How to Treat A Person Who Had Acute Hepatitis B, Window Period, then Chronic Hepatitis B
Heredity materials (DNA) are well protected by surface protein, core protein, and nuclear capsid to ensure perpetuation of hepatitis B virus
Graphical presentation of acute and chronic hepatitis B
Blood test gives some answers to questions about hepatitis B
A person who was infected by hepatitis B virus cannot completely eliminate the virus when he gets well. The hepatitis B vaccine cannot completely eliminate the virus from the body. The virus has developed resistance to drugs now used to treat hepatitis B.
Since the discovery that infusion chelation therapy can treat hepatitis B in 2012, there have been several questions asked by victims of the disease. Or those who suspect they have hepatitis B. That is why they would like to have a blood test for hepatitis B. They want answers to several questions:
What is hepatitis B? It is inflammation of the liver caused by hepatitis B virus. (‘Virus’ is used in the plural and singular sense)
What is a hepatitis B virus? This question looks simple but it needs a complicated answer.
Structure and functions
First let us take a look into the structure of hepatitis B virus in its cross section as shown above.
For simplicity we identified eight only of the several parts of hepatitis B virus.
Protein surface encapsulates the whole virus. This protein is not infectious.
The hepatitis B surface antigen is a marker. This is the marker that is easily seen by simple blood test. The protein surface antigen is sometimes not considered part of the virus because it is a marker attached by the macrophage, a component of the immune system. The antigen is the marker by which the antibody will find the virus. (More of this below.)
The early antigen is produced after infection and during the acute stage of hepatitis B.
The hepatitis core protein antigen marks the core protein. It cannot be detected by ordinary blood test. It can be “seen” by electron microscope, obtained from the liver by means of biopsy. That is, a small portion taken from the liver by means of a small needle. One proof of its presence is an increase in the population of hepatitis B virus. However, there is now a new gadget that can detect it which is not yet widely used. It can give test results in 4 to 5 days.
The nuclear capsid protects the DNA (deoxyribonucleic acid) and DNA polymerase.
DNA contains the information code. This is an instruction as to what kind of virus will be produced during replication.
DNA polymerase is responsible for the multiplication or replication of virus. Absent this polymerase and the virus cannot replicate.
Knowledge of these parts of the virus will become useful in showing the things that can be found about hepatitis B by means of blood test and biopsy.
What is an acute hepatitis B? A chronic hepatitis B?
These two questions can be answered by serological course. That is by looking into what hepatitis virus is doing by means of blood test and biopsy.
Let us take a look at the graphical presentation of acute and chronic hepatitis B above. At the X axis are tilers, at the y axis is time, in terms of months.
The Y axis also shows the times of acute hepatitis B, window period, and chronic hepatitis B. Acute hepatitis B lasts for about 3 or 4 months. Chronic hepatitis B starts from the 6th month and may last during the lifetime of the victim. There is a window period that may last one or two months when a blood test cannot detect any hepatitis B antigen. This window period can be brought about by vaccination or natural control of hepatitis B virus by the antibodies.
At the start of infection with hepatitis B, near 0, the virus replicates at a very high rate. This is shown by the marker, HbsAg, obtained by simple blood test. That high rate of replication is also shown by the high population of early antigens
The body fights back the infection by producing antibodies, one against the core protein antigen (IgM anti HBc); and another antibody (IgG anti HBs) against the surface protein antigen; still another antibody against the early antigens, IgG anti HBe. All of these occur during the acute hepatitis B stage.
These antibodies can control the virus thus the virus population goes down in about 2 or 3 or 4 months.
As the population of virus goes down the population of antibodies against the HB core protein, IgM anti HBc, also goes down. However, the population of another hepatitis B antibody that is produced next, IgG anti HBc, remains steady up until the chronic hepatitis stage. You should not be scared of the high population of antibody IgG anti HBc. In fact, you should welcome it because it means that the antibodies are always around trying to control the hepatitis virus. However, they are not altogether successful as we shall see.
Its time to review what is antigen and what is antibody.
An antigen is “any substance either within or outside the body that triggers the immune system to produce antibodies against it” (Internet. March 23,2014).
An antibody is “a protein (immunoglobulin) [indicated as Ig; IgG; IgM] produced by B lymphocytes in response to specific triggers by ‘foreign’ substances. They identify and neutralize their target” (Internet. March 23,2014, in brackets supplied).
B lymphocytes (B cells) are components of the immune system. "Produced in the bone marrow, B cells migrate to the spleen and other secondary lymphoid tissues where they mature and differentiate into immunocompetent B cells. ... B cells are responsible for generating antibodies to specific antigens...." (Internet. March 25,2014)
Transmission and symptoms
Hepatitis B can be transmitted by blood, blood transfusion, syringe, nippers or nail cutters, and sex.
About 75% of hepatitis B cases are asymptomatic. That is, no symptoms are felt or show up. About 25% of cases show severe symptoms: flu-like, nausea, vomiting, loss of appetite, headache, chills, fever, jaundice and stomach pain at the ride side (location of liver). About 5% of cases become chronic hepatitis B carriers.
Acute hepatitis B and chronic hepatitis B are not measures of viral load. They mainly show duration of infection although they give some clues of viral load . There is another test for viral load that is more accurate. This will be tackled in another Hub.
Surface proteins versus DNA infectious particles
Let’s review the structure of the virus. There is the surface protein and there is the DNA and DNA polymerase protected by the nuclear capsid. The surface protein can be separated from the nuclear capsid (including its contents). The surface protein is not infectious. It does not have the capability to replicate. It is the DNA particles (DNA and DNA polymerase) that can replicate.
In fact, one gene controls the production of surface protein that had been isolated and used to mass produce surface proteins. This gene is inserted into yeasts that when they multiply they also multiply surface proteins. Yeasts serve as factories of surface proteins. These surface proteins are used as vaccines. However, this surface protein retains some proteins of yeast that is why hepatitis B vaccine cannot be given to a person who is allergic to yeast.
There are more surface proteins (50 trillion) than DNA infectious particles (500 million) in a teaspoon of blood, according to Paul Offit, MD and L.M. Bell, MD in their book "Vaccines: What Every Parent Should Know. (I have a Hub on this topic, “Theories of Hepatitis B as Guides in Treatment.”)
During the chronic hepatitis B stage, there are antibodies against the surface protein. There are also antibodies against the HB core protein. Unfortunately, there are surface protein antigens.
That is why doctors say that a person who had been infected by hepatitis B virus cannot completely clear himself of hepatitis B. Remember that the DNA and DNA polymerase (infectious particles) are inside the HB core protein and are further protected by the nuclear capsid. That is, the DNA infectious particles are still around during the chronic stage of hepatitis B.
Drugs for treatment
The drugs (alpha interferon, de fovir, lamivudine, tenofovir, entecavir, telbivudine) being used for treatment cannot completely eliminate hepatitis B virus. They are not cures. The hep B virus has developed resistance to them.
These drugs operate within the germ theory of disease. They are supposed to kill the virus the way they kill bacteria. They are designed to inhibit the activities of the polymerase. They must penetrate through the surface protein, core protein and nuclear capsid. However, the virus does not neatly fall under the germ theory. Although it is very small, it is not even considered as dead or alive. Virus are either DNA or RNA, neither is a cell like the one-celled bacteria. A virus can be considered as a half cell because a cell must contain both DNA and RNA (ribonucleic acid). RNA transmits the blueprint (embedded in DNA) used to construct a house to the carpenters, as it were. In fact, the DNA virus commandeers the RNA of the host cell to replicate. The hepatitis B virus is a DNA virus that has a positive charge.
Viral load is the basis of the treatment for hepatitis B. Viral load may range from 8 million copies per milliliter to 110 million per ml of blood. The load of a former patient of hepatitis B who is considered cured is 10,000 copies per ml of blood. This topic deserves another Hub.
Suppose your test results are: HBsAg+ /HBeAg+ /IgG anti HBs+. You have acute hepatitis B.
Suppose your test results are: HBsAg_ /IgG anti HBs+. You have been vaccinated and you are responding to the vaccine.
Suppose your test results are: IgG anti HBc+ /HBsAg_ /IgG anti HBs+. You have just recovered from your hepatitis B infection.
Suppose your test results are: IgG anti HBc+ /HbsAg_ /IgG anti HBs_. Your hepatitis B is in the window period. That IgG anti HBc+ shows that the nuclear capsid and its contents, the DNA infectious particles are still around but undetected by ordinary blood test. (Reference: ftplectures.com).
Suppose your laboratory test results show: IgG anti HBc+ /IgG anti HBs+ /HBsAg+. You are positive for two antibodies, one against the core, IgG anti HBc and another against the surface protein antigen, IgG anti HBs. However, you are also positive for the surface protein antigen. Therefore, you are a chronic hepatitis B carrier.
You can live a normal life (without symptoms) with this condition. However, there is a possibility that the DNA infectious particles will escape from the antibodies. There is always a risk that you will develop cirrhosis or liver cancer.
Recall that during the window period (in the 4th to 5th months), virtually no surface protein antigen can be found. A blood test conducted at this time will not show positive for antigen. Only positive for antibodies. And you may believe that you have been cured. However, in about the 6th month the antibodies against hepatitis B surface protein antigens will appear. They show that the viral load is either infectious or non-communicable. A proof that the load has DNA infectious particles is an increase in population of hepatitis B virus. Another proof is that a member of your household got infected with hepatitis B virus for which you are most likely responsible.
There is a possibility that the blood test catches only empty surface protein. These are not infectious,.however, these are marked by surface protein antigens. That is why the treatment standard allows as cured a patient with 10,000 copies per ml of blood. Remember the ratio 50 trillion surface protein is to 500 million infectious particles per teaspoon of blood? If we extrapolate that ratio, 10,000 copies per ml might be showing only empty surface proteins. However, that is a mathematical extrapolation. Infectiousness must be proven by laboratory test of culturing specimen from the person to see that the viral load of a little over 10,000 copies per ml does not increase in population.
Infusion chelation therapy
The main ingredient of infusion chelation therapy is EDTA (ethylene-diamine-tetra-acetate) that has a negative charge. It has six claws, as it were, that pinch on positively charged minerals, including the virus. EDTA binds with and removes the virus through the urine. Early on EDTA has been used to chelate out lead. EDTA and propriety mineral bind with the whole hepatitis virus and carries it away, including the core protein, nuclear capsid, DNA and DNA polymerase.
That is unlike the drugs that must penetrate or destroy the surface protein, core protein and nuclear capsid to get to the DNA polymerase and inhibit its ability to induce replication.
The formation of a ligand between EDTA and hepatitis virus is the basis of the new discovery of Dr. Arturo V. Estuita, a Filipino internist and chelationist. He started treating hepatitis B patients in March 2012. So far, over 20 patients have been successfully treated. The reason is that only this number of patients had come for treatment in his clinic. Dr. Estuita, MD holds the property rights over that propriety mineral.
One patient came from Zimbabwe; another from United Kingdom. Most patients are Filipinos who are seeking for employment abroad.
New entries as of April 8,2014
Chelation therapy is safe and effective
These were the findings of the Institutes of Health of USA by means of double blind randomized with control study called "Trials to Assess Chelation Therapy" (TACT). This was launched in 2002 and completed in March 2011. Results were presented at a meeting of the American Heart Association held in Los Angeles, California on November 14,2012.
One beneficial side effect of chelation therapy is that it can treat diabetes. Among the participants (1,708 in all divided into treated group and control group) the occurrence of diabetes in the treated group was 37 less than those in the control group.
Of course, no one among them had hepatitis B. In 2012 Dr. Arturo V. Estuita, MD discovered that chelation therapy also treats hepatitis B patients.
Hubs related to hepatitis B written by conradofontanilla