Infections as Triggers for Autoimmune Disease with Dr. Aristo Vojdani: Rational Wellness Podcast 192

Dr. Aristo Vojdani speaks about Infections as Triggers for Autoimmune Disease with Dr. Ben Weitz at the Functional Medicine Discussion Group meeting on January 28, 2021.

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Podcast Highlights

8:10  The way the immune system works is that after infection with a virus you develop antibodies, which disappear after a number of months, but this does not mean that you no longer have immunity.  Our first line of defense is our macrophages which break up the virus particle into smaller pieces called antigens. The antigen is presented to antigen presenting cells, which are T helper cells. T helper cells produce various cytokines, which become cytotoxic lymphocytes, which kill viruses and also target tumor cells. The T helper cells then communicate with B cells, which divide to become plasma cells that produce antibodies against the viral antigens. It takes about 14 days for these plasma cells to produce different isotypes of antibodies (IgM, IgG). If the phagocytes could not finish the job and the cytotoxic lymphocyte could not do the job, then the antibody will bind to the virus and then the complex of the antibody plus the virus will be more easily destroyed by our immune system. Also, when the T helper cells become activated and present the information to the B cells, another subset of T helper cells, memory T cells will be created that last forever and give you lifetime immunity.  There are also memory B cells that are also in your body forever.  If the same virus were to re-enter the body, the memory T and the memory B cells will produce antibodies within hours that will protect you against the virus.

14:57  We often hear public health experts on TV saying that we don’t yet know if you get long term immunity after getting COVID-19, but Dr. Vojdani says that we should expect that there will be long term immunity because this is what always happens after viral infection. This is written in immunology textbooks and this infection is similar to others in many ways.  When the body gets exposed to any antigen, including the SARS-COV-2 viral antigen, IgM antibodies will be produced, followed by IgG antibodies. IgM will stay in the body for two to four weeks and the IgG will typically stay in the body for up to three months. The same thing happens when you get vaccinated.  When you get your second vaccination you will get a similar IgM response but the IgG response will be 10 times the original IgG response.  But then within 3 months the antibodies will tend to fade to a low background level or disappear.

18:42  Viruses have been in the environment for millions of years and scientists estimate that 380 trillion viruses live on or inside the human body.  There is a lot of discussion about the microbiome, but few people talk about the virome. And there are many beneficial viruses in our body. Viruses are made up of particles of DNA and RNA and they cannot replicate on their own. They have to infect cells in order to replicate and once they get inside a cell, they use material from that cell in order to replicate. During this replication, the virus mutates to acquire proteins that share that homology, so that it can hide from the immune system. This encourages cross reactivity of the immune system, which may result in autoimmunity.  Dr. Vojdani published about cross reactivity between wheat gliadin and the brain.  The lymphocytes react to wheat gliadin and make antibodies against gliadin. Because components of gliadin look like cerebellar tissue, the immune system will attack the cerebellum of the brain.  This is an autoimmune reaction against the brain resulting from eating wheat due to cross-reactivity.  Cross-reactivity is also why off target vaccines such as with the BCG vaccine or certain childhood vaccines can cause secondary activation of adaptive immunity and induction of effective secondary hypo-inflammatory antiviral immune response.  This can cause a drastic reduction in CD3 T cell activation, dampening of innate immune hyper activation, and finally, the result of that will be regeneration and recovery of the host health and survival.  So, that’s why giving vaccines other than SARS-CoV-2 to individuals suffering from COVID-19 may help to subvert the immune system from attacking the tissue through this process and save that individual from the virus.

27:05  Dr. Vojdani has published lots of scientific papers about cross-reactivity, including the following article in 2018 in the Journal of Alzheimer’s Disease: Vojdani A, Vojdani E, Saidara E, Kharrazian D. Reaction of Amyloid-β Peptide Antibody with Different Infectious Agents Involved in Alzheimer’s Disease. J Alzheimer’s Disease, 2018;63(2):847-860.  Dr. Vojdani looked at various pathogens, toxins, and foods that show cross-reactivity against amyloid peptide antibodies and this is part of Cyrex’s screen for the triggers of Alzheimer’s Disease, the Alzheimer’s LINX testThis includes an oral pathogen, enterococcus bacteria very similar to E.coli in our gut, cytolethal distending toxin, candida albicans, Giardia, Borrelia burgdorferi the agent of Lyme disease, and then some molds such as aspergillus and penicillium. These potential triggers also include HSV1 and EBV.  This test can play a role in screening for autoimmune reactivity and then use Dr. Bredesen’s methodologies for the 46.7 million Americans who have preclinical Alzheimer’s but do not have obvious symptoms and the two and a half million who have mild cognitive impairment. The earlier we can detect these preclinical triggers and make lifestyle changes, the better we can prevent Alzheimer’s Disease.  Here is the paper that Dr. Vojdani mentioned that was published by Dr. Christiana Franke, et al. published in Brain, Behavior, and Immunity in December 2020 on High Frequency of Cerebrospinal Fluid Autoantibodies in COVID-19 Patients with Neurological Symptoms.

35:24  Many pathogens can be triggers for autoimmune diseases, including bacteria, viruses, parasites, molds, yeast, and spirochetes like Lyme.  These are included in Cyrex’s Array 12, which is the Pathogen Associated Immune Reactivity Screen.  Dr. Vojdani recommends using a panel like this to test for antibodies against mold rather than using a urine mycotoxin test, which might be measuring mycotoxins coming from the food you are eating.




Dr. Aristo Vojdani is the Father of Functional Immunology and he has dedicated his life’s research to helping us figure out what are the triggers for autoimmune diseases and many of the tests he has developed for Cyrex Labs are focused on this.  Dr. Vojdani has a PhD in microbiology and immunology and he has authored over 200 scientific papers published in peer reviewed journals. Dr. Vojdani is the co-owner of Immunosciences Lab in Los Angeles, which offers testing for various types of infections, including Lyme Disease. He is the Chief Science advisor for Cyrex Labs, whom he has developed all of the testing for. He is also a professor in the Department of Preventative Medicine at Loma Linda University.  Dr. Vojdani recently published the following paper:  Vojdani A, Vojdani E, Kharrazian D. Reaction of Human Monoclonal Antibodies to SARS-CoV-2 Proteins With Tissue Antigens: Implications for Autoimmune Diseases. Front. Immunol., 19 January 2021.

Dr. Ben Weitz is available for nutrition consultations, including remote consults via video or phone, specializing in Functional Gastrointestinal Disorders like IBS/SIBO and Reflux and also specializing in Cardiometabolic Risk Factors like elevated lipids, high blood sugar, and high blood pressure and also weight loss, as well as sports chiropractic work by calling his Santa Monica office 310-395-3111 or go to www.drweitz.com. Phone or video consulting with Dr. Weitz is available.



Podcast Transcript

Dr. Weitz:                            Hey, this is Dr. Ben Weitz, host of the Rational Wellness Podcast. I talk to the leading health and nutrition experts and researchers in the field to bring you the latest in cutting edge health information. Subscribe to the Rational Wellness Podcast for weekly updates, and to learn more, check out my website, drweitz.com. Thanks for joining me, and let’s jump into the podcast.

                                                Autoimmune diseases are on the rise today, and there are at least 100 different autoimmune diseases and at least 40 other diseases that are suspected to have an auto-immune origin. If we include diseases that have an autoimmune basis, autoimmune diseases are the third leading cause of death in the United States, since most of these diseases are chronic and often life-threatening. Some of them are common autoimmune diseases, including Alzheimer’s disease, Parkinson’s disease, rheumatoid arthritis, Hashimoto’s hypothyroid, celiac disease, Graves type one diabetes, psoriasis, multiple sclerosis, Crohn’s disease and irritable bowel disease. But most of you probably know this already.  The immune system is designed to protect us from bacteria and viruses and parasites, et cetera, and to repair our tissues went damaged among other functions. Auto-immune diseases, as most of us know, are diseases where the immune system, instead of attacking pathogens, start attacking our own cells and organs. The immune system is out of balance, often referred to as immune dysregulation. While the conventional medical community is often content with simply prescribing an immune blocking or modulating medication to help control symptoms such as Humira or Enbrel. as functional medicine practitioners, we want to find out what are some of the root causes and correct these.

                                                There are three major categories of triggers for autoimmune diseases, and these are toxins like pesticides, bisphenol A, heavy metals, mycotoxins. We have food sensitivities and we have infections, which are our topic for tonight.  Now I would like to invite Heather Ngo from Cyrex Labs, who is our sponsor for this evening, to tell us some information about Cyrex Labs. Heather, go ahead and unmute yourself.


Heather Ngo:                     Hello, everyone. Thank you so much. My name is Heather Ngo, territory manager at Cyrex Labs, and our lab is based in Arizona and our focus is auto-immunity. We do offer barrier testing, evaluating the intestinal and blood-brain barrier integrity. We have environmental trigger testing, identifying reactivity, which includes dietary proteins, chemicals, and heavy metals. We have predictive antibody testing to define precursors of autoimmune disorders. A panel of cognitive health, identifying early signs of neural cognitive decline.

                                                We also have a saliva test evaluating possible outcomes of a compromised mucosal tolerance. We can ship out the serum or saliva kit directly to your patients, especially during this crazy time. And we are providing a show special for today.  It is $100 off on our pathogens panel. This panel has a 29 markers, consists of viral, bacterial, spirochete, parasite, yeast, and mold.  We are assessing just the IgG, the latent pathogens that may lead to multiple autoimmune reactions.  I just want you to know this promotion expires March the 15th, ’21, of this year, and if you have any questions or would like to schedule a one-on-one education, please call, text, email me to schedule it. I will also provide my contact information via the chat room. Thank you so much, Dr. Weitz, for having us, and I’m going to pass this invisible mic back to you. We’re so excited to listen to Dr. Vojdani’s presentation.



Dr. Weitz:                            Absolutely. Me too, and I promise not to drop the invisible mic. So our speaker for tonight is Dr. Aristo Vojdani, who I’m sure most of you already know. He is the father of functional immunology, and he’s dedicated his life to helping us figure out what are the triggers for autoimmune diseases, and many of the tests that he has developed for Cyrex Labs are focused on this, including the Array 12, which is the pathogen associated immune reactivity screen that Heather referred to. Dr. Vojdani has a PhD in microbiology and immunology, and he’s authored over 200 scientific papers published in peer reviewed journals. Dr. Vojdani is the co-owner of Immuno Sciences Lab in Los Angeles, which offers testing for various types of infections, including Lyme disease. He is the chief science advisor for Cyrex Labs, whom he has developed all the testing for.  He’s also a professor in the Department of Preventative Medicine at Loma Linda University, and I would like you to indulge me for one minute to tell you an anecdotal story. So I’ve been putting on these Functional Medicine meetings for about five years, and we’ve been honored to have Dr. Vojdani speak almost every year, except for last year. Usually I get the opportunity to have dinner with Dr. Vojdani about a week or so before we have the meetings so I can find out what he’s going to be talking about and I’m in a better position to try to ask some intelligent questions.  Usually Dr. Vojdani shows up for dinner with this huge stack of scientific papers that we ended up discussing, which is very exciting for a research geek like myself.  But the reason I’m telling you this is that if you don’t know, any statement that Dr Vojdani makes is informed by hundreds of scientific research papers.  So thank you so much for honoring us with your presence tonight, Dr. Aristo Vojdani.

Dr. Vojdani:                        Thank you.

Dr. Weitz:                           So Dr. Vojdani, if questions come up, would you like me to chime in, or do you want me to wait till the end?

Dr. Vojdani:                        Wait to the end and then please read the questions for me.

Dr. Weitz:                           Okay. You got it.

Dr. Vojdani:                        Okay. Thank you so much. So, first of all, thank you, Dr. Weitz, for your introduction. I’m happy to see many of you, many familiar faces. Heather, Michelle from Cyrex and in particular, I’m very proud to see my son Elroy. He’s one of the doctors who is participating tonight in this Zoom. So I’m going to talk about chronic infections as triggers for auto-immune diseases. So this is my disclosure. Already Dr. Weitz talked about this, Immuno Sciences Lab, Cyrex and Loma Linda University. 

There is a reason I’m going to start with the immune system tonight because, honestly, in the past year, almost past year or so, we heard so much about antibody, antibody, antibody.  And the antibodies do disappear after a month or two months and three months, and after that, we don’t have immunity against COVID.   That’s the reason I’m putting this slide to clarify this point.  So when we get exposed to a virus such as corona, SARS-CoV-2, this virus particle is too big for our T cell and B cells.  So macrophages, which are part of first line of defense, our innate immunity, will taking that up and breaking into smaller pieces called an antigen. Then they take that antigen, presenting that to antigen presenting cells, presenting that to T helper cells. However, let’s stop for a few seconds in here. So what will happen to that virus when macrophages is breaking that to smaller pieces?  It’s not anymore a virus.  So this is the most important part of our defense system, that our macrophages should be able to take that virus and break that to the pieces, and then give that to antigen presenting cells to the T helper cells.  This process will take probably a few seconds or few minutes. So that’s the most important part of our immune defenses. Then the antigen presenting cells, presenting that antigen to T helper cells.  T helper cells, by producing different types of cytokines become, cytotoxic lymphocytes. What is the job of cytotoxic lymphocyte? If the macrophages were not able to take care of some of these viruses and break them down to smaller pieces, the cytotoxic lymphocyte will go after any virus particles in our cells. Any cells, in fact, which are infected with that virus and destroy that virus, plus the cell, which is infected with that virus. This process will take few hours. Also, the job of cytotoxic lymphocyte is to kill tumor target cell. So this is our defense also against tumor cells.

                                         Now, T helper cells in the presence of different type of cytokines become T helper 1, or T helper 2, and then T helper cells communicate with B cells, giving all the information to the B cells about this viral antigens to start to divide to become plasma cells and to start producing antibodies against the viral antigens, process which takes about 14 days. Why it takes 14 days?  Because all this process of putting together the factory that manufactures antibody takes about 14 days. So after 14 days, these plasma cells will produce different isotypes of antibodies.  So if in case the phagocytes could not do the job or finish the job, the cytotoxic lymphocyte could not do the job. The antibody will bind to the virus and now complex of antibody plus viruses will be destroyed by our immune cells.    Furthermore, I would like to present in here that when T helper cells become activated and present the information to the B cells, another subset of T helper cells, which I don’t have it in here, just imagine should be right here, is going to be called memory T cell. That memory T cell will remember forever that had some kind of reaction to, in this case, SARS-CoV-2. Could be Epstein-Barr virus. So remember that computer called memory T cell is going to stay in the body forever.

Dr. Weitz:                           Is there any controversy about that, or is that absolute, definitely true, no matter what?

Dr. Vojdani:                        It is absolutely true, no matter what. Thank you for asking that. Okay, there is a reason, again, I put this slide in the beginning. So memory T cells, there are short-term memory T cells, as you see the name, may disappear in few months.  But there are long term memory T cells, will stay in our body forever. Now you see in here, I emphasized memory B cells.  Also, they are short-term and long-term.  The long-term memory B-cell will stay in our body for forever. So together memory T cell and memory B cells are going to be in our body. They’re waiting for entry of the same virus into our body for second time or the third time, and this time they are not going to wait 14 days to start making the antibodies. They will start making antibodies within hours and maximum within 24 hours. That was the reason I decided to put this slide.

Dr. Weitz:                           But why do we hear all these public health experts say, “Well, we don’t really know if there’s long-term immunity.”

Dr. Vojdani:                        I’m sorry. They are not public health experts. They don’t understand immunology. This is written in a textbook of immunology. Memory T cells and memory B cells stay in our body forever. They are talking about disappearance of antibody.  Yes, antibody will disappear in some people after 30 days, in some people after 60 days, in some people after 90 days. So that’s why I emphasize here the memory B cell when second time the same virus get into the body, they are going to react to that and immediately they are going to produce antibodies. So when, for the first time, our body get exposed to that antigen, in this case SARS-CoV-2, IgM antibody is going to be produced, followed by IgG.  IgM is going to stay in the body for about, let’s say, two weeks.  Maximum, three weeks, not longer than four weeks.  The IgG will pick up and stay in the body up to three months.  Okay, and then we’ll go down almost to background level.

                                                Now when the same virus … So imagine that you had your first vaccine. Okay? So this is what happened when you had your first vaccine. This is your IgM, and this is your IgG. Now you are going to get your second vaccine. Look what is going to happen. Immediately your body is going to produce IgM the same level as before, but the IgG is going to be 10 times. This is logarithmic. If this was only, let’s say, 50 units, now you’re going to produce 500 units of antibody. Because the half-life of IgG is about 21 days, if you made 500 units of IgG, imagine how long that is going to be in your body. Probably months or sometimes years. So therefore this is the principle of vaccination and if you get the third vaccine or the third antigen, this time this antigen goes all the way up to the roof.

Dr. Weitz:                           But does that really matter if we have long-term memory T cells? Do we really want that? Does it help?

Dr. Vojdani:                        The memory T cells and memory B cells are going to immediately to wake up the B cells to start making antibodies.

Dr. Weitz:                           So do we really need the second big spike in IgG?

Dr. Vojdani:                        The second spike in IgG we need. The more antibody, the better virus will be neutralized if the virus will get into our body.

Dr. Weitz:                           Only during the period of time that the IgG antibodies are here.

Dr. Vojdani:                        Yes, otherwise the antibodies circulating in blood, doing nothing. We need those antibodies only if the virus get into our body, and the antibody is going to bind to the receptors or antigens and the virus, neutralizing it and preventing the virus from division and replication. Okay?

Dr. Weitz:                           Okay.

Dr. Vojdani:                        All right. Now, viruses have been in the environment for millions of years. This is absolutely true. Actually, I took all of this from an article from Science about two months ago. Scientists estimate that 380 trillion viruses live on or inside the human body. The human virome is 10 times the number of microbiome.  Guess what?  We always hear about our microbiome.  We hear nothing about our virome.  Believe me, there are many, many beneficial viruses in our body.  Not all viruses are bad.  So almost half of all the biological materials within our body is not human, meaning it’s bacteria or viruses or fungi or parasites.

                                           So what are viruses made up? They are made up pieces of DNA and RNA. They’re biological particles. They cannot replicate on their own, but they do it with the help of the host. That’s why they have to infect cells, epithelial cells, nerve cells, heart or muscle cells. As soon as they get inside the cell, they use whatever material available from that cell and replicate, and from one they become two and then four and thousands and millions. Unfortunately, during this replication, the virus mutate to acquire proteins that share homology.  Remember, tonight, I’m going to talk a lot about this. With human tissue cells, which they reside. Why they do that? To hide from the immune system. The viruses use this strategy to look like human tissue antigens. In the process, they hide from immune attack. We’ll talk more about this later.  So what is mimicry or similarity or cross-reactivity?  Cross-reactivity refers to the direct competition between two different molecules for the same binding site, and an antibody due to structural similarity. You’ll see example here.  I published about 10 years ago, published an article about wheat gliadin cross react with cerebellum.  So when our lymphocytes react to wheat gliadin, they make antibodies against gliadin.  But because components of gliadin looks …  So anti-gliadin binds to gliadin, right?  But because components of gliadin partially looks like cerebellum, the same antibody also react to cerebellum.  We call this cross reactivity.  Let me give you another example, because cross reactivity is not only about IgG.  Could be about the IgE.  Imagine that you are allergic to house dust mites. So every time you get exposed to house dust mites, you sneeze and you have type one IgE mediated allergic reaction.  But because, I’m giving you an example, peanuts or cat or dog danders also cross react with house dust mites, so your memory lymphocytes remembering your reaction to house dust mites. Now you get exposed to the dog dander, immediately also you start sneezing.  This is cross reactivity between house dust mites and antigen from dog or cat or food antigens such as peanuts. So the world of cross-reactivity is very vast.  So that’s why the virus trying to change its structure to look like human cells in order to hide from the immune system.  But there will be a huge price we are paying for that strategy. I will explain that later on.

                                                So I did publish an article, but I’ll talk about that later, but this article in Frontiers in Immunology, it’s all about potential cross-reactivity, cross-reactive immunity, to SARS-CoV-2 from common human pathogens and vaccines.  You heard that if you get vaccinated with polio or with child vaccines or with BCG, you will not get infected with SARS-CoV-2.  Is this true?  Absolutely, yes.  So here an article and a slide from an article in Journal of Immunology, they called that off target revaccination. So imagine, say, an individual is having high load of SARS- CoV-2, and having severe inflammation, cytokine storm and all of that, which we know what is the consequences of that. But if we take that person and give him BCG, they call that off target vaccination. What will happen? Causes secondary activation of adaptive immunity and induction of effective secondary hypo-inflammatory antiviral immune response. Drastic reduction-Drastic reduction in CD3 T cell activation, dampening of innate immune hyper activation, and finally, the result of that will be regeneration and recovery of the host health and survival.  So, that’s why giving vaccines other than SARS-CoV-2 to individuals suffering from COVID may help to subvert the immune system from attacking the tissue through this process and save that individual from the virus.  There was a question there?

Dr. Weitz:                           No, we’ll save it to the end. I mean, there’s lots of questions that have been coming in.

Dr. Vojdani:                        Yes, please. Okay. Now back to the world of cross-reactivity, as you know, I published lots of articles about cross-reactivity, one of them in 2018, in Journal of Alzheimer’s Disease. What did we do in this case?  We took antibodies made against amyloid beta peptide 1-42, which is responsible for production of amyloid plaque. When we applied that to 30 or 40 different pathogens, we found that amyloid peptide antibody not only reacted with amyloid peptide itself, this is like the hundred percent reaction, but reacted with oral pathogen. That’s why oral pathogen is playing a role in Alzheimer’s disease, enterococcus bacteria very similar to E.coli in our gut, candida albicans, Giardia, Borrelia burgdorferi the agent of Lyme disease, and then some molds such as aspergillus and penicillium.  These pathogens, if we make antibody against them, those antibodies can turn against our amyloid beta causing amyloid beta aggregation. That’s the message. Furthermore, that antibody reacted slightly with West Nile virus HSV1. That’s why HSV1, herpes type 1 playing a role in Alzheimer’s. EBV, early antigen, Influenza. So, I’m not here to answer or say whether or not you should be vaccinated with influenza A and B. Cross-reactivity with amyloid beta, rabies and look at HPV. Again, I’m not here to say get vaccine against HPV or do not get vaccine against HPV. The data is very clear. These viruses and bacteria cross react with amyloid beta. Some may…

Dr. Weitz:                            I would just like to point out to everybody that Cyrex has the Alzheimer’s LINX test, and you can use that to screen patients for all these different pathogens and other immuno reactants for preventing Alzheimer’s disease.

Dr. Vojdani:                        Thank you, Ben. Some may explain this a little bit different saying, well, if we vaccinated with HPV we make antibody against amyloid beta. It’s good because they inject monoclonal antibodies against amyloid beta to prevent Alzheimer’s disease. Then my question is, did it work? The answer is no. Close to 40 different monoclonal antibodies were tried for Alzheimer’s disease prevention and treatment, and based on articles published in the literature, I believe none of them worked.   So, this is the world of cross-reactivity, you can interpret the results both ways. That’s why I’m showing here the pathogens, and Ben was kind enough to mention what Cyrex is doing. And we’re very proud with our publications emphasizing the oral pathogens, E. Coli, bacterial cytolethal distending toxin and herpes type 1 and why it’s important to detect some of these cross reactivities. Because, we do not work today or sleep tonight and we wake up tomorrow with dementia or Alzheimer’s disease. From normal to abnormal, sometimes takes many many years. It takes years to get from normal to early Alzheimer’s, 20 years or more before diagnosis. 46.7 million in America, they’re in preclinical Alzheimer’s but they do not have obvious symptoms. Two and a half million, they have mild cognitive impairment which can get better with Dr. Bredesen’s methodologies, and finally three and a half million with dementia.

                                                So, ladies and gentlemen, we should not wait until 46.7 million to end up either with mild cognitive impairment or with dementia. If we detect the environmental triggers, we change our lifestyle, all of the above can prevent individual to move from normal to preclinical stage, from preclinical stage to mild cognitive impairment, and from mild cognitive impairment to full-blown dementia. This is the panel that Alzheimer’s LINX that Dr. Weitz was talking about. It’s not about cross-reactivity just with pathogens, cross-reactivity with foods such as casing and gliding toxic peptides. We test for blood-brain barriers, we test for gut barriers and we test for proteins involved in Alzheimer’s and Parkinson’s disease, and also the nerve growth factors as well. Also, let’s not to forget the [interregnum 00:07:59] which is major component of this panel. I highly recommend to do these tests and if any abnormalities, then you remove some of these cross-reactive foods and hopefully by that you will stop progression of Alzheimer’s from the first stage to the second and third and fourth.  Here is an article from Alzheimer’s and Dementia, forecasting the prevalence of preclinical and clinical Alzheimer’s disease in the United States. The diagnosis of persons with preclinical disease is potentially important because persons may be more likely to benefit from disease modifying treatments such as the one Dr. Bredesen is doing, such as the one my son Elroy is doing. If interventions occurred before the occurrence of significant brain damage. Doctors can help you before significant damage is done to the brain. That’s the message of this article.

Now, let’s go to additional pathogens, pathogens in general, pathogens associated immune reactivity screen. Bacteria, viruses, parasites, molds, yeast, spirochetes, all of these have a component, antigens, which cross react with human tissue. That’s why I emphasized in the beginning the issue of what viruses are doing in order to hide from the immune system. Same thing bacteria, parasites, spirochetes and yeast are doing in order to hide from the immune system. They have a component which is similar to human tissue including brain, the brain.  That’s why Cyrex is offering these 29 different antibody for 28 different antigens and if you have any elevation of antibodies against some of these pathogens, then the doctor will help you to treat and reverse the course of auto-immune diseases. In particular, I would like to draw your attention to the three molds in here. I know most of you when you have patients with mold exposure, you do not measure the most important lab test which is measuring antibodies against the mold antigens itself, aspergillus, penicillium, and stachybotrys, which is part of this panel. What most of you do, going measuring mycotoxins in the urine which nobody knows where really they are coming from. Are they from the food? Are they from the bacteria? Are they from the viruses in the gut? Nobody really knows. But when you make antibodies against the aspergillus, penicillium, stachybotrys, that shows that you live in the moldy environment, the mold releases the antigens, get into your body and you make antibody against them. Please ladies and gentlemen, do not waste your money on useless testing such as-

Dr. Weitz:                            Urine mycotoxin.

Dr. Vojdani:                        … Urine mycotoxin which is not a reliable method. Maybe it’s important for some other environmental factors, but they are not meant to measure exposure to molds Aspirgillus, penicillium and stachybotrys. Thank you so much. I made my point. Now, let’s have some fun. You see this beautiful slide, very simple right? So far in the literature, Epstein-Barr virus was the queen of auto-immunity. For years, the scientist, the auto-immunologists were discussing and claiming that we should find a vaccine against EBV because EBV is responsible for 20 different auto immune diseases, including Lupus and multiple sclerosis. This was true and it’s still is true, but HHV-6 came along, she started saying that I am the queen of auto immunity. Believe it I’ll show you some data that it is true that HHV-6 is so far the queen of auto immunity, more than EBV. But that was true until a year ago, 10 months ago, who? SARS-CoV-2 was discovered.   When there is conversation… There’s by the way, a comic that Joel and I we are putting together, hopefully we’ll be able to finish it soon, next year or next time I’ll present it to you. There is conversation between EBV, HHV-6 and SARS-CoV-2. Who is the real queen of auto immunity? So, after back-and-forth, SARS-CoV-2 saying that I am the queen of auto immunity, if you don’t believe me, look at my structure. If you don’t believe me, then why they call me Corona? Meaning I have many crowns on my surfaces. Believe me, you’ll see some data that I’m presenting to you that after, EBV was the first one, HHV-6 the second one, but now number one, queen of auto immunity is SARS-CoV-2. So I’m going to share with you.

Dr. Weitz:                            That Dr. Vodjani, does it really make any sense to give people a vaccine against EBV to prevent auto-immunity when isn’t it quite likely that the same immuno reactivity that occurs from the virus is likely to occur in the vaccine?

Dr. Vojdani:                        Absolutely. Let’s get to last sentence of my talk tonight, will be exactly about that. So, here test results of a patient, 58 years old lady went to 10 different doctors and had a pile of laboratory test results, including urine mycotoxin. Honestly, none of them could help her, and I’ll tell you why. Until one of the doctors sent the request for viral panel and Lyme disease from Immunosciences Lab, which is our specialty. When I got the results, look at some of the abnormalities, HSV-1 and 2 IgM red, highly positive compared to the highest normal range. EBV early antigen very high, meaning EBV reactivation. EBV nuclear antigen IgM, highly elevated. CMV IgM, elevated. Measles IgM, can you believe it? One probably in a hundred tests that we do, measles IgM is positive. But look at this, three times of the reference range. Then, when I looked at HHV-6 results, very high level of HHV-6 IgM.

                                                Then next slide. When we looked at lyme disease, six different antigens from Borrelia elevated antibody against that. Four different subspecies are elevated. Three different co-infections, Babesia, Ehrlichia and Bartonella elevated. So what’s happening in here? The patient is having Lyme disease, herpes infection, EBV infection, cytomegalovirus infection, measles, ongoing measles infection, and HHV-6. What do you think? Which one is the right diagnosis in here? And by the way, it is a requirement by department of health if measles IgM is elevated and Borrelia IgM is elevated, we have to report that to department of health. Think about the laboratory who do not have an immunologist like me. They are going to report this to department of health saying that we have patient with measles. So, what I did I called the doctor, I said, doctor, please tell me if your patient is having any symptoms of ongoing measles infection. I was told no, absolutely not.  Then, I came to conclusion actually, it is reaction to HHV-6 and IgM antibody produced against HHV-6 cross-react with measles, with CMV, with EBV and HSV-1 and 2. I told the doctor, if you treat your patient for HHV-6, all these antibodies will disappear probably in three months. I hope that’s the case, this is ongoing right now. That’s very important. It is very important to use a laboratory with an individual who is able to interpret the test results for you the way that can help the patient and can help the doctor as well. Because imagine that department of health are busy with COVID, now we are going to overwhelm them with measles and Lyme infection unjustified. I wanted to share with you that case.

                                                Now, lets go to the COVID, the queen of auto-immunity. Between March and April 2020, upon the availability of blood test for SARS-CoV-2 we took first five and later additional blood specimens that had been confirmed positive for COVID-19 and tested them for biomarkers of auto immunity, ANA, ENA, double-stranded DNA, Actin, mitochondrial antibody, rheumatoid factor and immune complexes. Elroy and I were very surprised to find out that three of the five initial specimens had significant elevation in the biomarkers of auto-immunity. Usually we find this in one in 20, one in 50, but here three out of five. So these results, I would like to show you how the brain of researchers work. These promoted us to investigate patterns of cross-reactivity between SARS-CoV-2 and auto immune target proteins.

                                                Now, when we reviewed the literature, so far during 2020, at least 10 different groups published articles about anti-nuclear antibody and COVID, lupus anticoagulant, ENA, cardiolipin. Our work, ANA, ENA, Actin, mitochondrial antibody, anti interferon, anti MDA5 antibody, myelin basic protein antibody, NMD receptor antibody, and more. These are all in COVID patients. So, upon availability of mouse and rabbit monoclonal antibodies made against the spike protein of SARS-CoV-2 and nuclear protein, we took those antibodies made specifically against SARS-CoV-2 antigens and applied them to 50 different tissue antigens, and we found that those antibodies reacted with mitochondria, with ENA, anti-nuclear antigens, Actin, Actomyosin, Tropomyosin, collagen, Thyroid peroxidase, brain growth factors and brain antigens, blood brain barrier proteins, MBP (myelin basic protein) in the brain, Transglutaminases, scheme in the gut and tight junction proteins, occludin, zonulin, claudin, also found in epithelial cell tight junctions of the lungs.

                                                So, compare that to reaction of monoclonal antibody to SARS-CoV-2 spike protein which is a hundred percent, look at transglutaminase 3, look at extractable nuclear antigens, mitochondria. So, SARS-CoV-2 cross-react with many human tissue antigens and no one can deny this fact. Also, we took anti nuclear protein antibodies and reacted to those 50 human tissue antigens. Look at mitochondria as if this is nuclear protein or SARS-CoV-2, again, ENA, ANA, Actin, actomyosin, thyroid peroxidase, Thyroglobulin, transglutaminase 6, myelin basic protein, other antigens as well. So, let me go back to this and then I will share with you another piece of the story. When we send this for publication to clinical immunology… within 24 hours at that time around May was accepted for publication. In clinical immunology, it was online, 24 or 48 hours later, but it was published in August 2020 officially. When this article was published, some of my colleagues were saying that the antibody that used are made in mouse and rabbit. “These are not kind of antibodies that are humanized antibodies that are used or will be used for treatment of patients with COVID. Why don’t you do the same study with human monoclonal antibodies?” Okay. I said, “Thank you so much, but those are not available.”   So while I was thinking about this on July 7, I got exposed to SARS-CoV-2. Two weeks later, I had to be hospitalized, Ellroy took me to the hospital. And you see couple of days later, my CRP, 156, my ferritin… But thanks to the treatment at Cedars, four days later I got released from the hospital and by July 29 and August, everything is back to normal.

Dr. Weitz:                           What treatment did you receive?

Dr. Vojdani:                        Remdesivir and Dexamethasone.

Dr. Weitz:                           Okay.

Dr. Vojdani:                        Okay. Now, I really don’t know, you see the knee, right? For almost 90 days post COVID, I was suffering from knee pain and knee inflammation. Was that because of the medication or because of COVID? And again, I would like to share with you that in my family, my mother suffered from rheumatoid arthritis and osteoarthritis for 47 years and she passed away from the disease, so that’s the weak part of my body. So is it because of COVID or because of the medication? I really don’t know. Okay. So this experience made me more serious to further investigate cross-react activity between SARS-CoV-2 with human tissue using monoclonal antibodies, human monoclonal antibodies.  So what is human monoclonal antibody? The polyclonal antibody, let’s say we inject something to a rabbit many clones from spleen or lymph nodes, they are going to make that different type of antibodies. The antibodies made by different clones that’s why they call them polyclonal antibodies. If we inject that to human, that will develop some kind of sickness, we can not do that. Maybe once is good, but if you repeat that the individual will develop serum sickness or something like that.

                                                Monoclonal antibody is an antibody is made by a clone of cells, but many very recently, they found that if we take an individual human lymphocytes from individual infected with a virus, and by the way, this is the memory lymphocytes, okay? And we take that memory lymphocyte who knows how to produce antibody IgG antibody against SARS-CoV-2, that lymphocyte becomes activated and ready to produce antibodies. There is a method in the clinical labs or research labs called immortalization of B cells. For example, if you add Epstein-Barr virus, Epstein-Barr virus is going to activate the B cells to divide crazy and make antibodies. So they add all kinds of reagent and these cells become immortalized.

                                                But if we take one of these cells or some of these cells, okay? Which became activated, they know how to produce antibodies against SARS-CoV-2, fuse them with human myeloma cell, human myeloma cell is a factory for production of proteins in this case antibody. So that’s why you see half of these cell is called human hybridoma, half of it from myeloma, the other half is from B cell. And then when these cell, hybridoma cell make antibodies, we call that human monoclonal antibodies. You can inject them safely to human without having any side effects. So that was important to explain to you.

                                                So when human monoclonal antibody became available around August 2020, immediately we purchased those antibodies. And we repeated that experiment that I explained before. And we reacted it this time with 55 different tissue antigens, 28 of them reacted from moderate to strongly. And by the way, whatever I’m going to explain to you from an on is published in Frontiers in Immunology, very prestigious journal eight days ago. And if you look at the journal right now, we had more than 20,000 views, which is unheard of in this journal. That shows how much people and scientists are interested about possible cross-reactivity between SARS-CoV-2 and human tissue and its implication for auto-immune diseases.

                                                So here are the results, they are almost similar to what I showed you. So this is nice because not only polyclonal antibody reacted with human tissue, now monoclonal antibody made against spike protein reacted almost with the same antigens, okay? Acting mitochondria, ANA, histone, brain antigens, collagen, alpha-myrosinase, thyroid peroxidase, liver gut 65, transglutaminases and tight junction proteins. Also, we used human monoclonal antibody made against nuclear protein, the results, again, identical with some variation, but very similar. Look at mitochondria almost, I would say 60% reaction of monoclonal antibody to nuclear protein, which is in red, two items, mitochondria and insulin receptor reacted very, very strongly, occludin claudin which are tight junction proteins, which are measuring antibodies. Part of array too cross-reacted strongly with SARS-CoV-2 proteins. So brain alpha-myrosinase, liver gut 65 and tight junction proteins are cross reacting with SARS-CoV-2 nuclear protein.

                                                In order to show specificity of this antigen-antibody reaction, meaning monoclonal antibody reaction to specific antigens when you do serial dilution like what we did in here from 1 to 200 to 1 to 25,600, you should see the decline in the level of the antibody, and that’s the case. Also, we did inhibition study and again, in proportion to the amount of antigen put in competition, we see decline in the antigen-antibody reaction. All of that support, that the reaction that we detected between monoclonal antibodies made against SARS-CoV-2 spike and nuclear protein with human tissue antigens is very specific.

                                                So when we send this for publication, the reviewers from the journal asked us to do epitope mapping. What is epitope mapping? Another meaning compare peptides from human tissue to SARS-CoV-2 and see if their fingerprint is similar to each other, if that’s the case, then proves that our experiments are 100% correct. So we did that. And they asked us to do it with mitochondria. And we found 30 different peptides from mitochondria that had more than 50% identity or similarity with spike protein, but less with nuclear protein. I’m showing only two peptides. So in order to clarify this for you, ladies and gentlemen, you need only five of these red amino acids to be similar between mitochondria and spike protein in order to cross-react with each other, meaning antibody against mitochondria will react with spike. Antibody made against spike will react with mitochondria. And here we have eight of them. And we had cases even we had more than that. So that’s about mitochondria.

                                                How about actin? The same thing about actin, we found between 20 to 30 proteins for peptides who cross-reacted with spike protein. And finally, they asked us to do it with thyroid peroxidase. Again, we see a significant cross-reactivity between TPO and spike protein. What does that mean? Patient with COVID may develop thyroid auto-immunity in the future, or even some individuals get vaccinated may have cross-reactive antibodies against CPO? Time will tell. We don’t know. I cannot really answer that question, but I’m just asking that question.

                                                So we proved that concept of cross-reactivity, it is real antibody made against spike protein. And nuclear protein react with cellular components, such as mitochondria with liver, muscle, joints, thyroid nervous system, skin, GI and tight junctions, and some other antigens that I’m not mentioning here. So if that is the case, okay? Are we the only one?  No, I already shared with you earlier that there are at least 10 different groups who showed auto antibodies in patients with SARS-CoV-2.  Not only auto antibodies under top right here. Also, look at diseases detected in patients with SARS-CoV-2, type one diabetes and Guillain-Barre syndrome, vasculitis, and many other auto-immune diseases. By the way, the credit for this slide is going to Professor Schoenfeld who presented this in a mosaic of autoimmunity about a month ago.  So we are not the only one claiming that there is cross-reactivity between SARS-CoV-2 and human tissue.   So molecular mimicry between SARS-CoV-2 to spike glycoprotein and mammalian proteomes implication for the vaccine. And this was published by professor from Italy, by the name of Kanduc with Yehuda Schoenfeld.  [Kanduc, Schoenfeld. Molecular mimicry between SARS-COV-2 spike glycoprotein and mammalian proteomes: implications for the vaccine.And another article by Schoenfeld group and Gilad Halpert, SARS-CoV-2, the auto-immune virus. And then I did not put additional slides that by scientists from the U.S. Lyons Weiler, professor Ernfeld also from Israel, professor from Germany, her name is-

Speaker 1:                           Franke.

Dr. Vojdani:                        Yeah, Dr. Franke or Professor Franke, who published a very elegant, I’ll show you the slide later on an article that recently. So I am not alone, we are not alone. At least 10 to 15 different groups in the world published about SARS-CoV-2 an auto-immunity and cross-reactivity and even showed epitope mapping similarities between SARS-CoV-2 and human tissue. So what is the meaning of cross-reactivity? So in this very simple slide, we get infected with the virus, or we get injected with the vaccine. Our plasma cells are going to produce antibody to SARS-CoV-2 or to the vaccine antigen.  These antibodies are going to bind to the receptor on the virus and neutralizing the virus, and the virus will not be able to bind to ACE receptor, that’s the goal. But unfortunately, due to cross-reactivity, some of these antibodies may bind to different human tissue antigens and causes auto-immunity 5 years down the road, 10 years down the road, a year down the road due to mimicry. So remember this very simple slide, our goal is to make neutralizing antibodies to neutralize the virus. But unfortunately some of those antibodies act like friendly fire causing auto-immune reactivity at this level, I’m calling it not auto-immune disease.

Dr. Weitz:                           Can I just throw in a question right here? Dr. Rahbar had asked after someone gets infected, do they get just IgG antibodies or do they have neutralizing antivirus? There been a big controversy in popular press or the doctors who come on TV who say, well, you may have antibodies, but if they’re not neutralizing antibodies then they’re not going to be protected.

Dr. Vojdani:                        I am sorry. Again, they are not immunologists, okay?  I don’t call them experts.  You make antibodies, your body is making neutralizing antibodies.

Dr. Weitz:                           So there’s no situation where they make antibodies that are not neutralizing.

Dr. Vojdani:                        I don’t think so. Let’s say if you make 100 units of antibodies, at least 50% of those are neutralizing antibodies.

Dr. Weitz:                           Does it matter how severe an infection someone has? Like if somebody has more severe infection, do they get more protection or more antibodies versus somebody who has a mild infection?

Dr. Vojdani:                        Really, we don’t have the answer for that.

Dr. Weitz:                           Okay.

Dr. Vojdani:                        Okay. So let’s continue. And I’m very close to finishing my talk in about 10 minutes. So after this introduction, look at this very simple slide, immunity from the virus, like the one I have, or from the vaccine, we know antibody against the virus cross-react with human tissue. We know antibody made against component of the virus, which is this fight proteins also cross-react with human tissue. So what will be the future consequences?  Time will tell.  However, let’s go ahead and look at this slide. We know that when we make IgG, IgM antibodies against SARS-CoV-2 spike protein, they disappear after 30 days, in some people earlier, even that. But these antibodies unfortunately appear in the body with additional auto-antibodies, anti-nuclear antibodies, rheumatoid factor, [inaudible 01:13:03], interferon gamma antibodies, MDA5 antibodies, myelin basic protein antibodies, tight junction protein antibodies, all of that.  So we know there is some consequence of auto immunity due to viral infection. So we should not vaccinate the public and let them develop the disease, some of them will die and some of them may develop auto-immune disease. But we are lucky that these antibodies are shorter because if those antibodies will stay in the body for a long time from auto-immune reactivity may end up with auto-immune disease. So that’s one side of the coin. The other side, we vaccinate, we make circulating IgG and IgM antibody against spike protein. Our goal is to repeat the vaccine and make enough antibodies to stay in our body for a long term. But the question I’m going to ask, what will be the consequence of these long-terms or presence of these long-term antibodies made against spike protein that cross-react with human tissue? Again, the answer, time will tell.

                                                So I just wanted to share with you this article by Dr. Franke from Germany. Look at the title, just published very recently. I think I end of up December, high frequency of cerebrospinal fluid auto-antibodies in COVID-19 patients with neurological symptoms. So where they did from very severe-ill patients removed serum and spinal fluid, majority of these patients unfortunately died. They reacted them with myelin basic protein and tissue antigens, you will see the results and they reacted with many, many sections of mouse brain cells, which is identical to human brain cells. And also they detected antibodies in blood, I guess, myelin basic protein and NMDA receptor.  So auto antibodies may already now explain some aspects of multiorgan disease in COVID-19 and can guide immunotherapy in selected cases. So here clear picture when they took spinal fluid from COVID patients and added them to brain cells, you see that fluorescents indicate reaction of those antibodies in spinal fluid with brain cell antigens, in this case, best cells in the brain, Purkinje cells neurons in the brain, and many other components of the brain. [Dr. Christiana Franke, et al. published in Brain, Behavior, and Immunity in December 2020 on High Frequency of Cerebrospinal Fluid Autoantibodies in COVID-19 Patients with Neurological Symptoms.]

                                                This is very elegant study proves the concept of cross-reactivity and auto-immunity against the brain due to COVID. The article was so important that Dr. Kreye in that Nature Reviews Immunology wrote this commentary, “In summary cross-reactive antibodies generated in response to SARS-CoV-2 may contribute to some of the clinical phenotypes seen in COVID 19, and could provide a mechanistic explanation for the persistence of symptoms in patients who have recovered from initial viral infections. Finally, although preliminary, these findings suggest that monitoring for self reactive antibodies and post challenge auto immunity should be incorporated into vaccination trials.” And with that before recommending type of testing.

PART 3 OF 4 ENDS [01:18:04]

Dr. Vojdani:                        For recommended type of testing and I would like to read the final couple sentences, and I would like all of you to remember that Aristo Vojdani on the January 28, 2021 said the following, “While I am not against vaccination, I am worried about the rise of autoimmunity post COVID vaccination. Okay. Until the time will tell, please consider to test your patients for possible autoimmune reactivity, not autoimmune disease, autoimmune reactivity, as part of their yearly checkup.”   And with your permission, I’m going to read this because history will judge me in the future.   “While I’m not against vaccination, I’m worried about the rise of autoimmunity post COVID vaccination. Until the time will tell – as I mentioned in my slides – please consider to test your patients for possible autoimmune reactivity as part of their yearly checkup”   How to do that? By considering Array five, multiple auto immune reactivity screen from Cyrex, or simple auto immune panel from Immuno Sciences Lab. And I’m not really selfish in here. You can use any laboratory you want to do anti-nuclear antibody, rheumatoid factor, immune complexes, acting and mitochondrial antibodies, which you saw the evidence of cross-reactivity with SARS-COV-2 antigens. Thank you.

Dr. Weitz:                           So we got a bunch of questions here. One of the questions is, is there cross-reactivity between flu vaccine and COVID?

Dr. Vojdani:                        The answer is yes, there are lots of publication who shows that memory lymphocytes, memory lymphocytes taken from patients with flu vaccine, who had flu vaccine before, put them in culture with COVID antigens. Those memory lymphocytes immediately started reacting to COVID antigens. And so therefore that’s the best indication of cross-reactivity between flu and SARS-COV-2. But we can go on online NIH Plus and look for structural similarity and believe me, it does exist,

Dr. Weitz:                            [inaudible 01:21:27]

Dr. Vojdani:                        but this is the most elegant way of to show first memory lymphocytes stay in the body, and also you can demonstrate evidence of cross-reactivity

Dr. Weitz:                           By the way- [crosstalk 01:21:44].

Dr. Vojdani:                        In SARS-COV-2.

Dr. Weitz:                           Is there a way to test for memory B cells or memory T cells?

Dr. Vojdani:                        Yes.

Dr. Weitz:                           How?

Dr. Vojdani:                        You just put them in culture with what antigen you think the memory T-cells and B-cells for SARS-COV-2.

Dr. Weitz:                           Yes.

Dr. Vojdani:                        Okay. So if you have a patient where you’re not sure the antibody is negative, but you think the patient had SARS-COV-2 or COVID.

Dr. Weitz:                           Okay.

Dr. Vojdani:                        You can take blood from that patient, put them separate the white blood cells, put them in culture with COVID specific antigens and incubate that in incubator at 37 degrees for 48 hours. And then you look at finger print of cytokine production, interferon, gamma, even you can wait for few days and check for antibody production. So yes, that is possible. There are methodologies and it is possible to do that.

Dr. Weitz:                           Right. But there aren’t any labs available right now?

Dr. Vojdani:                        No, no, no.

Dr. Weitz:                           Okay.

Dr. Vojdani:                        Only for research.

Dr. Weitz:                           So Dr. Rahbar asked another question. What is the mechanism of persistent IgM in Chronic Lyme?

Dr. Vojdani:                        I think most of the Chronic Lyme is due to cross-reactivity that we call it Chronic Lyme [crosstalk 01:23:21] and I showed you, but, but, [crosstalk 01:23:24] but I’ll answer that question. And because we have memory lymphocytes, right, Dr. Rahbar and Dr. Ben. If my memory lymphocytes made against EBV and I did publish an article, then EBV cross react, with Borrelia burgdorferi, agent of Lyme disease. So now imagine I have memory lymphocytes for Epstein-Barr virus or vice versa, have memory lymphocytes for Lyme, and these memory lymphocytes can cross with each other. So I can get [inaudible 01:24:29] my memory lymphocytes could be exposed to EBV antigens and produce antibodies against burgdorferi or release cytokines. And that’s why I’m really against the method, that first of all, I published about it about 10, 12 years ago, that you can culture lymphocytes with Borrelia antigens and look for cytokine production.

                                                So now there is a method called Elispot. Instead of measuring the level of cytokines, you look at the spot formation and they call, if that spot is positive, this is the lab in Germany, and you say, they say you have Lyme disease, but I argue with that, you could have also memory lymphocytes made against EBV. You expose it in culture with Lyme antigens, now they produce the same cytokines and will give you positive spot. And you tell the doctors that your patient is having chronic Lyme. So chronic Lyme could be due to cross reactive memory B cell, which can make cross-reactive antibodies.

Dr. Weitz:                            So if somebody chose to get a COVID vaccination to protect themselves, what we know so far about the two vaccines that are available, the Pfizer and the Moderna, and soon we’ll have the Johnson and Johnson, and with a different mechanism of action is if you were to just speculate, would you think one of them would be more or less likely to lead to possible autoimmunity or immunoreactivity in, you know, as somebody who just happens to be vulnerable to that.

Dr. Vojdani:                        First of all, we are right now in the dark. That’s why I emphasized time will tell. All of them they are using, I think the same, almost the same, RNA. RNA For spike protein.

Dr. Weitz:                           I think the first-

Dr. Vojdani:                        Even if they use, even if they use RNA for another fruit in nuclear protein, and if you read my article, by the way, that we use two other antigens as well, those other two antigens, the membrane and the nucleocapsid, and whether the two more antigens – it’s in the article, in Frontiers in Immunology – also cross-reactive with many tissue. And so the world of crushed the activity is not limited only to spike protein. It also applies to other antigens of SARS-COV-2. That’s why I called the COVID or SARS-COV-2, the queen of autimmunity after EBV, NHS, V6.

Dr. Weitz:                           Right, I don’t know a lot about this, but I believe that the AstraZeneca and Johnson and Johnson have a slightly different mechanism than the Pfizer in the Moderna. And they use an adeno virus as part of how they provide protection rather than a strand of messenger RNA.

Dr. Vojdani:                        Yeah. It doesn’t matter, honestly. What is the goal? The goal of vaccine is the patient or the individual will produce antibodies that, if in the future will be exposed to the virus, will have enough neutralizing antibodies to neutralize the action of the virus. That’s the goal.   Now, really, we don’t know any if these viruses that were injected the patients made antibodies, how much antibodies they made, how much neutralizing antibody they made. We are going to learn more in the future. That’s why I said I’m not against vaccination. They’re vaccines right now saving lives. Because if not, they will get the disease like I got. And not everybody is lucky like me, who I survived, but many people died from the disease. So I’m not again against the vaccine, but we should learn more about mechanism of action of the vaccine and whether or not these cross-reactive antibodies that our body is going to generate. Is it going to protect us or is it going to damage our tissue? And again, time will tell.

Dr. Weitz:                            Are you going to consider getting a vaccine in six months?

Dr. Vojdani:                        Because I got the disease, no.

Dr. Weitz:                            Okay. Somebody asked about patients who already have, say, elevated antiphospholipid antibodies. Are they more at risk for, you know, immunoreactivity, if they either get sick or get a vaccine?

Dr. Vojdani:                        Okay. I have many relatives. Unfortunately, some of them have autoimmune disease. They called me and they wanted my advice. And this is my advice to my own family. I’m sorry, I don’t want to generalize these. Okay. I told them if you have an autoimmune disease, please wait at least six months. Let’s see what will be the results of vaccinations and then consider vaccination.

Dr. Weitz:                            For somebody who’s sick, as part of their treatment, would you think that monoclonal antibodies or convalescent plasma therapy, meaning taking antibody, say from somebody like you, would one of those more likely be effective and/or safer?

Dr. Vojdani:                        I know they’re using lots of monoclonal antibodies. And from patients who had the disease, the latest article about a week ago I read, was that when they take plasma from a person like me, of course now I don’t have the antibody anymore, let’s say two weeks after I released from the hospital, it doesn’t work. It didn’t work.

Dr. Weitz:                            Okay.

Dr. Vojdani:                        But again, this is only one study that I read.

Dr. Weitz:                            Yeah, somebody has the same thing. Let’s see. Same question. Why are some people asymptomatic if there is so much cross-reactivity? I think that just depends on the person, right? Do you have an opinion as to the efficacy of the PCR test for viral?

Dr. Vojdani:                        Unfortunately, many false positives, many more false positives than false negatives. Also the antibodies I had experience with our employees in here that some of them were tested in two different labs, you know, we let them go for 14 days and we wanted them to be negative, right? And they were tested again and again and again, one lab negative, the other lab positive. So what do you do? Tell them stay home again. And so, unfortunately it turned out one of the labs was reporting many, many false positive results for antibody and antigen even.

Dr. Weitz:                            I think the latest guidelines from the CDC are that after you test positive, after 10 days, you can return to wor if you don’t have symptoms. They recommend not testing again, because it’s not unusual for people to test positive for two or [crosstalk 01:33:24]

Dr. Vojdani:                        Because at my work, we have one person who did not develop the disease and we wanted, we did not want to put him in the injured. So we told the person until you bring the evidence of negativity, you cannot come back to work.

Dr. Weitz:                            Right. People ask is it being recorded. Yes. It’ll be included in my weekly podcast. I’ll post it sometime next week. You can listen to it on Apple podcasts, and there will be a video version on YouTube autoimmune disease.

                                           Why did ferrets die after exposure to Coronavirus after vaccination? Are you concerned about this?

Dr. Vojdani:                        Again again? Can you repeat?

Dr. Weitz:                           This is referring to animals. Why did ferrets, I guess these furry animals, apparently they died after exposure to Coronavirus after getting vaccinated.

Dr. Vojdani:                        I’m not aware of that, I’m sorry.

Dr. Weitz:                           Okay.

Dr. Vojdani:                        The person can educate us. I’ll be very happy to.

Dr. Weitz:                           Yeah.

Dr. Vojdani:                        [01:34:37]

Dr. Weitz:                           Dr. Lalazar, are you, are you still on the call? Did you want to unmute yourself and ask the question again?   Maybe she’s not. Let’s see. What do you think about the recent paper in Nature, “Immunology to suggest in cases of severe COVID long term antibody mediated immunity to the virus has been shown to be absent” cardiovascular 19, or COVID 19 disease can yield development of new auto-immunity the messenger RNA vaccines may confer protection against both effects”?

Dr. Vojdani:                        Well, first of all, the first part is yes. I agree that the antibody disappeared. My antibody disappeared after 60 days.

Dr. Weitz:                           Right.

Dr. Vojdani:                        But the second part [crosstalk 01:35:32]

Dr. Weitz:                           Doesn’t matter if it’s severe or not severe.

Dr. Vojdani:                        Yeah. The second part was about autoimmunity. Cardiovascular. What? I didn’t understand.

Dr. Weitz:                            I’m sorry. I think I said it wrong. I was saying cardiovascular. I think he just abbreviated COVID-19 can yield development of new auto-immunity. We know that. I think the point he’s trying to make is does the messenger RNA vaccine protect against the auto-immunity and I think you’ve answered that question.

Dr. Vojdani:                        Again. Time will tell, I don’t know if these antibodies that right now people are producing they’re protective or pathogenic. Time will tell, they are protective against the virus, but against autoimmunity, we don’t know.

Dr. Weitz:                           Okay. So the virus is mutating. Do we think it’s likely that somebody like yourself who has protection against the SARS-COV-2, would you still have protection against these mutated forms and the same question related to vaccination?

Dr. Vojdani:                        Yes. Thank you. I believe that I will have 99.9% protection. 

Dr. Weitz:                           That sounds pretty good to me.

Dr. Vojdani:                        That is when you’ll get sick and then you’ll have memory T-cells in your body that stays forever.

Dr. Weitz:                           Right.

Dr. Vojdani:                        So.

Dr. Weitz:                           I’m curious if you got the flu shot. Is this the reason you got so sick? Because you did not?

Dr. Vojdani:                        No, I never got flu shot. And because again, I believe in cross-reactivity and immunity. Because of my family history of autoimmunity, I never considered flu shots. I believe in my new strength of my immune causal immune system, how to keep my new causal immune system, my first line of defense strong in order to keep me safe against viruses. But unfortunately that was enough against our scope to.

Dr. Weitz:                           Is there a big benefit to doing antibody testing? And if so, when’s the best time to do it?

Dr. Vojdani:                        Antibody testing against what?

Dr. Weitz:                           Let’s say you contracted the virus afterwards. Is there a benefit to testing your antibodies? Does it really matter?

Dr. Vojdani:                        Well, if they disappear after two or three months, I don’t think that it does matter.

Dr. Weitz:                           Okay. But,

Dr. Vojdani:                        But, but if you get vaccinated-

Dr. Weitz:                            Right.

Dr. Vojdani:                        And you have long-lasting antibodies, I will test, as I recommended, I will test for possible autoimmune reactivity once a year, in order to make sure an individual with family history of autoimmunity are not going to develop an autoimmune disease.

Dr. Weitz:                            Right. I didn’t really understand this question. J.L. Asked, why are some patients asymptomatic? I think that’s just people have different reactions to any disease, right?

Dr. Vojdani:                        Okay. The answer is that really it’s the inoculum or the number of viruses that we get get into our body also plays a role. And also the not – we each one of us, we have different number of receptors and our epithelial cells or [crosstalk 01:39:18].

Dr. Weitz:                           Like the Ace 2 Receptor, which is [crosstalk 01:39:19].

Dr. Vojdani:                        Yes [crosstalk 01:39:20] So that’s really is another factor. So more number of viruses attacking you at the same time, you get more sick than the one who less viruses are attacking.

Dr. Weitz:                           And we know the level of vitamin D, it plays a big role in how likely you are to get sick, the status of your immune system.

Dr. Vojdani:                        Absolutely. Vitamin D is because strengthening your immune system.

Dr. Weitz:                           Absolutely.

Dr. Vojdani:                        It regulates your T-Reg cells. You know that.

Dr. Weitz:                           Absolutely. And of course we know about the benefits of vitamin C and zinc, and quercetin and melatonin.

Dr. Vojdani:                        Right. Right.

Dr. Weitz:                           So we’ve been infected – It’s the same question again, if you’ve been addicted, are you permanently protected? Most likely.

Dr. Vojdani:                        Yes. I believe I said 99.9%. Let’s say 99%. I believe I’m protected. And all these claims that even if you are, had the disease, even if you have been vaccinated, there is some information on the internet. Still, you have to wear a mask still. You have to do all steps required by law.

Dr. Weitz:                           This question is, let’s say you recovered from SARS-COVID-2, you get the autoimmune screen and you have autoimmune reactivity, what do you do to prevent yourself from getting an autoimmune disease?

Dr. Vojdani:                        There is a lot you could do, you know, you find what are the triggers and remove the triggers and you’ll reverse or stop the course of autoimmune disease. That’s really my, you know, I wrote that in my book in relation to food. Hopefully one day I’ll have time to finish the other two books. One about toxic chemicals, the other about pathogens. But then unfortunately this year I became busy with SARS-COV-2 and research and all of that.

Dr. Weitz:                           Right.

Dr. Vojdani:                        I could not finish my second book.

Dr. Weitz:                           Well, I think the answer is from a functional medicine approach. There’s usually not just one trigger for an autoimmune disease. So even though you may have reactivity from SARS-COVID-2, there are likely going to be other triggers. You may have toxins, you may have food sensitivities.

Dr. Vojdani:                        Or pathogens.

Dr. Weitz:                           Yes. You want to clear all those out, reduce your overall level of immune reactivity. And then even if you have some reactivity to a virus you’re less likely to develop the full disease. And this’ll be the last question.   What is happening in the brain post vaccination? When people get a memory loss, brain fog, is that a guaranteed blood-brain barrier breach and autoimmunity, or it could have been some other mechanism?

Dr. Vojdani:                        I think the article by Dr. Franke, which I highly recommend to read is very clear that the antibodies made against SARS-COV-2 attacking different components of the brain and causing damage to the neurons.

Dr. Weitz:                           Okay. Excellent. Thank you. Thank you so much for your valuable time. I know you actually have another presentation.

Dr. Vojdani:                        Thank you very much.

Dr. Weitz:                           Thank you so much Dr. Vojdani, that was awesome.



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