 The purpose is to build resistance to that stressor, as when a doctor gives us vaccines with low amounts of antigens to build up our immunity, or we strain muscles to fatigue in order to build them back stronger.

Although many gene-therapy protocols are now being actively explored, one of the most exciting and widely covered in the media is genetically enhancing the ability of a person’s T cells, white blood cells that play an essential role in the body’s natural immune response. In CAR-T therapy, blood cells are extracted from the body of a person with specific cancers and then engineered to boost the ability of their T cells to express a chimeric antigen receptor (CAR) before being put back into the person’s body with cancer-fighting superpowers.

Carcinoembryonic Antigen (CEA),