Related Articles

Major Rewrite – Version 2.0

12.6.2023

Open AI ChatGPT is definitely the future …

28.1.2023

Open AI ChatGPT comments ALS disease, Part III.

21.1.2023

Some strange and for people currently more or less invisible infection is being mentioned by some sources. Can it be at least partially relevant?

In general, the idea there is something which we are unable to see is in my opinion quite rational, despite it lacks scientific proof yet. In theory it could explain some hard problems. It can be relevant in those peculiar autoimmune like processes. If our immune system reacts and sometimes even overreacts on something not obvious to us, it would be still in line with the general and correct immune function. A very wild association popped out in my mind when I was thinking about it – please take it with a great deal of reserve.

In the cult movie Predator (1987) there is this famous scene of guerilla camp elimination. From the point of the commando lead by Dutch (Arnold Shwarzenegger), it is quite precise ambush resulting in annihilation of all enemies. This could be sort of wild analogy of immune cells (CTLs or NKs) when they encounter site of known infection and routinely eliminate the threat associated. Good job!

However then there is an enemy of a different kind. Enemy which the commando is not trained for. This enemy is a space monster equipped with advanced technology – unknown to the human commando. Besides the weapons like laser cannon, the greatest tactical advantage the monster has is the camouflage ability and scanning options in multiple light spectres, with infrared vision being the most handy. The result is very different. Here the analogy lies in more aspects or views. In the jungle shooting scene the trained killers are alerted by death of one of them and from this obvious reason they tend to overreact – innocent jungle is destroyed and the single monster escapes thanks to the camouflage. The monster is gone but the commando is still devastating everything at the place of the contact (autoimmunity?). After that those remaining soldiers are being eliminated in one by one fashion as the monster fully utilizes its advantages including human voice recording! 😃 Only once chances equalize a bit, Arnie can kill the Predator.

What if something similar is happening with all those strange, autoimmune or weird diseases we have no cure for? Science fiction, right. However it would make sense – the body accused for decades from going wrong would deserve some vindication. Now the new theory would need to state something else. The body can sometimes spot the enemy (virus, bacterium, toxic substance) so it employs an attack but it struggles significantly in this guerilla war and is unable to get fully in control, in certain case it can be loosing gradually and more or less slowly. An unpleasant situation which can be changed only with some smart external intervention.

Anthony William

Let´s start with the medical medium, Mr. William. He mentions mainly Epstein-Barr virus and also other herpetic viruses (HHV-5, HHV-6 etc.) but also the cofactors like toxic metals and bacterial infections. At the same time he says there are much more variants of EBV – tens of additional virus types or mutations, some more pathogenic and aggressive, some less. This is not the biggest controversy yet. New viruses are being observed from time to time. For example let´s remind how time went with various hepatitis viruses^​1​. The jaundice as a disease was known for some time – centuries. The bacterial cause was identified once people came with the appropriate technology. During 1940s it was observed there are more infectious agents and it gave raise to A and B versions. It took another 40 years to reveal the C version in 1987. It would be very shortsighted to think mankind revealed all major viruses on this planet which infect people. It is quite likely there are viruses which live inside us and nobody revealed them yet. The micro-world is just too complex and we all are actually full of microbs – there is no surprise we struggle in revealing all the environmental and microbial relationships in the maze of human body. The Human Microbiom project is dealing with this and in upcoming decades new observations will come for sure. With this information in mind we may tend to be quite OK with Anthony William statements on additional herpetic like virus types. However what about that EBV? It is known virus so why it should represent stealth enemy like mystery? I tried to look at this and I was a bit surprised – a room for such stealth theory can be actually there and I will share some thougts in different section. Besides that there could be some strain which is yet to observe similarly as it was with hepatitis C virus.

What is already a bit weird even for me are those statements regarding viral particles which actually move and drill into our thyroids or sinovial tissues, liver etc. The problem is that virus does not have “legs” or any other own means of locomotion. Virus is considered to be edge form of life – it has genetic information and can replicate but in order to do that it needs cells, so in our case our human cells. Virus cannot move and thus it travels by other means of transportation – our air respiration paths and fluids circulating in our bodies, mainly blood and lymph. This way it can certainly get from lungs to different places but it certainly cannot start drilling through tissues on its own – here I have slight problem with Anthony William. It can be good to still not reject the whole theory just because of this flaw. The virus can actually do many things. It is an intracellular parasite so it can hijack our cells – for example red blood cell and thus it can get to any place where blood gets. Virus can also hijack cells which are part of our immunity – for example T-lymphocytes, B-lymphocytes or macrophages and once done it gets ability to move. I would not imagine it as if someone steals a car and can drive where needed but the fact viruses can make use of our cells to achieve their goals is unquestionable. The primary goal is known to everyone and pretty simple – get into cell, hijack the cell machinery so it can reproduce and survive. Sometimes very rapidly and resulting in killing the cell (literally tearing it apart) and sometimes becoming latent or rather passive and waiting inside the cell. As I learned herpetic viruses are often those latent ones and they are known to target B-lymphocytes, so those cells which produce antibodies. That is why it can become confusing and complex for science to link viruses directly with some disease. If some virus is considered common in people – both healthy as well as those ill, it gets complicated. However the theory here has the trigger part and it really seems relevant after comparing this with other information. Invisible and hard to recognize pathogens can exist and those known (EBV, cytomegalovirus, HHV-6, HSV-1 and HSV-2) can – under some rare circumstances – have role which is unknown as well. Some magical activation function can occur and we may not see that. There is another key thing – the pathogens are told to excret toxins and these toxins then travel through the body as well, causing damage in locations far from site of infection which may contribute to autoimmune observations whre no virus is found. I shall also remind the fact Anthony William is assigning ALS not to single virus but actually to something I would call multi-factor infection where more virus types are present, then there needs to be bacterial infection present and last but not least heightened levels of toxicity in the form of heavy metals and other followed with significantly weakened body toxin neutralization and excretion functions. I will do a favor to readers and repeat his full statement^​2​​ here in full parade.

Modern Science

Is scientific world aware of some similar behaviors? Stealth capabilities? What science knows about Epstein-Barr virus besides infectious mononucleosis? Well, it seems to me there is definitely something strange happening here – judged fully based on various scientific sources. I need to say the EBV really appeared almost everywhere and it is time to describe the highlights. However as I wrote above, virus itself does not have the capabilities Anthony William assigns to it. Virus cannot move through tissues like that based on quite trustworthy scientifical information, see for example this book^​3​. Besides our cells, a virus can hijack also bacteria which have “legs” similarly as come of our cells. Such viruses are called bacteriophages or just phages. So who knows how it is with the motion?

This means there are basically two options. Either Anthony William is wrong or there is an additional complexity or layer which needs to be identified. There can be something else in this puzzle besides herpetic virus strains.

Epstein-Barr virus (EBV)

In order to introduce this virus let me first cite National Institute Of Health (NIH) website.

The Epstein-Barr virus (EBV), the first isolated human tumour virus, was identified in 1964 by Epstein’s group in a cell line derived from Burkitt lymphoma (Epstein et al., 1964). EBV is a human herpesvirus, classified within the gammaherpesviruses subfamily, and is the prototype of the Lymphocryptovirus genus. In keeping with the systematic nomenclature adopted for all human herpesviruses, the formal designation of EBV is human herpesvirus 4 (HHV-4)^​4​.

From above we can understand the virus is known for more than 50 years and it was first identified in a context of analyzing tumor – so cancer research. This is in line with A.W. theory as he claims EBV and its variants are responsible for 90% of all cancer cases. This is probably not shared with modern science as I´m not aware the cancer treatments would be primarilly targeted to immune system support and reinforcement. Many of my relatives died on cancer which is very sad story but treatments mostly involved chemotherapy or other invasive procedures. Science knows about HPV viruses though. I also found article where EBV is suspected to be major factor in cancer development besides genetic and environmental factors^​5​.

Many studies suggest that the focal distribution of nasopharyngeal carcinoma (NPC) may be influenced not only by host genetics, diet and environments but also by interplay with Epstein-Barr virus (EBV) genetics. Specific EBV gene variants (theAand C types, the BamHI f configuration, a C terminal 30 bp deletion and aNterminal loss of an XhoI site in the BNLF1 gene) have been explored in high incidence areas in southern Asian NPC patients^​5​.

Another, for me very interesting information, is following.

Two major EBV types have been detected in humans: EBV-1 and EBV-2 (also known as types A and B). EBV-1 and EBV-2 differ in the sequence of the genes that code for the EBV nuclear antigens (EBNA-2, EBNA-3A/3, EBNA-3B/4, and EBNA-3C/6) (Sample et al., 1990). EBV-2 immortalizes B cells less efficiently than EBV-1 in vitro, and the viability of EBV-2-infected lymphoblastoid cell lines is less than that of EBV-1-infected lines (Rickinson et al., 1987). The differences in the immortalizing efficiency of the EBV subtypes may relate to a divergence in the EBNA-2 sequences (Cohen et al., 1989)^​4​.

For viruses we should always try to identify which cells they prefer and with EBV people can confirm it likes B-Lymphocytes. Isn´t it strange? B cells are part of our immunity and it is these cells which produce antibodies and in above statement we can read the virus makes B cells immortalized! I don´t know why but link to autoimmune processes popped out in my mind in light speed fashion. We can think about it like our body created certain specific B cells to respond to some antigen presence because unquestionable threat was detected but then a virus comes, hijacks these cells, makes them immortalized and thus they are not garbage collected and can already cause damage by creating antibodies which are already not needed. Is that science-fiction or too simplified and naive idea? Perhaps yes, but that was my instant deduction. Please consider what Polly Matzinger wrote in her alternative hypothesis on autoimmunity.

Perhaps PRRs have not evolved to bind to pathogens at all. Perhaps the pathogens have evolved to bind to them! Many cell surface molecules involved in normal physiological functions are targeted by pathogens. Human immunodeficiency virus, for example, binds to CD4, CCR5, and CxCR4, and Toxoplasma also seems to bind to CCR5 (30), whereas Staphylococcus and Streptococcus bind to a conserved loop on T cell receptors and to the Fc portion of antibodies. Coxsackievirus binds to intracellular cell adhesion molecule–1 (ICAM-1), rabies to N-CAM, and Epstein-Barr virus to complement receptor 2, thus activating a B cell as it enters.

I understand it in a following way. In human bodies there can be many instances of B cells. Each configured for slightly different antigen and due to the very smart algorithm^​6​ used for creating them there is a good chance even autoreactive B cells are created. However the immune system counts with these collisions and has mechanisms how to quickly eliminate and suppress these autoreactive B cells before they get activated and start creating antibodies against body tissues (e.g. collision with some organ). One such way how this is achieved if such B cell is detected (perhaps it already did some minor damage and thus alerted other security guys like T cells), is to approach the “collision B-cell” and request it to commit suicide (apoptosis). Problem is solved and any minor damage is reconstructed/healed. Suppose this is the good old primary positive use case. Things can go wrong and surprisingly for me we know there is something like EBV, a virus which likes B cells and which carries a gene for disabling managed suicide feature called cell apoptosis. Let´s imagine what can happen if this virus finds autoreactive B cell and hijacks it within very specific short time period, a period starting with creating this not really useful B cell and ending with relatively quick elimination of it. An analogy to rubish/rejects in industrial production of things may be imagined. If the virus timing in B cell ambush is as above then it can result in pretty serious problem – somewhere in the body a B cell intended for garbage collection was activated and even worse refuses to die, or to commit suicide. In my language it would mean the cell refuses to execute its destructor or the destructor was actually overriden and instruction like “return” or “return false” is added as the first line of code so it never gets to the instructions which destroy the cell. This was analogy with software programming. This logically describes autoimmune process, or not? Such immortalized B-Lymphocyte could be analogy of so called memory leak problem in computer science or software development. These are nasty issues – I have some experience with hunting these bugs though 🦗🔨🕵️‍♀️

Logically there needs to be some additional mechanism of cell death, otherwise EBV suppressing apoptosis would become the ultimate winner. Still I would see this viral capability a big problem. Let´s open google and take a look at cell death types^​7–10​. I found additional interesting findings including ALS link.

Abnormalities in cell death regulation can be a significant component of diseases such as cancer, autoimmune lymphoproliferative syndrome, AIDS, ischemia, and neurodegenerative diseases such as Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, and Amyotrophic Lateral Sclerosis. Some conditions feature insufficient apoptosis whereas others feature excessive apoptosis^​10​.

And there is other relevant information. I would need to cite the whole article. For anyone interested I recommend reading it, mainly section Pathologic Apoptosis. Science definitely made great progress here – it all looks like many of the internals are described to great extent. EBV role in cancer seems to be 100% confirmed. Those descriptions mentioning B cell proliferation with pathogenic apoptosis modes seem highly relevant and thus in line with pseudoscientific theory. My understaning is that problems just in apoptopic cell death (refusal to die when requested or easy die when not desirable) already cause big issues.

Because of the diversity of B cell receptors, there is essentially no limit on what they can recognize – including our own proteins, carbohydrates, and fats. Most B cells which can recognize our own molecules are eliminated shortly after they are born in the bone marrow (much more on this in Lecture 9). However, this screening process is not 100% effective, and there are self-reactive B cells in circulation which could cause autoimmune disease if they produced antibodies (autoantibodies). To guard against this possibility there is a fail-safe mechanism in place which allows B cell activation only when there is real danger^​6​.

Please note the fail-safe mechanism involves T cells so that both B and T cells need to agree but we already know EBV can infect T cells too and if the mechanism is same then the cell is activated at the moment of entering the cell. As a result the real and very problematic scenario can actually be enabled. Let´s not make big conclusions yet, anyway good point to remember.

EBV virus primarilly infects people but primates are known to have their own EBV similar viruses. Now let´s focus on the target cells in slightly more detail. All this information is available on NIH page.

Like other gammaherpesviruses, EBV establishes latent infection in lymphocytes and can induce proliferation of the latently infected cells (Young & Rickinson, 2004). EBV infection of B cells is mediated through the interaction of the viral envelope glycoprotein gp350/220 with the cellular receptor for the C3d complement component CR2 (CD21) (Fingeroth et al., 1984, 1988; Tanner et al., 1987). After binding of the viral particle to the surface of the host cell and endocytosis, the viral envelope fuses with the host-cell membrane by a mechanism involving three other viral glycoproteins: gp85, gp25, and gp42 (Li et al., 1995). It is worth noting that gp42 can bind to major histocompatibility complex (MHC) class II, and EBV uses this as a cofactor in the infection of B lymphocytes (Li et al., 1997).

It has been shown nonetheless that EBV can also infect cells, albeit at low efficiency, via CD21-independent mechanisms. Indeed, cells that do not express CD21 (as some epithelial cells) can be infected by the virus, and furthermore a virus deficient in gp350/220 was shown to be still infectious (Imai et al., 1998; Janz et al., 2000).

Although EBV is considered to be a B-lymphotropic virus, it can also infect T lymphocytes or epithelial cells because it is found in some T-lymphoma cells and several important diseases of epithelial cells, including nasopharyngeal and gastric carcinomas, and oral hairy leukoplakia (Thompson & Kurzrock, 2004). Other CD21-independent pathways may be responsible for EBV infection of cells other than B lymphocytes (Imai et al., 1998; Janz et al., 2000).

Current evidence suggests that EBV infection in healthy chronic virus carriers is largely restricted to B cells, although in certain situations the virus can be detected in epithelial cells. The most likely role for epithelial cells is as a site for replication and amplification of EBV rather than as a site of persistent latent infection, however, this remains controversial (Kieff, 1996) (see Section 1.1.6 and Fig. 1.2).

Above statements are included to increase trust in the information which I then try to interpret. No need to have deep understanding of that – I´m no expert either.  We should just remember mainly B cells but sometimes also T cells, complement proteins are somehow involved too. Another key information is related to the virus life cycle. What science says?

EBV, probably the most potent transforming human virus in culture, is nonetheless known to infect and persist for life in > 90% of human adults without causing disease.

Several reviews have described how EBV exploits the physiology of the normal B-cell differentiation, and uses different combinations of latent viral gene expression to progress from initial infection to long-term persistence within the memory B-cell pool of the immunocompetent host (Thorley-Lawson & Gross, 2004; Young & Rickinson, 2004; Thorley-Lawson & Allday, 2008).

The memory B cells eventually return to the tonsil, where they occasionally undergo plasma-cell differentiation, which triggers viral replication. The resulting virus may be released into saliva for spreading to other hosts or may infect other B cells (Young & Rickinson, 2004; Thorley-Lawson & Allday, 2008).

Primary EBV infection elicits a strong cellular immune response which brings the infection under control, and newly infected cells are thought to be efficiently removed by the latent-antigen-specific T-cell response. The virus can persist for life in the host only in the resting memory B cells in which no viral proteins are expressed, and is therefore shielded from the immune system (Thorley-Lawson & Gross, 2004; Young & Rickinson, 2004; Thorley-Lawson & Allday, 2008).

What we basically can learn from above statements is that we may know how the latency of the virus is actually achieved. The virus survives immune responses in memory B cells and this can last for life of the host organism, i.e. human person. I don´t see any conflict with multi stage EBV theory presented by pseudoscientist Anthony William so far!

So far we are rather in cancer world but we now know much more about one specific herpetic virus, the variant with code name HHV-4, Epstein-Barr virus. I need to find some link to ALS and similar diseases which affect nerve system – both PNS as well CNS. If we take a look at below table we know what to do next – look closer at EBV „brothers“ … or „sisters“? 🙄

• 

These other strains are mainly the first three (HSV-1, HSV-2, HHV-3) and another three (HHV-6x, HHV-7) from lower part of the table. It looks like these guys like neurons in PNS as well as CNS and surprisingly this is exactly what Anthony William states.

Please note we already have certain link between ALS and MS diseases. This enables us to construct an indirect EBV to ALS link and I would like to support it with following statement.

Our findings indicated that EBV was present in most (90%) cases of MS and the virus could be detected in multiple tissue samples from each case. Surprisingly, we found EBV not only in B-cells, but also in astrocytes and some microglial cells. Significantly, the virus was transcriptionally active in these cells and expressed EBNA-1, and to a lesser extent the early lytic cycle protein BZLF1. Taken together, these findings support a role for EBV in the pathogenesis of MS^​11​.

We have just moved from B cells to glial cells and this has in my opinion absolutely critical importance. Why? Because we should already know what glial cells do and what is their function. These are support cells which work for neurons and they are very close to them. Microglia cells are the bodyguards, the brain macrophages which are supposed to seek & destroy any uninvited guests – for example bacteria or viruses. Astrocytes are big cells which as per my information are also capable of phagocytosis but mainly these cells have to also manage the amount of glutamate, one of the most common exhibitory neurotransmitter which enables us to pass signals throughout our neural networks. Astrocyte cells need to process or let´s say neutralize the excessive amount of extracellular glutamate. Bright reader as well as passionate researcher like me should already know there is a big catch regarding glutamate amount^{​12–14​} – if there is too much glutamate then nearby neurons die and by the way this is the signature finding for ALS (moto neurons are dying). What can be the logical deduction then? Astrocytes may not work, they can be striking or … they could be somehow crippled because EBV hijacked them or corrupted them somehow? Who knows, but I see the potential here for sure. The below related finding blames SOD1 gene but is that bullet-proof? The astrocytes might recruit or activate the microglia, which could then direct motor neuron degeneration^​15​.

It is good to expect these other virus strains share similar capabilities as EBV (HHV-4) but they do different damage because they prefer different cells. It is time to look at HHV-3 as an representative of the neuron attacking herpetic viruses. It is this virus which I highly suspect due to what I have seen and what information I gathered later.

Primary infection with varicella-zoster virus (VZV) causes varicella (chickenpox), after which the virus becomes latent in the cranial nerve and dorsal root ganglia. Reactivation of the latent virus produces shingles (herpes zoster), mainly in elderly or immunosuppressed patients. VZV causes a wide range of CNS manifestations including encephalitis, meningitis, Ramsay Hunt syndrome, cerebellitis, myelitis, and vasculopathy. The CNS manifestation caused by VZV can occur as a result of both primary and reactivated disease. In rare cases, CNS diseases caused by reactivation of the VZV vaccine virus can occur^​16​.

Varicella Zoster Virus

The zoster virus is known very well and its symptoms are usually visible which significantly helps with detecting it. Let me write it also using different words. The zoster virus is known very well and its symptoms are usually visible which significantly helps and your physician will believe you and won´t give you hypochondriac label right away. The associated rash and blisters cannot be denied. The problem is the virus may not manifest its presence with skin expressions – it can be deeply in your nerves and you may just feel strange discomfort – often in area of forearms, wrist etc. I would not be surprised if some carpal tunnel diagnoses were actually deep and progressing, reactivated infections of this painful virus. If the patient suffers or suffered with occasional shingles it is clear evidence he has the virus, it is very rarely eradicated completelly. In my opinion it is responsible for the PNS unpleasant symptoms even in ALS diagnosed patients. Poor and unlucky people are most likely under simultaneous attack of more viruses – each sitting somewhere else in the body and together silently contributing to work of doom. Speculation? Yes, well perhaps it is expert guess despite I´m not official expert but instead I witnessed something in reality which complies with such hypothesis.

HHV-6 & HHV-7

Science is aware of heightened levels of HHV-6 and HHV-7 in Alzheimer disease patients and this disease again is considered similar to ALS – the difference is just in the brain and corresponding center (memory, speech, motoric) which gets infected. Alzheimer disease incidence is much higher than ALS but they really are not that different when it comes to tracking the root cause – at least that is my experience and guess.

Our results offer evidence of complex viral activity in the aging brain, including changes specific to AD clinical traits and genetic factors, particularly implicating Herpesviridae, HHV-6 and HHV-7. Taken together, these data provide compelling evidence that specific viral species contribute to the development of neuropathology and AD^​17​.

Lots of studies show the association of HHV-6 with other diseases like chronic fatigue syndrome (Chapenko et al. 2006), multiple sclerosis (Leibovitch and Jacobson 2014), drug rash with eosinophilia, systemic symptoms (Gentile et al. 2010), etc.; however, the cause relationship between HHV-6 infection and these diseases still needed to be elucidated. Strikingly different from other human herpesviruses, integration of HHV-6 full genome into host genome has been reported (Arbuckle et al. 2010); the mobilization and reactivation of HHV-6 virus from integration have also been reported (Prusty et al. 2013; Kaufer and Flamand 2014)^​16​.

Human endogenous retrovirus (HERV) sequences are assumed to be remnants of ancient retroviral infections of our ancestral germ-line cells and constitute ~8% of the human genome (1). Although these viral sequences were generally silenced through diverse evolutionary mechanisms, some HERV genes have been shown to be expressed in controlled tissue-specific manner (2). Interestingly, some HERV were suggested to be involved in the pathogenesis of several autoimmune diseases, including multiple sclerosis (MS) (3–5) and type 1 diabetes (6), neuropathological syndromes like schizophrenia and bipolar disorder (3), as well as degenerative diseases, including amyotrophic lateral sclerosis (7, 8)^​18​.

I think I could continue and make this long post unreadable but I think this is enough. For my own purpose I gathered sufficient amount of scientific information about these viruses and that they can be critical component in development of amyotrophic lateral sclerosis and most likely even other diseases, namely Alzheimer, Parkinson and multiple sclerosis.

Cell Wall Deficient Forms (CWD)

Another stealth principle within scientifical circles can be the theory about so called cell wall deficient forms of bacteria. To my surprise science is aware of this phenomen for a long time. There is a confirmed theory about bacterial pleomorphism, meaning there are bacteria which can exist in more than one form. Usually we imagine bacteria as some small bug where the usual sizes are in one or few micrometers, sometimes smaller. In this common form the bacterium has its cell wall and this wall is the target of antibiotics which we eat when suffering with bacterial infections. The problem is that some bacteria can break into or switch to different much smaller form (virus size form) which does not have cell wall and thus it is called cell wall deficient form. There are some synonyms like L-form or spheroplasts.

One scientist which was intensively focused on this research was Lida Mattman (1912-2008), I have decided to include her introduction from her book. She died in 2008.

As is apparent, her research work was focused on Lyme, ALS and MS – she tried to find out what the role of spirochetal infections can be in the development of these diseases.

A spiral-shaped organism has been noted in multiple sclerosis (MS) by so many investigators, over so many decades, in so many countries that it can hardly be ignored. The search for the spirochete concerns three aspects: (I) visualization in brain at autopsy or in spinal fluid, (2) growth of the organism in laboratory animals, and (3) culture of the agent. European pathologists led in finding spirochetes by silver staining of brain tissue or spinal fluid sediment. One patient’s spinal fluid contained approximately 35 spirochetes/ml, Steiner, who named the organism Spirochaeta myelophora. (Figure 25-8) was the most persistent in applying staining. He located the organisms even within the brain’s glial cells^​19​.

Above citation regarding multiple sclerosis is in certain conflict with other sources – the hunt for causative microb was intensive but never successful. The problem might be the spirochetes are found in healthy people as well. On contrary perhaps the same can be said about people who may have EBV and do not suffer with any unplesant symptoms. It should be all about measure, if immune system is in control or not.

A spirochete was found in eight MS brains at a titer as high as 10^9/g of tissue and in sera of patients with active disease at titers up to 10^3/ml. It multiplied to high titers in the central nervous tissue of inoculated animals and was serially passed in mice using brain homogenates . Fascinating studies also support a viral etiology for MS. Spongiform degeneration on the central nervous system was produced in sheep and mice inoculated with MS brain tissue. Cultures were negative. Carp et al. and Koldovsky et al. demonstrated an organism by the effect on the neutrophiles of mice. The agent was not cultivable and passed through 50 nm filters but not smaller filters ; hence, they concluded that the agent was viral. Neither of these characteristics rule out the possibility that the organism is a spirochete prone to forming filterable particles. The relationship of the organism to MS was again shown, this time by its neutralization by sera from patients whose disease was quiescent^​19​.

Regarding Lyme disease and ALS she was realizing some commonalities. If she would talked to Anthony William what she would hear? He states bacteria are not the root cause, problem are viruses.

It was once published that amyotrophic lateral sclerosis (ALS) was probably a form of Lyme disease, but the possibility was discarded upon discovery that many cases lack circulating antibody to the spirochete . Now it is known that severe cases of spirochetal disease often do not have antibody free in plasma; it is bound in the tissues in immune complexes. The 18 cases of Lou Gehrig’s disease which we have cultured, all have a spirochete in their blood, which reacts with Borrelia burgdorferi antibody. Only a more complete biochemical analyses of major components will determine how closely the ALS spirochete may be related to the pathogene of Lyme disease and of MS^​19​.

This spirochetal branch attracted my interest from one additional reason. In Stephen Harrod Buhner work^​20​ I learned spirochetes excret QUIN or QA (Quinolinic Acid) which together with the ROS (reactive oxygene species) cause damage. Have you noticed that so far I haven´t mentioned one missing factor here compared to Anthony William theory? So far I´m discussing the viral factors but what about those heavy metals? I should cite Wikipedia here, an easily confirmable statement.

Exogenous sources
The formation of ROS can be stimulated by a variety of agents such as pollutants, heavy metals, tobacco, smoke, drugs, xenobiotics, or radiation. In plants, in addition to the action of dry abiotic factors, high temperature, interaction with other living beings can influence the production of ROS^​21​.

This can basically tell us that presence of heavy metals can rapidly accelarate the brain damage because they stimulate formation of ROS. Stephen Harrod Buhner states that if ROS forms are present the neuron damage can increase by 80%. This can help explaining the very variable length of life of ALS patients. As we can see it is not just about heavy metals but also other factors from lifestyle category which science registers as big risk factors. Similar negative effect can have another finding regarding producing matrix metaloproteniases (MMP). Buhner states presence of spirochetes attracts immune system which is then stimulated to produce these MMPs but this has harmful effect on tissues, mainly sinovial tissues. Especially MMP-1, MMP-3 and MMP-9 are registered and are considered as a cause of Lyme arthritis. Buhner concludes spirochetes leverage immune system for its own purpose – movement in extracellular matrix and escape. Huh, isn´t it strange? It reminds me the historical name for autoimmune diseases, collagen diseases, and also the delayed return phenomen which was observed in ALS patients^​22​. The critical importance of super oxid dismutase in controlling ROS is mentioned on the same Wiki page. Scientists overstress the SOD1 gene defect in some ALS patients but as I wrote earlier that, in theory, could be just consequence of viral or toxicity mutations.

The way QUIN was described by Buhner reminded me the glutamate factor so I started searching if there is any QUIN-2-glutamate relationship and found below statement – it is actually just abstract of some scientific paper which I don´t have in full copy. Also bear in mind that Lida Mattman gave us evidence spirochetes indeed can be found in brains, especially in MS and ALS patients, but also Lyme patients.

Enhanced synaptosomal glutamate release, associated with inhibition of glutamate uptake into astrocytes induced by QA could contribute to increase extracellular glutamate concentrations which ultimately lead to overstimulation of the glutamatergic system. These data provide additional evidence that neurotoxicity of QA may be also related to disturbances on the glutamatergic transport system, which could result in the neurological manifestations observed when this organic acid accumulates in the brain^​23​.

Summary & Open Question

I personally find the information I put together here quite interesting – my wish is if some research department could review that. It looks to me there are relationships which actually can lead to description of ALS mechanics on pretty low level (viruses, bacteria, cell interactions, chemicals and receptors involved). Please also note that I tried to build mainly on scientifical works of many people (see References section below).

Below images includes citations^{​4,11,24​}. Unfortunately I´m unable to understand how it is all realted if at all. It would be nice if some educated person explained this to me. I started with pretty insane Predator analogies but at the end I don´t think it is that insane, something strange may be happening – I have included another two citations which would not fit the picture.

B cells can transport complement (C3d)-opsonized immune complexes in the bloodstream, and B cells also have access to the lymphatic system. Thus, in principle, a B cell can transfer C3d-opsonized immune complexes between these compartments^​25​.

Autopsy of GBS patients who died 3–9 days after disease onset reveals products of complement activation (complement activation marker C3d and MACs) bound to the outer rim of many peripheral nerve fibers and Schwann cell membranes (87). In these patients, disruption of myelin occurs after complement activation but before the invasion of the region by macrophages (87). This indicates that the initial nerve damage is complement mediated and associated with MAC, rather than macrophage, attack (87). This damage is then amplified by macrophages which, in addition to engulfing myelin, may further the damage by releasing injurious molecules such as ROS, NO, proteases, acids, eicosanoids, and proinflammatory cytokines (97)^​26​.

And finally a role of microbial agents.

A role for complement C3 cleavage products as regulators of B cell signaling and humoral immunity has been appreciated for decades (1, 2). Activated C3 forms covalent bonds with foreign Ags and generates C3dg and C3d cleavage products that can supply physiologically relevant ligands for the human CD21 and mouse CD21/35 complement receptors expressed by mature B cells and follicular dendritic cells (3, 4). C3dg and C3d also function as natural adjuvants to enhance humoral immune responses to Ags, including pneumococcal capsular polysaccharide, hen egg lysozyme (HEL),5 streptavidin (SA), HIV gp120, and influenza or measles virus hemagglutinin (5, 6, 7, 8, 9, 10). Moreover, deficiencies in either C3 or the common gene that generates C3 complement receptors 1 (CD35) and 2 (CD21) result in impaired Ab responses in mice (11, 12, 13, 14, 15, 16, 17). However, complement components may also exhibit immunosuppressive activities (18). For example, C3 depletion by cobra venom factor can inhibit primary, yet enhance secondary, humoral immune responses to both unmodified and protein-conjugated pneumococcal polysaccharide (19). Furthermore, C3d attachment to certain Ags can inhibit humoral responses to the nontoxic diphtheria toxin fragment B (DT), human chorionic gonadotropin, bovine rotavirus VP7, bovine herpesvirus type 1 glycoprotein D, and malarial circumsporozoite protein (20, 21, 22, 23). Thus, in addition to its positive role in regulating immune responses, complement may negatively regulate humoral immunity through unknown mechanisms^​27​.

• 

References

1. 1.

   Hepatitis Table. CDC. Accessed December 2020. https://www.cdc.gov/hepatitis/resources/professionals/pdfs/abctable.pdf
2. 2.

   William A. Medical Medium Celery Juice: The Most Powerful Medicine of Our Time Healing Millions Worldwide . Hay House Inc.; 2019.
3. 3.

   Ryan F. Virusphere. WilliamCollinsBooks; 2019.
4. 4.

   Epstein Barr Virus. National Institute Of Health. Accessed December 2020. https://www.ncbi.nlm.nih.gov/books/NBK304353/
5. 5.

   Ayadi W, Feki L, Khabir A, et al. Polymorphism analysis of Epstein-Barr virus isolates of nasopharyngeal carcinoma biopsies from Tunisian patients. Virus Genes. Published online January 11, 2007:137-145. doi:10.1007/s11262-006-0051-2
6. 6.

   Sompayrac LM. How the Immune System Works. 6th ed. Wiley-Blackwell; 2019.
7. 7.

   Cell Death. Wikipedia. Accessed December 2020. https://en.wikipedia.org/wiki/Cell_death
8. 8.

   Galluzzi L, Vitale I, Aaronson SA, et al. Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018. Cell Death Differ. Published online January 23, 2018:486-541. doi:10.1038/s41418-017-0012-4
9. 9.

   Tait SWG, Ichim G, Green DR. Die another way – non-apoptotic mechanisms of cell death. J Cell Sci. Published online May 15, 2014:2135-2144. doi:10.1242/jcs.093575
10. 10.

    Elmore S. Apoptosis: A Review of Programmed Cell Death. Toxicol Pathol. Published online June 2007:495-516. doi:10.1080/01926230701320337
11. 11.

    Khan G, Hassani A. Epstein-Barr Virus in Multiple Sclerosis. In: Multiple Sclerosis [Working Title]. IntechOpen; 2019. doi:10.5772/intechopen.85222
12. 12.

    Odoya E, Norris M. Anatomy & Physiology For Dummies. 3rd ed. John Wiley & Sons, Inc.; 2017.
13. 13.

    Schwartz M, London A. Neuroimmunity: A New Science That Will Revolutionize How We Keep Our Brains Healthy and Young. Yale University Press; 2015.
14. 14.

    Adaes S. What Is Glutamate? Neurohacker.com. Accessed December 2020. https://neurohacker.com/what-is-glutamate
15. 15.

    Believe It: Astrocytes Kill Neurons in New ALS Model. AlzForum. Accessed December 2020. https://www.alzforum.org/news/research-news/believe-it-astrocytes-kill-neurons-new-als-model
16. 16.

    Kawaguchi Y, Mori Y, Kimura H, eds. Human Herpesviruses (Advances in Experimental Medicine and Biology Book 1045). 1st ed. Springer; 2018.
17. 17.

    Readhead B, Haure-Mirande J-V, Funk CC, et al. Multiscale Analysis of Independent Alzheimer’s Cohorts Finds Disruption of Molecular, Genetic, and Clinical Networks by Human Herpesvirus. Neuron. Published online July 2018:64-82.e7. doi:10.1016/j.neuron.2018.05.023
18. 18.

    Charvet B, Reynaud JM, Gourru-Lesimple G, Perron H, Marche PN, Horvat B. Induction of Proinflammatory Multiple Sclerosis-Associated Retrovirus Envelope Protein by Human Herpesvirus-6A and CD46 Receptor Engagement. Front Immunol. Published online December 6, 2018. doi:10.3389/fimmu.2018.02803
19. 19.

    Mattman LH. Cell Wall Deficient Forms: Stealth Pathogens. 3rd ed. CRC Press; 2000.
20. 20.

    Buhner SH. Healing Lyme: Natural Healing and Prevention of Lyme Borreliosis and Its Coinfections. Raven Press; 2005.
21. 21.

    Reactive Oxygen Species. Wikipedia. Accessed December 2020. https://en.wikipedia.org/wiki/Reactive_oxygen_species
22. 22.

    Ono S, Toyokura Y, Mannen T, Ishibashi Y. “Delayed return phenomenon” in amyotrophic lateral sclerosis. Acta Neurologica Scandinavica. Published online February 1988:102-107. doi:10.1111/j.1600-0404.1988.tb05879.x
23. 23.

    Tavares RG, Tasca CI, Santos CES, et al. Quinolinic acid stimulates synaptosomal glutamate release and inhibits glutamate uptake into astrocytes. Neurochemistry International. Published online June 2002:621-627. doi:10.1016/s0197-0186(01)00133-4
24. 24.

    Hafer-Macko C, Hsieh S-T, Ho TW, et al. Acute motor axonal neuropathy: An antibody-mediated attack on axolemma. Ann Neurol. Published online October 1996:635-644. doi:10.1002/ana.410400414
25. 25.

    Lindorfer MA, Köhl J, Taylor RP. Interactions Between the Complement System and Fcγ Receptors. In: Antibody Fc. Elsevier; 2014:49-74. doi:10.1016/b978-0-12-394802-1.00003-0
26. 26.

    Watkins LR, Maier SF. Beyond Neurons: Evidence That Immune and Glial Cells Contribute to Pathological Pain States. Physiological Reviews. Published online January 10, 2002:981-1011. doi:10.1152/physrev.00011.2002
27. 27.

    Lee Y, Haas KM, Gor DO, et al. Complement Component C3d-Antigen Complexes Can Either Augment or Inhibit B Lymphocyte Activation and Humoral Immunity in Mice Depending on the Degree of CD21/CD19 Complex Engagement. J Immunol. Published online December 8, 2005:8011-8023. doi:10.4049/jimmunol.175.12.8011

Series Navigation

<< My Story – Program XVerdict >>