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Theories of Hepatitis B as Guides in Treatment
Diagram of EDTA clawing on hepa B virion; take note of negative charge that binds with the positive charge of virion
Structure of hepatitis B
Hepatitis B virion becomes alive in a live host cell, inserting genes and replicating as host cell divides into two daughter cells
Theories in hepatitis B that explain, point out flaws and a new method of treatment
Hepatitis B is a serious disease. It is even more dangerous than acquired immunodeficiency syndrome (AIDS). Both are caused by virus. Hepatitis B is caused by hepatitis B virus. AIDS is caused by the human immunodeficiency virus (HIV).
Hepatitis B virus (HBV) causes inflammation of the liver, cirrhosis and liver cancer. Some symptoms are jaundice, fatigue, nausea, and stomach pain
Several theories are involved in hepatitis B. We will elaborate each. Then we will show:
1. why some treatment or cures are not effective,
2. some flaws in standards,
3. a new effective method of treatment.
By theory we mean: concepts and relationship(s) among concepts that had been verified true (Einstein, A. Ideas and Opinions. 1954). Einstein was a theoretician in nuclear physics.
In doing science, we have what is called theoretical and experimental. In theoretical, we use concepts and relationships formulated by other scientists that had been proven. In experimental, we conduct experiments to verify hypothesis. A hypothesis is a scientific guess used as guide in conducting experiment. It also consists of concepts and relationship(s) among concepts. Once these concepts and relationship(s) are verified true the hypothesis is true. Then it graduates into a theory. Put another way, a theory is a hypothesis that is verified true. Here, we will use results of experiments done by other scientists or doctor of medicine.
While we are dealing with a scientific subject we will try to use layman’s language.
Theory one. The hepatitis B virion consists of a double-stranded helical deoxyribonucleic acid.
The concepts are “hepatitis B virion” and “deoxyribonucleic acid.” The relationship is “consists.” (Virus is plural, virion is singular.)
Deoxyribonucleic acid (DNA) is a heredity material that contains the information code. This code, transmitted by the ribonucleic acid (RNA) controls the making of protein. Proteins make up a cell, Cells make up a tissue. Tissues make up an organ. Organs make up a person. In short, information codes, as transmitted by RNAs, translate into a person. There are trillions of information codes found in DNA of a human being. An information code consists of three nucleotides in sequence. (My Hub “Criminals can neither fool nor escape from DNA fingerprinting” gives more details on information code).
We emphasize the partnership between DNA and RNA. They work together, DNA alone will not translate into a cell. RNA alone will not translate into a cell.
We will not elaborate in more detail the nature of DNA or RNA. Suffice it to say that viruses are either DNA or RNA like hepatitis A. A virion is neither alive nor dead, according to our present criteria of what is alive or dead. They do not need food to stay potent.
In a sense the hepa B virus, being DNA, is more powerful than RNA virus. It contains DNA that largely controls the nature of new hepa B virus. It also has a large effect on the transformation of the chromosomes of the host cell. It commandeers the RNA of the host cell.
A virion is very small; it cannot be seen by the naked eye. Light particles used by the eyes cannot strike its surface because a light photon is larger than the virion. Photons curve away from the surface of virion. Its size and shape can be constructed with the use of electron microscope, the electron being smaller than virion thus strikes it. There are over 50 trillion copies of hepa B virus in a teaspoon of blood.
Prevention. The base hosts of virus are fowls and pigs. Their virus that had mutated attack humans. In 1997, thousands of chicken in Hong Kong were incinerated to prevent the spread of H5N1 flu virus. (See picture below). Hepa BV are transmitted by blood, shared wash clothes, nail clippers, razors, and body fluid.
Theory two. The immune system reacts to hepa B virion as a foreign body.
Virus attack plants and animals. We talk of humans here. The body considers hepa B virion as a foreign body to which the immune system reacts. The immune system consists of T helper cells, T killer cells, macrophage, suppressor cells, and memory cells. The T helper cells are bodyguards roaming the whole body that alarm the T killer cells and macrophage when they sense the presence of foreign bodies. T killer cells and macrophages so alarmed multiply very fast by means of cloning. A macrophage plucks an antigen from the surface of the foreign body; antigen serves as marker of the foreign body. That way, each foreign body is marked with an antigen. T killer cell produces an antibody (surface protein antibody) and latches it on the surface of hepa B virion that it finds by means of the antigen. The antibody latched on the surface of the foreign body changes its size and shape (Jaret, Peter. Our Immune System: Wars Within. National Geographic. June.1986) Hepa B virion attacks cells and get food from them. Effects on the person are jaundice, cirrhosis and liver cancer, among others.
Infection occurs this way: A hepa B virion looks for a hole in the membrane of cell that fits its shape and size. Once it finds that hole, it gets into the cell and gets into the nucleus, then chromosomes. Any hepa B virion that cannot get inside the cell stays outside or in spaces between cells. These hepa B virus are engulfed by the macrophages and neutrophils that can "eat" even asbestos fibers. However, as humans advance in age, 19 to 25 years old, the T killer cells or macrophages become weak and may fail to engulf all the hepa B virus (Estuita, A, personal communication, August 26,2013). Also the T killer cells may fail to produce antibodies to latch onto the hepa B surface protein antigens, hepa B early antigens, and hepa B core protein antigens.
Treatment. Chelation therapy can revive the production of antibodies, according to Dr. Estuita. A strong immune system protects the body from attacks by hepa B virus.
[The suppressor cell slows down the production of T killer cells and macrophages when the enemy had been defeated. Most of them die off; some macrophage remain as memory cells. When the same kind of microbe or virion infects the body, the memory cells induce the immune system to battle the foreign body. That is how vaccination works; the vaccine induces the production of memory cells without causing disease.]
Tests. The antigens of hepa B virus located outside the cells are also found in the blood. They can be detected by blood test. Antigens of hepa BV inside the nucleus (hepa B core protein antigens) are not found in the blood or are not detected by blood test. They can be detected by DNA test or biopsy. A small part of the liver is taken and examined in the laboratory.
Blood test results of one infected with hepa B may be as follows: total bilirubin, 5.2; direct bilirubin, 0.4; HBsAg positive; anti-HBc IgM positive; IgG negative; HBeAg positive (Kim, S. I. and T. A. Swanson. Underground Clinical Vignettes, Internal Medicine. 2007:147-48).
Bilirubin is a pigment responsible for jaundice. HBsAg indicates antigen in the blood. Anti-HBc IgM positive indicates acute infection or infection of patient is in a short time. IgG negative indicates that patient have not had past infection or had not yet been vaccinated. HBeAg positive means that cells, especially liver cells of patient, have hepa B virus capable of infection and replication.
A blood test can show a result of false positive. That is, there are surface proteins but infectious particles are absent. A blood test reads the antigens for both. This fact has an implication of standards of viral load. (More of this later).
Acute hepatitis means infection for a short time. Chronic hepatitis means infection for a long time. Acute or chronic is not a measure of the intensity of disease, inflammation, cirrhosis or liver cancer. Viral load is a measure of intensity of disease. An acute hepatitis B or chronic hepatitis B does not mean automatic conversion to cirrhosis or cancer. To clarify further: when a person had just been infected by hepa B virus in, say, two months, he has acute hepatitis B. By that time his viral load may be 24,000 and is now a carrier. Given that he is a carrier for about six months, he now has chronic hepa B, the consideration is length of time. Since virus doubles their population every 20 minutes he may have 9 million hepa BV copies by that time. Their great number may cause scarring in liver cells that result in symptoms like jaundice. Or may result in cirrhosis. Their preponderance may cause mutations in one mitotic cell that result in cancer. Cancer can occur even at acute hepatitis B (more of this below).
For more information on acute and chronic hepatitis B, please read my HuB "Acute and chronic heptitis B: Answers to questions obtained by blood test and biopsy."
“Hepatitis B core antigen (HBcAg) is an intercellular antigen that is expressed by infected hepatocytes. It is not detectable in serum” (Same source as above). Hepatocyte is a liver cell.
That means the blood test does not detect infectious particles inside the nucleus or viral genes inserted in the chromosomes of host cells. These are like antigens expressed by cancer cells. That antigen is called carcinoembrionic antigen (Kuroki, M. “Gene Therapy in Cancer Via Use of a Retrovector Having a Tumor Specificity and Expressing Inducible Nitric Oxide Synthase.” Hassid A. Editor. Nitric Oxide Protocols. Second edition. 2004:201-211)..
Theory three. The infectious particle inserts its genes into the chromosomes of the host cell.
The concepts are “infectious particle,” “genes,” “chromosomes,” and “host cell.” The relationship is “inserts.”
A gene is a specific part of a chromosome. Genes make up the hereditary materials of a chromosome A gene designated as HbA, in the language of genetics, controls production of normal hemoglobin. A gene designated as HbB controls the production of abnormal hemoglobin that is shaped like a sickle. The disease is called sickle cell anemia. A human being has 3 trillion genes (The Genome Project, Internet, Aug. 30,2013) A gene consists of two alleles, one comes from the father, another comes from the mother. For example, the gene of normal hemoglobin is indicated as HbA,HbA.
The process of insertion of viral genes into the chromosomes of host cell is called transduction. (We will not explain transduction in detail.) A virion may have 5 to 10 genes. After transduction, a human being may have 3 trillion and 10 genes.
Protection. The first line of defense against transduction is prevention of the entry of hepa B virion into the cell. That is done by the immune system, the T killer cell latching an antibody to the virion. "T" means thymus. T killer cells originate from the bone morrow then develop in the thymus gland. The secret is to revive the thymus gland to produce a lot of T killer cells, according to Dr. Arturo V. Estuita. The macrophages will engulf virus that T killer cells failed to latch with antibodies, although sometimes they also partly fail. They die and become pus. Neutrophil, a chemical produced by the prostaglandins, also "eats" virus..
Theory four. A virion becomes alive by entry into the host cell and insertion of its genes into chromosomes of a live host cell.
The concepts are in italics; relationships are in hold letters.
Infection starts in the entry of a virion into a host cell. Once inside the cell, an infectious particle, consisting of surface protein and DNA, inserts its genes into one chromosome of a liver cell. When this cell produces a daughter cell in a process called mitosis the infectious particle also becomes two. (See diagram above) The daughter cells are no longer identical to the mother cell because they have viral genes. In virus, the production of daughter cells is called replication. We make infection and replication as criteria of being alive. So the virion has now turned alive.
In the quote that follows Dr. Jonas E. Salk indirectly said that the virion is alive if it has the capacity to infect and replicate..
“The theory of the killed-virus vaccine rests on the well-established fact that an inactivated virus, though it has lost the power to infect or multiply, may still act as an antigen stimulating the body to produce antibodies against specific virus” (Salk, J. E. “Vaccines for Poliomyelitis.” Scientific American April. 1955. Microsoft Encarta. 2009, emphasis supplied).
Protection. Hepa B virus take 70 days to produce symptoms.That is why the hepa B vaccine can be effective if administered within 70 days. Hepa B virion favors the liver cells because these contain a lot of folate that are used in the production of new daughter cells. The hepa B virion adds one more property to the liver cell; fast replication. This is the term that means multiplication or growth. A hepa B virion makes the liver cell, now with hepa B genes in its chromosomes, replicate into two every 20 minutes. The population is doubled every 20 minutes; that is why the infection by hepa B is very fast.
Theory five. An infectious particle consists of surface protein and DNA.
Let us call a virion with surface protein and DNA infectious particle. New cells within the matrix have infectious particles. They are virtually hepa B virus. When the matrix bursts owing to overpopulation of virus, the matrix releases thousands of infectious particles and surface proteins. The surface protein can be separated from the DNA. Each surface protein is marked by an antigen. Also each infectious particle is marked by an antigen. The surface protein is empty and not infectious.
HBV produces more surface proteins than infectious particles. There are 50 trillion surface protein in a teaspoon of blood. There are 500 million infectious particles in one teaspoon of blood (Offit, P., MD and L. Bell, MD. Vaccines: What Every Parent Should Know. 1996: 77-79).
Vaccine. The gene that controls the production of surface protein had been isolated. It is used in recombinant DNA such that the gene is inserted into bacteria (yeast) to produce surface proteins. These are harvested and used as vaccine. The hepa B vaccine consists of surface proteins only.
Since surface proteins are grown in yeast bacteria, the hepa B vaccine contains some yeast proteins. This vaccine can cause allergy to people allergic to yeast.
Blood test for hepa B counts the antigens for surface protein and infectious particles; test result is indicated as HBsAg. (Kim, S. I. and T. A. Swanson. Underground Clinical Vignettes, Internal Medicine. 2007:147-48).
Theory six. An infectious particle uses folate of the liver cell to replicate.
Foliate is a vitamin that assembles nutrients into proteins that make up new molecules that make up new cells. Foliate works with other vitamins, minerals, and nutrients. For example, vitamin B2 works with other co-factors like zinc, folic acid and selenium to assemble glutamate, cystine and cysteine into glutathione sulf-hydril (GSH). GHS consists of three molecules; it supplies glutathione peroxidase that protects against free radicals (Pressman, A. DC, Ph.D. CCN, and S. Buff. Glutathione: The Ultimate Antioxidant. 1998). [More of this below]. We emphasize foliate because it is abundant in the liver cell. Without foliate the host cell cannot produce a daughter cell. On the part of the liver cell, the infectious particle is taking away its foliate. The doctor interprets this as parasitism.
Replication can be observed in the host cell. One cell divides into two cells, that divide into four cells, that divided into 16 cells and so on. A cell is confined by a matrix like a balloon. The air inside the balloon is like a virion that when it divides into thousands of virus, the balloon will burst, Each of the thousands of new virus will be marked by an antigen. These antigens are detected by blood test as viral load.
Remedies. Not much can be done by conventional medicine against hepa V virus parasitizing on liver cells. One consolation is that liver cells can replace themselves like a lizard growing a cut tail. Another way is operation to remove the infected part, commonly done on those suffering from cirrhosis. May be stem cell therapy can help. But the ultimate remedy is to kill or chelate infectious particles.
Theory seven. An infectious particle that infects liver cell induces mutation.
Given that an infectious particle had entered a liver cell and inserted its genes to the chromosomes of the cell. The virion genes can start mutation that results from a rearrangement of amino acids, or substitution, or deletion of amino acids in DNA; from break, or deletion, or thinning, or thickening of chromosomes (Cummings, M. Human Heredity, Principles and Issues. 2009). Alone, or in combination, these result in abnormality. Mutation can be detected by the Bioarray kit.
Cirrhosis. When alcohol adds its effect to abnormality the most likely result is cirrhosis. This is the replacement of normal liver cells with hardened and scarred cells. Seen another way, cirrhosis is a sort of embalming while the person is still alive (Cranton, D. MD. Bypassing Bypass. Updated 2nd edition. 1995). This is brought about by alcohol that if unmetabolized forms formaldehyde. Formalin is 67% formaldehyde that kills and hardens tissues. It was used by Dr. Jonas Salk to kill poliovirus and harden its coat in developing the Salk killed-poliovirus vaccine (Kluger, J. The Splendid Solution. 2009). Formalin is used in embalming.
That is why it is wise to avoid the alcoholic drink, or minimize intake. A healthy liver can metabolize 30 to 40% alcohol (vodka, whiskey, gin) at the rate of 30 ml per hour (WorldBook 2005). Six cans of beer per day puts one at risk. Wine is a no-no for a person with hepa B.
Liver cancer. Mutations in liver cells also result in cancer. Imagine the causes as links in a chain. The first link is infectious particle, the next link is copying error. The division of one mitotic cell into two involves copying such that the daughter cell is identical to the mother cell. Since there are viral genes added to the normal genes, copying errors occur. Cells have a way to correct such error but some errors may escape detection and correction. This is especially because the cell infected by infectious particle replicates much faster than normal cells. Remember the body is copying 3 trillion genes anytime. Copying error may result in cancer. Cancer starts with one mitotic cell.
A strong immune system can help remedy copying errors.
Free radicals (superoxide) and their derivatives (hydrogen peroxide, hydroxyl radical) may cause mutation then cancer. Macrophages shoot virus with nitric oxide produced by the inducible nitric oxide synthase. Nitric oxide kills the infected cells together with the virus. However, neighboring healthy cells are also hit. Nitric oxide induces mutation in healthy cells that may result in cancer.
The more viral load, the more macrophage, the more nitric oxide.
We cannot escape from free radicals, However, their population can be reduced by antioxidants, oral (fruits, vegetables, vitamins) and infusion chelation therapy. (More of this below).
Theory eight. Each infectious particle and each surface protein has a positive charge.
An infectious particle or surface protein has a positive charge, It is like hemoglobin that Dr. Linus Pauling, a two-time Nobel prize winner, found to have a positive charge. It is like a battery that has a negative end and a positive end. A positive end attracts a negative end.
That hepa B virion has a positive charge is proven with the use of chelators like vitamins A, C, E, magnesium, and EDTA (ethylene-diamine-tetra-acetate). Magnesium can be obtained from the chlorophyll of green leaves. like that of papaya. Chlorophyll is a chelate of magnesium.
Chelation therapy. Vitamin C given to patients suffering from dengue fever raises the platelet count that counters bleeding. Cristina Reyes, MD and Rowena Pua, MD, both pediatricians at the Los Baños Doctors Hospital and Medical Center, had treated dengue fever patients with administration of 500 mg of vitamin C for children. Dengue fever is also caused by virus.
Dr. Pauling had used vitamin C to prevent heart disease. Vitamin C has eight hydrogen atoms in its molecule, each atom can neutralize one free radical or derivatives. I take 2,000 mg of vitamin C daily for my heart disease.
Dr. Arturo V. Estuita, MD, a Filipino internist and chelationist, uses EDTA to treat patients afflicted with hepa B. A viral load of 8 million to 10 million was reduced to 10,000 by the administration of about 35 sessions of infusion chelation therapy (Estuita, A, MD. personal communication. 2013).
EDTA has a negative charge; it is a chelator (Brown, M, et al. Chemistry the Central Science. 7th ed. 1997). EDTA forms a ligand with hepa B virion. That is, it binds with and removes the virion through the urine. This process is called chelation. EDTA has six coordinates, or pincers, that claw on the virion. (See diagram above).
Review of standards
Infection by hepa B can be prevented by vaccination. The hepa B vaccine consists of surface protein only. However, a person so vaccinated will have antigens and antibodies for hepa B virus unless infusion chelation therapy is prolonged. A count of zero is unnecessary and may not be attainable. It is possible and highly probable that the blood test is false positive.
A person who had been infected with hepa B virus cannot completely eliminate virus when he gets well. That is unlike infection with hepa A virus; a person completely eliminates hepa A virus when he gets well.
Some countries like United Kingdom require that a person has a viral load of 1000 to 1500 copies per milliliter of blood to be considered as non-infectious. This standard may be unattainable and unnecessary. This standard must be reviewed.
To recall, there are more surface proteins than infectious particles. The ratio is 100,000 surface protein is to one infectious particle. So a person with a viral load of 14,000 or 10,000 most probably has no infectious particle.
One reason in the misinterpretation of viral load is the method of laboratory test. The blood test measures only the antigens outside cells. To recall, each surface protein and each infectious particle is marked by one antigen. The blood test reacts with the antigen. Blood test does not read the infectious particle inside the cell indicated as HBcAg. This is counted with the use of biopsy or the new gadget that test DNA, a CPR machine that is not yet widely used. .
The use of drugs (hepsera, lamivudine, barraclude) to treat hepa B is not entirely satisfactory. Antibiotics will not do because antibiotics kill bacteria and fungus but do not kill virus.
There is also the possibility of reinfection of a treated or vaccinated person. That is why there is a need for booster shots of hepa B vaccine.
How do we know that the viral load is not infectious? Dr. Estuita has methods as follows:
"On (a patient earlier treated with infusion chelation therapy) return I want to check for HBV proliferation or replication and infectivity (HBeAg), immune response (HBsAg) and HBV load."
To start with, the person so treated will always show positive for antigens and antibodies of hepa B virus shown by HBsAg. However, that is false positive. After treatment, for example by infusion chelation therapy, the viral load does not increase. Here, the use of blood test is reliable. The reasoning is that, if there were infectious particles within cells shown by HBeAg, these are sure to replicate and would cause an increase in the population of hepa B virus.
The test for HBsAg should be done 6 months after treatment. The reason is that there is a window period (about the 4th and 5th months) when the patient is negative for surface protein antigen. Please review my Hub on acute and chronic hepatitis B.
Likewise, liver cells are not inflamed or other diseases related to hepa B virus (jaundice) do not occur. Cancer does not occur. Cirrhosis does not occur. Cirrhosis sometimes turns into cancer. Inflammation is easier and faster to find than cirrhosis or cancer.
We have explained hepatitis B in terms of theories. These theories also serve as bases of modes of prevention and treatment, the latest being infusion chelation therapy. Conventional medicine has been dealing with virus along the germ theory of disease. However, the fact that hepatitis virus has a positive charge makes it amenable to the free radical theories of disease. Under them, the most effective treatments are antioxidants and chelators. EDTA works to revive the thymus gland and to chelate out hepa B virus.
Moreover, these theories clarify tests being used. They point out some flaws in standards that need to be reviewed and corrected.
More medical research and formulation of theory on the nature of hepatitis B and methods of control should be done. .
New entries as of February 25,2014
“Hepatitis B Virus (HBV) DNA test can detect the presence of viral DNA and measure the amount of DNA ( viral load ) in the patient’s blood.” DNA test is done by quantitative real-time PCR in Rotor-GenTM 6000. This is superior to the hybrid-capture PCR method in that it is more sensitive. Also it can quantify viral DNA load in the range of 5X102 to 1X108 copies per milliliter without dilutions (sksingha. Hepatitis B - Detection, Quantitation and Molecular Characterization Hubpages.com. February 25,2014).
This DNA test can give read-outs or results in four days, according to Dr. Arturo V. Estuita, internist and chelationist who is administering chelation therapy to cure hepatitis B.
The hepa B virion has four recognizable genes. One controls the production of surface protein. Another gene controls the production of core protein; another gene controls production of X protein. Still another gene controls the production of DNA polymerase that is responsible for replication or multiplication. In other words, DNA polymerase is the infectious part that is the target of developers of drugs. Such drugs are designed to inhibit the activity of DNA infectious particle.
Today the anti-hepatitis B virus drug in use is lamivudin. However, hepatitis virus have developed resistance to it. A long-term treatment with lamivudin induces mutation of hepatitis B virus resulting in a resistant strain. Such strain can infect a person and multiply within him or her. (Same source as above).
Hubs related to hepatitis B written by conradofontanilla