Title:
Autoimmune Cross-targeting Hypothesis. The "ins and outs" of the immune system.
Abstract:
The trigger of autoimmunity has remained elusive. Genetic susceptibility and infections contribute to the development of autoimmunity but the pathogenesis has not been clear. This Cross-targeting hypothesis suggests that simultaneous infections on one target triggers autoimmunity. One infection on the outside of the target cell and one infection on the inside of the target.
Introduction:
Paul Ehrlich called it Horror autotoxicus when the immune system attacks self tissue, we call it autoimmunity. Under normal healthy conditions our immune system does not attack self tissue because the immune system has built up a tolerance to self proteins by educating it's B cells and T cells. T cells are educated to recognize the inside of cells while B cells are educated to recognize the outside of our own cells. Both of these "educations" must be compromised for the immune system to attack self.
Hypothesis:
It is my contention that in order for autoimmune disease to occur two different infections must be attacking the same target tissue. Cross-targeting is a military term for when a target is attacked from 2 different platforms. I will use this term for the 2 branches of the immune system attacking at the same time on the same target. Those immune cells attacking the outside of a cell to kill large infections and those attacking viruses on the inside. It is this state of both B cell and T cell educations uncoupling and attacking at the same time that causes autoimmunity. There is nothing to hold the immune system back from killing the entire cell thus autoimmunity develops.
Evaluation of Hypothesis:
The pathogenesis of autoimmune disease can be elucidated if autoimmune diseases are analyzed as a group and the overlapping characteristics are established as key. Think of autoimmune diseases in terms of the target tissue and infections.
Most autoimmune diseases can have multiple infection triggers and they don't have a specific time table until you look at it in terms of infection. One virus on the inside and one larger infection marking the outside. Typically the larger infection take hold first first and for some reason has not been eradicated before the second infections appears. Then a virus can mark the inside of the target cell but you only need one to mark the inside. The autoimmune disease is not triggered unless infections are marking both the inside and the outside at the same time.
When autoimmune diseases appear linked together it is because they share an infection. For example they could all have e.coli as the larger infection marking the outside. E.coli has been found in the bladder, in the intestine, in the pancreas, and in the liver. It is only when one is unlucky enough to have simultaneous inner and outer infections on the same target that autoimmunity develops.
Some autoimmune diseases have associations to gluten sensitivity but this is not a digestion issue or needed for autoimmunity to develop rather an indication of the type of infection involved in the disease. Different infections cause gluten sensitivity because they are barrier breaking infections with the ability to cross the intestine or the blood brain barrier. I will attempt to show evidence of this.
The pathogenesis of autoimmunity can be elucidated if we just look at the areas of overlap we can see the significance of the autoimmune target, of the infection’s similar abilities, and of the autoimmune diseases having shared infection triggers. Think of autoimmunity in terms of target and infections.
The significance of
the target in autoimmune disease
Autoimmune disease is when the
immune system has decided to attack self tissue. Each autoimmune disease has a core target tissue that is being
attacked. The hypothesis is that cross-targeting is occurring at this target. This pattern can be found in all autoimmune diseases.
For example, in type one diabetes the immune system has decided to attack the pancreas. The development of the autoimmunity on this target is not random but selected by the infections. Two viruses have been associated with the development of type one diabetes the coxsackie virus and the flu virus. Both of these viruses can and do replicate inside of pancreatic cells but it only takes one virus to mark the inside.
Viruses do not infect all body cells rather they only gain entry into target cells by using specific receptors as door knobs. Flu viruses have a tendency to infect dopamine-2 receptor organs which makes me suspect this receptor. The pancreas has the D2 receptor which might explain how the flu viruses replicate there.
Larger infections have also been found infecting pancreatic cells from the outside: mycoplasmas, e.coli, and candida. So which infection is responsible for the development of autoimmune type one diabetes out of these lists? All of them and yet only one of them on the outside at a time is needed to trigger type one diabetes.
The trick is that the outside and the inside of the pancreas cell must be under attack simultaneously for autoimmunity to result. Imagine a pancreatic cell having a flu virus on the inside and the outside infected at the same time by mycoplasmas. It is this state of cross-targeting that I believe causes the immune system to go into an autoimmune attack and destroy the entire target tissue. The immune system has lost it's tolerance education. Normally if the immune system is attacking an infection on the outside the immune system's education of the inside protects the cell from complete destruction and vice a versa. Remember B cells have been educated to know all of the outside self proteins and Tcells have been educated to know all of the inner cell proteins. If the immune system decides that both of these areas need destruction what would save the target tissue?
For example, in type one diabetes the immune system has decided to attack the pancreas. The development of the autoimmunity on this target is not random but selected by the infections. Two viruses have been associated with the development of type one diabetes the coxsackie virus and the flu virus. Both of these viruses can and do replicate inside of pancreatic cells but it only takes one virus to mark the inside.
Viruses do not infect all body cells rather they only gain entry into target cells by using specific receptors as door knobs. Flu viruses have a tendency to infect dopamine-2 receptor organs which makes me suspect this receptor. The pancreas has the D2 receptor which might explain how the flu viruses replicate there.
Larger infections have also been found infecting pancreatic cells from the outside: mycoplasmas, e.coli, and candida. So which infection is responsible for the development of autoimmune type one diabetes out of these lists? All of them and yet only one of them on the outside at a time is needed to trigger type one diabetes.
The trick is that the outside and the inside of the pancreas cell must be under attack simultaneously for autoimmunity to result. Imagine a pancreatic cell having a flu virus on the inside and the outside infected at the same time by mycoplasmas. It is this state of cross-targeting that I believe causes the immune system to go into an autoimmune attack and destroy the entire target tissue. The immune system has lost it's tolerance education. Normally if the immune system is attacking an infection on the outside the immune system's education of the inside protects the cell from complete destruction and vice a versa. Remember B cells have been educated to know all of the outside self proteins and Tcells have been educated to know all of the inner cell proteins. If the immune system decides that both of these areas need destruction what would save the target tissue?
Most autoimmune diseases appear to fit this inside and outside cross-targeting problem. Multiple sclerosis for example has been found to appear after shingles but not everyone with shingles develops it. People with psoriasis also have higher rates of multiple sclerosis but not everyone with psoriasis gets it. Now put into place the cross-targeting hypothesis. Shingles is the herpes zoster virus that would mark the inside of the nerves while psoriasis if it is a mycobacteria infection which likes the myelin sheath marks the outside of the nerve. The inside and the outside of the nerve would be marked to the immune system at the same time. Are people who have shingles while they have psoriasis the ones at risk for multiple sclerosis?
What about the vaccine induced autoimmunity? This cross-targeting hypothesis can be applied to vaccine reactions. The DTP vaccine has three bacterial infections that it inoculates for : diphtheria, pertussis, and tetanus. Only one of these bacterial infections exists in the temporal lobe of the brain and that is tetanus. When the vaccine is given even if the disease is prevented a small amount of antibodies would end up at the temporal lobe because those virus pieces bind there. Why pick tetanus out of this list ? Some autism patients have HHV6 with the neural autoantibodies. This 6th disease known for it’s rash Roseola is a virus that replicates in the temporal lobe of the brain. Applying the cross-targeting hypothesis on the temporal lobe suggest that if a child with 6th disease gets the dtp vaccine they could develop an autoimmune attack of the temporal lobe thus developing an autism disease of this part of the brain.
What about the infamous MMR vaccine? Autoantibodies for the measles part of that
vaccine have been seen in a group of autistic kids and measles migrates to the cerebellum. Clusters of autistic kids have been
found to have sutterella bacteria in their system too. Sutterella is closely related to campylobacteria which can infect the cerebellum. Does the cross-targeting of the measles vaccine and sutterella cause an autoimmune attack of the cerebellum? Is this
possible?
What about the children born with autism that were not induced by vaccines? Pregnant women with Rheumatoid arthritis are more likely to have autistic children. Women who catch the flu during pregnancy are more likely to have autistic kids. If we apply the cross-targeting hypothesis and look for a specific target we find the frontal lobe in this form of autism. Antibodies to the frontal lobe have been found in mother's with rheumatoid arthritis. The flu (H1N1) when it has infected the brain of the young children has been found in the frontal lobe region. It is possible that an unborn fetus develops an autoimmune form of autism on the frontal lobe when both of these infections occur at the same time in a pregnant woman.
Are children the only ones susceptible to autoimmune brain disease? I don't think so. Parkinson's disease has been associated with psoriasis' mycobacteria and nocardia which are infections capable of crossing the blood brain barrier. Parkinson's has also been connected to the flu H5N1, west nile, and dengue viruses. These infections like the basal ganglia area of the brain specifically the Substantia Nigra area. Parkinson's could very likely be cross-targeting autoimmunity of the substantia nigra.
The key theme here is knowing the core target tissue of the autoimmune disease. If you know the target tissue and you know what can infect this tissue then be careful not to cross-target. Prevention would be to kill the current infection as quickly as possible or vaccinating when healthy.
For example if the d68 virus is cross-targeting with staph on the nerves causing paralysis and we know that there is a strong association of eczema with staph then we know what group of children are vulnerable to paralysis. Maybe we should be treating kids with eczema for staph during outbreaks of d68. Watching for and preventing infections before the risk of paralysis.
The exception to this infection driven hypothesis is the drug-induced autoimmunity. Cross-targeting is still occurring triggering when drugs are triggering the immune system but a drug replaces an infection.
Drug induced lupus can be triggered by monocycline and hydralazine. Hydralazine is a muscle relaxer and works inside the muscles cells. Monocycline which is an acne medication is known to penetrate muscles and cause severe muscle cramping. Either of these drugs could replace the viral infection which marks the inside of the cell. A patient with autoimmune liver disease makes anti-muscle antibodies which would mark the outside. If the outside and the inside of the muscle appears marked or foreign to the immune system cross-targeting autoimmunity could result.
The reverse scenario can also occur. Hemolytic anemia is triggered when a drug like penicillin coats the outside of the red blood cells. Normally this would not be an issue but if the person had recently had the RSV virus which replicates in bone marrow or had chronic hepatitis C which might try to infect red blood cells and the virus was still visible in the red blood cells it might trigger autoimmunity.
This leads us to the next autoimmune issue of recognizing and diagnosing what you are infected with. People who host parasites like t.gondii, yeasts, mycobacterias or mycoplasmas will find this hard to accept and it is still hard to diagnose. Very little is known about the good verse the bad microbes even in our digestive system but we must learn what is there and what they can do.
What about the children born with autism that were not induced by vaccines? Pregnant women with Rheumatoid arthritis are more likely to have autistic children. Women who catch the flu during pregnancy are more likely to have autistic kids. If we apply the cross-targeting hypothesis and look for a specific target we find the frontal lobe in this form of autism. Antibodies to the frontal lobe have been found in mother's with rheumatoid arthritis. The flu (H1N1) when it has infected the brain of the young children has been found in the frontal lobe region. It is possible that an unborn fetus develops an autoimmune form of autism on the frontal lobe when both of these infections occur at the same time in a pregnant woman.
Are children the only ones susceptible to autoimmune brain disease? I don't think so. Parkinson's disease has been associated with psoriasis' mycobacteria and nocardia which are infections capable of crossing the blood brain barrier. Parkinson's has also been connected to the flu H5N1, west nile, and dengue viruses. These infections like the basal ganglia area of the brain specifically the Substantia Nigra area. Parkinson's could very likely be cross-targeting autoimmunity of the substantia nigra.
The key theme here is knowing the core target tissue of the autoimmune disease. If you know the target tissue and you know what can infect this tissue then be careful not to cross-target. Prevention would be to kill the current infection as quickly as possible or vaccinating when healthy.
For example if the d68 virus is cross-targeting with staph on the nerves causing paralysis and we know that there is a strong association of eczema with staph then we know what group of children are vulnerable to paralysis. Maybe we should be treating kids with eczema for staph during outbreaks of d68. Watching for and preventing infections before the risk of paralysis.
The exception to this infection driven hypothesis is the drug-induced autoimmunity. Cross-targeting is still occurring triggering when drugs are triggering the immune system but a drug replaces an infection.
Drug induced lupus can be triggered by monocycline and hydralazine. Hydralazine is a muscle relaxer and works inside the muscles cells. Monocycline which is an acne medication is known to penetrate muscles and cause severe muscle cramping. Either of these drugs could replace the viral infection which marks the inside of the cell. A patient with autoimmune liver disease makes anti-muscle antibodies which would mark the outside. If the outside and the inside of the muscle appears marked or foreign to the immune system cross-targeting autoimmunity could result.
The reverse scenario can also occur. Hemolytic anemia is triggered when a drug like penicillin coats the outside of the red blood cells. Normally this would not be an issue but if the person had recently had the RSV virus which replicates in bone marrow or had chronic hepatitis C which might try to infect red blood cells and the virus was still visible in the red blood cells it might trigger autoimmunity.
This leads us to the next autoimmune issue of recognizing and diagnosing what you are infected with. People who host parasites like t.gondii, yeasts, mycobacterias or mycoplasmas will find this hard to accept and it is still hard to diagnose. Very little is known about the good verse the bad microbes even in our digestive system but we must learn what is there and what they can do.
The significance of similar infection abilities
Gluten sensitivity has appeared in
multiple autoimmune diseases. Autism,
schizophrenia, celiac disease, pandas, parkinson's, and
psoriasis to name a few . The infections
associated with these diseases are e.coli, sutterella, strep, candida, and
mycobacterias. The associations are unproven but suggestive because they all have the ability to cross the intestine and the blood
brain barrier. Gluten is a macromolecule. It is huge. The sensitivity to gluten
could be because these infections have made a hole in the barrier which then
allows the gluten across to interact with the immune system at the other side. Obviously these infections attack differently
but all of them break barriers by crossing them.
The notorious t.gondii which first crosses the intestine then crosses into the brain where it nests around the amygdala is probably the easiest to study. Days after infection with t.gondii, mice become gluten sensitive and will show an antibody response to gluten.
The notorious t.gondii which first crosses the intestine then crosses into the brain where it nests around the amygdala is probably the easiest to study. Days after infection with t.gondii, mice become gluten sensitive and will show an antibody response to gluten.
I believe Celiac disease has a magnified
reaction to gluten compared to the other autoimmune diseases only because of the location of this autoimmune disease target at the intestinal lining where the barrier is broken. Autoimmune reaction on top of barrier breaking. Gluten has been considered to be “the trigger” of celiac disease causing the immune system attacks upon the intestinal lining. This is indirectly true because gluten has been demonstrated to ramp up the immune system. Gliadin has been shown to interact with the immune system ramping up macrophages. The immune system becomes hyper right where the cross-targeting autoimmunity is occurring at the intestine with e.coli thus the reaction to gluten will be stronger because of the location getting mixed up with the autoimmune reaction.
Patients of celiac disease often have a history of bladder infections. E.coli is the most common culprit of bladder infections. If the infection spreads to the intestine E.coli would cling in a feather like attachment all over the intestinal lining. At first the patient would only have gluten sensitivity. Then, in time, a stomach virus like the adenovirus or hepatitis C could infect the lining. Gluten would hype up the immune system when it leaks across the barrier hole made by e.coli making the autoimmune reaction even worse. Other bacterial infections might cause autoimmunity but the intestine is filled with bacteria that normally don't set off the immune system. Understanding how the immune system discriminates here will be key to figuring out the cause of celiac disease.
Think of gluten as potentiating the immune reaction once it gets to the other side of the barrier. Gluten has been shown to inflame the immune system after crossing the barriers. Wise not to eat gluten because it hightens the inflammatory response.
Patients of celiac disease often have a history of bladder infections. E.coli is the most common culprit of bladder infections. If the infection spreads to the intestine E.coli would cling in a feather like attachment all over the intestinal lining. At first the patient would only have gluten sensitivity. Then, in time, a stomach virus like the adenovirus or hepatitis C could infect the lining. Gluten would hype up the immune system when it leaks across the barrier hole made by e.coli making the autoimmune reaction even worse. Other bacterial infections might cause autoimmunity but the intestine is filled with bacteria that normally don't set off the immune system. Understanding how the immune system discriminates here will be key to figuring out the cause of celiac disease.
Think of gluten as potentiating the immune reaction once it gets to the other side of the barrier. Gluten has been shown to inflame the immune system after crossing the barriers. Wise not to eat gluten because it hightens the inflammatory response.
If we say that Gluten
sensitivity occurs at both the barriers: the brain and the intestine and that gluten sensitivity occurs by breaking the barrier we can now predict other gluten sensitive infections.. Strep for instance is suspected for it's ability to cross the blood brain barrier to trigger the Panda's autoimmune reaction called Sydenham's chorea. Suspiciously gluten sensitivity has also been associated with chlorea. Would a strep infection of the intestine eventually lead to gluten sensitivity? Strep does break the barriers.
Gluten sensitivity, I believe, can warn us when we are vulnerable. When we are sensitive to gluten we have "holes". Normally our immune system and any viruses we have do not normally have access to the brain. Many of us have different forms of herpes viruses hiding out in our body. Once a hole has been created in the blood brain barrier mental issues may result not just from the entering infections, not just from gluten, but from the viruses seeping in the hole after these infections. In other words gluten sensitivity should not just be about avoiding gluten but figuring out what infection is there as quickly as you can before you catch a virus. My hypothesis is the autoimmune disease will only appear when a virus triggers cross-targeting with an larger infection.
Allergies can also help us determine what infections we have by revealing an infection's reaction. Autoimmune diseases tend to have associated allergies. The staph of eczema makes a pigment with egg and milk which ironically are the allergies associated with eczema. Is the immune system reacting to a pigment change in the infection? What of other allergies? Bee venom has been found to kill t.cruzi and t.gondii. Could people with t.gondii or t.cruzi allergies be the ones with bee allergies? Allergists should compare the autoimmune histories of their patients with the known allergies. I am betting patterns appear.
Gluten sensitivity, I believe, can warn us when we are vulnerable. When we are sensitive to gluten we have "holes". Normally our immune system and any viruses we have do not normally have access to the brain. Many of us have different forms of herpes viruses hiding out in our body. Once a hole has been created in the blood brain barrier mental issues may result not just from the entering infections, not just from gluten, but from the viruses seeping in the hole after these infections. In other words gluten sensitivity should not just be about avoiding gluten but figuring out what infection is there as quickly as you can before you catch a virus. My hypothesis is the autoimmune disease will only appear when a virus triggers cross-targeting with an larger infection.
Allergies can also help us determine what infections we have by revealing an infection's reaction. Autoimmune diseases tend to have associated allergies. The staph of eczema makes a pigment with egg and milk which ironically are the allergies associated with eczema. Is the immune system reacting to a pigment change in the infection? What of other allergies? Bee venom has been found to kill t.cruzi and t.gondii. Could people with t.gondii or t.cruzi allergies be the ones with bee allergies? Allergists should compare the autoimmune histories of their patients with the known allergies. I am betting patterns appear.
The significance of
shared infection triggers
It has become accepted that some autoimmune diseases have
associated autoimmune disease families. If you have one autoimmune disease your risk for another autoimmune disease goes up, but specific ones. If you start looking for shared possible infections in these families you realize that
although an individual autoimmune disease has several culprits only one suspect is common
for the group.
Looking at the outer larger infection we can see families form. Parkinson’s, psoriasis, crohn’s, and multiple sclerosis are all mycobacteria associated. Celiac disease, type one diabetes, and autoimmune liver disease can all be associated with e.coli. Sjogren's, Hashimoto's, Microscopic colitis, and Vitiligo have all been associated with various fungal infections. (yeasts and molds) RA, graves, and type one diabetes have all been connected with mycoplasmas. Each autoimmune disease has a different virus associated but the large infections match.
Looking at the inner viral infections we see patterns linked to receptors. The Herpes viruses seem to use estrogen receptors which in nerves cycle to the mitochondria. The autoimmune diseases associated with the herpes viruses tend to involve the central nervous system: Multiple sclerosis, Guillian Barre, and Encephalitis. As mentioned earlier flu viruses use the D2 dopamine receptors which not all tissues have but the pancreas does.
Seizures often have associations with viruses. Enteroviruses may, no evidence to prove yet, be using nicotinic acetylcholine receptors. Enteroviruses could be infecting the hypothalamus and can cross-target with whatever parasite appears there. Is there an enterovirus causing seizures with t.gonidii in schizophrenia, with pertussis in dtp vaccines, and as polio with a parasite in Africa? The nodding disease of Africa, which is a type of seizure, could be the black fly parasite cross-targeting with the live polio vaccine which as an enterovirus replicates in the hypothalamus. Understanding how one infection family works lead to the ability to predict other families. The malaria seizures could be similar with autoimmune cross-targeting because severity of the seizure increases when both the parasite and virus are detected there.
Considering malaria, outside of seizures, could help explain Central America's Chronic kidney disease. A mysterious disease of sugar cane workers who we know are constantly infected with the malaria parasite. One of the organs infected by the malaria parasite is the kidney. If chronic kidney disease is autoimmune we need a virus marking the inside of the kidney cells. In this case enteroviruses don't infect kidneys. Adenoviruses on the other hand can infect the kidney. If a sugar cane worker with a malaria parasite catches an adenovirus then cross-targeting could occur on the kidney and result in an autoimmune chronic kidney disease. If we look maybe we will find this adenovirus.
Conclusion:
The pathogenesis of autoimmune disease can be elucidated if autoimmune diseases are analyzed as targets and infections. The overlapping characteristics are key to understanding what we are really looking at, which infections we are looking at. Think of the immune system cross-targeting on one target as the trigger for autoimmune disease. What infections are shared among autoimmune disease families, what is the target tissue, and what these infections have in common can give us not just insight into how autoimmune disease is triggered but how to prevent them and maybe even cure them.
I need to respectfully identify Dr. Andrew Church and Dr. Russel Dale who work on Encephalitis Lethargia.
Everyone remembers the 1990 Awakenings movie with Robin Williams as Dr. Oliver who in 1918 dealt with a cluster of encephalitis lethargia patients. In 1993 Dr. Andrew Church found himself with another Encephalitis cluster and he discovered that 2 infections were there not just the flu. Dr. Andrew discovered that a high number of his patients had a rare form of strep called Diplococcus along with the spanish flu. He has spent a life time trying to piece together this disease. In 2011 Dr. Andrew and Dr. Russel came out with a paper proving Encelpalitis lethargia was an autoimmune disease with antibodies directed at the Basal Ganglia. This is possibly the first paper supporting cross-targeting as the trigger for autoimmune disease.
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Looking at the outer larger infection we can see families form. Parkinson’s, psoriasis, crohn’s, and multiple sclerosis are all mycobacteria associated. Celiac disease, type one diabetes, and autoimmune liver disease can all be associated with e.coli. Sjogren's, Hashimoto's, Microscopic colitis, and Vitiligo have all been associated with various fungal infections. (yeasts and molds) RA, graves, and type one diabetes have all been connected with mycoplasmas. Each autoimmune disease has a different virus associated but the large infections match.
Looking at the inner viral infections we see patterns linked to receptors. The Herpes viruses seem to use estrogen receptors which in nerves cycle to the mitochondria. The autoimmune diseases associated with the herpes viruses tend to involve the central nervous system: Multiple sclerosis, Guillian Barre, and Encephalitis. As mentioned earlier flu viruses use the D2 dopamine receptors which not all tissues have but the pancreas does.
Seizures often have associations with viruses. Enteroviruses may, no evidence to prove yet, be using nicotinic acetylcholine receptors. Enteroviruses could be infecting the hypothalamus and can cross-target with whatever parasite appears there. Is there an enterovirus causing seizures with t.gonidii in schizophrenia, with pertussis in dtp vaccines, and as polio with a parasite in Africa? The nodding disease of Africa, which is a type of seizure, could be the black fly parasite cross-targeting with the live polio vaccine which as an enterovirus replicates in the hypothalamus. Understanding how one infection family works lead to the ability to predict other families. The malaria seizures could be similar with autoimmune cross-targeting because severity of the seizure increases when both the parasite and virus are detected there.
Considering malaria, outside of seizures, could help explain Central America's Chronic kidney disease. A mysterious disease of sugar cane workers who we know are constantly infected with the malaria parasite. One of the organs infected by the malaria parasite is the kidney. If chronic kidney disease is autoimmune we need a virus marking the inside of the kidney cells. In this case enteroviruses don't infect kidneys. Adenoviruses on the other hand can infect the kidney. If a sugar cane worker with a malaria parasite catches an adenovirus then cross-targeting could occur on the kidney and result in an autoimmune chronic kidney disease. If we look maybe we will find this adenovirus.
Conclusion:
The pathogenesis of autoimmune disease can be elucidated if autoimmune diseases are analyzed as targets and infections. The overlapping characteristics are key to understanding what we are really looking at, which infections we are looking at. Think of the immune system cross-targeting on one target as the trigger for autoimmune disease. What infections are shared among autoimmune disease families, what is the target tissue, and what these infections have in common can give us not just insight into how autoimmune disease is triggered but how to prevent them and maybe even cure them.
I need to respectfully identify Dr. Andrew Church and Dr. Russel Dale who work on Encephalitis Lethargia.
Everyone remembers the 1990 Awakenings movie with Robin Williams as Dr. Oliver who in 1918 dealt with a cluster of encephalitis lethargia patients. In 1993 Dr. Andrew Church found himself with another Encephalitis cluster and he discovered that 2 infections were there not just the flu. Dr. Andrew discovered that a high number of his patients had a rare form of strep called Diplococcus along with the spanish flu. He has spent a life time trying to piece together this disease. In 2011 Dr. Andrew and Dr. Russel came out with a paper proving Encelpalitis lethargia was an autoimmune disease with antibodies directed at the Basal Ganglia. This is possibly the first paper supporting cross-targeting as the trigger for autoimmune disease.
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