Jenn, I appreciate your dialogue and observations. With my first grandson just arriving last month, and son and daughter-in-law being artists, I felt compelled to give them some advice. My background is in transplant compatibility testing. Stay with me, this is relevant to the discussion. Ten years ago, I made a serendipitous discovery that shocked me and pushed me to research the literature. This ultimately led to dissent from mainstream theory that transplants are rejected by mismatched organs. I discovered through my research that this is only a consequence of viral superinfection complicated by stress (which can come in many forms).
While different vaccines have slightly different mechanisms of action, most have the capacity for a viral envelope protein to be stored in the nucleus due to a post-translational protein modification called SUMO2/3. I found that this can alter the structure of the viral protein and the way it is recognized by the immune system. It can also provide it with new and unknown functions. Bottom line, it lays the groundwork for an allo (in the case of transplants) or auto (in the case of autoimmunity) immune response.
With that being said, I just published the in silico evidence last month. The autoimmune component was not part of the paper.
I am not anti-vax. However, based on my experience and data, I now lean in favor of vaccine hesitancy because we are introducing an element that is not natural, tricked our immune system into seeing danger and responding to it, all in hopes of staving off a disease with a low frequency of consequences. I still have more work to do, and this is an uphill battle as you can imagine. But the combination of EBV reactivation by stress, compounded by the introduction of a second virus, may be a recipe for chronic suffering down the road depending on one's exposure, genetic makeup and stress levels (diet and general health play a role obviously).
If I had to do it all over again, I would be far more hesitant knowing what I know about the immune response that can be activated with these components at present. Am I saying that vaccines can cause disease? I cannot rule this out right now, because the confounding variables I have encountered are not accounted for in the vaccine studies I have reviewed. Am I saying that they can cause organ transplant rejection? Highly likely, especially influenza. But you will not read that in any study including mine (TBD). The literature and at least the data I've been exposed to support my hesitancy. To be fair, I do not advocate mainstream views but rather a dissenting viewpoint. I am trying to get funding to continue my investigation.
Not sure this helps. But until the variables are addressed, I will not be taking or advocating for anyone to be vaccinated. I don't like numbers involving death any more than anyone else. But is chronic suffering any worse in the long term? If I am able to prove that adjuvants and certain live-attenuated or killed vaccines or VLPs or mRNA can provide the necessary components for disease, why would I expose anyone to them intentionally? Wouldn't it be smarter to isolate until I'm no longer able to spread? Concentration is the key to disease. Vaccines concentrate viral components.
The problem, as I see it, is as much an obstacle by the scientific community as it is in the anti-vax community. This is why neither trust the other.
For what it's worth, those are my observations. I can overwhelm you with studies to provide you with evidence, but I don't think that will help right now until more work is done.
Thanks Steve for sharing your thoughts. Can you share some links to the research you mention? I'm aware of the danger of of latent herpesviruses like CMV in transplantation but have not seen any evidence around the potential mechanisms you mention.
As an adult living with long covid for the past 5 1/2 years, I can tell you that for the first 3yrs I wish I had died. Each moment was agony in physical suffering. It is isolating and takes a toll on the whole family. I now live the best life I can as a disabled person. (Prior to long covid I was an endurance runner & at the top of my career. I was fit AF. ) I can no longer work or do more than one activity a day. I cannot imagine the loss of this much health as a child & having to struggle with these issues the rest of their lives. The devastation is not only to the child, their family, and their friends, but to our community and future loss of what they could have contributed.
I strongly feel that we need to continue to improve the vaccines as we learn more about the virus. But vaccines are not enough. Society quickly moved away from isolating when sick due to pressure to influence the WHO’s & CDC’s recommendations despite them knowing Covid is Airborne. Work places went back to sick shaming when taking time off & schools punish kids for their absenteeism. Masks are now political when they are personal protective equipment (PPE). It is frustrating that health care providers rarely role model masking themselves. I have experienced them getting upset when asked to mask because my immune system is vulnerable. It is really scary to see so little masks in health care settings (and in public) when Covid spikes seasonally. We need more discussion about airborne transmission and the need for multi pronged approach based on science.
PS- surgical or cloth masks are not as protective as N95s & need to be fitted to your face.
All medical decisions are risk-benefit analyses. All medical decisions are prone to error. Your/our job is to choose on which side you want to err, since none of us make perfect decisions. A certain percentage of folks operated on for appendicitis will and should have normal appendices. Otherwise people will wind up with ruptured appendices too often. Which do you prefer? Get it?
I think the issue is that most people are making these decisions without knowing all of the risks and facts about Covid. I continue to meet people with newly diagnosed long covid saying they didn’t know that could happen. Most people think it is just like getting the flu and only vulnerable populations could have serious harm. (Side bar- it is also extremely disturbing how cavalier people are about protecting the vulnerable population as if their lives are expendable, but I digress). I’m not saying the vaccine is for everyone, but people could make different choices (stay home when sick, test, mask, ask known sick people to not attend a function, make a meeting virtual instead of in person, not travel when sick, etc) if they knew the real risks.
Let me start with my work, because it is the only known challenge to the narrative that I am aware of. Https://doi.org/10.1016/j.trim.2025.102197. In the discussion, I review the inconsistencies in the literature as a basis for my hypothesis. I don't know of any wet work that has been done to demonstrate superinfection in the context of disease, but here is an in silico study. Https://doi.org/10.1016/j.jtbi.2019.01.011. This study was my 2nd clue into identifying vaccines having the potential to cause transplant rejection. Doi.org/j.1600-6143.2011.03604.x. In case the doi is wrong, Katerinis et al De novo anti-HLA antibody after pandemic H1N1 and seasonal influenza immunization in kidney transplant recipients. AJT. 2911;11:1727-1733. In the same journal, another article immediately challenges the premise. Of course, at least one of the authors challenging the concept has a COI with pharma. I've been communicating with Dr. Mustafa who is interested in the concept of vaccines causing organ rejection. After he published this paper (Front. Immunol. Doi: 10.3389/fimmu.2025.156377) I ran an analysis using the algorithm I created. The patient's antibodies were most likely from the influenza vaccine and EBV reactivation and were a memory response exacerbated by the adjuvants in the RZV and PCV13 vaccines. Until you have enough data to tease these things apart, you can't unravel the patterns. There is way too much noise among adult transplant recipients to see this. It requires a pediatric population where there are no interfering pregnancies, transfusions or prior transplants (the old paradigm of sensitization), and shots or infections are staggered. The seminal study for determining that HLA were immunogenic took place in 1975 using a rabbit model injected with human lymphocytes. A negative control (1 of 4) made the same antibodies and it was blown off as being xenoantibody. Just so happens that rabbits are a great conduit for HSV-1. When you put HSV-1 gB together with EBV gp350, you come up with the same HLA antibody specificity as the lymphocytes that were injected into all the positive controls. No one ever challenged this study (Ferrone et al. Tissue Antigens 1975;5:41-7). And HLA Class 2 were never tested for immunogenicity. That's a problem, because the neonatal Fc receptor is important to antigen presentation and appears identical to HLA Class 1 in structure and sharing Ɓ2M, which requires an acidic pH to function (lysosome and ischemia/reperfusion injury).The problems go on and on. It starts in 1957 with Peter Medawar publishing an article (Ann. The New York Acad Sci. 1957;68(2):255-267) where he identified that the immunogenic subcellular particle causing transplanted skin rejections is a virus-like particle that is isolated from the cell nucleus derived from regional lymph nodes-susceptile to ischemia/reperfusion injury. HLA have NEVER been found in the cell nucleus. IR is a breeding ground for glycolysis and SUMOylation. Together, under stress, these post-translational protein modifications may induce the formation of viral neoepitopes. The immune system cannot distinguish one virus from another in the same lymph node, and therefore may make a lower affinity, higher avidity response to combat both simultaneously. Neither can be detected at this level. EBV upregulates hyaluronic acid which is incorporated into exosomes and can be oxidized under stress or ROS to become a DAMP (danger associated molecular pattern). Shall I go on? You can see more on my LinkedIn series, TidbiTs of Transplant Rejection, where I give some practical examples of problems with data analysis (from memory since I have to be careful legally). My audience appears to be dwindling, so I'm not sure how long I will continue that endeavor. I guess it's too complicated to comprehend and too overwhelming to consider after considering everything we were taught might be skewed, or wrong. Trying to get funding to continue the work as we speak. Hope that helps. Best regards.
I just realized I did not follow-through in order with a few points. The FcRn was not discovered until 10 years after HLA, and Ɓ2M is a much better indicator of kidney function than GFR. No one has ever determined whether the Ɓ2M in urine comes from FcRn or HLA Class I. It has always been assumed that it is from HLA. While there is room for argument here, without data this is a blind spot. Because of the pH dissociation with FcRn vs peptide loss determing dissociation from HLA, it seems more likely that FcRn is the more likely candidate providing the Ɓ2M. Stress and IR injury induce pH changes in localized tissue. FcRn is upregulated under cell stress and functions optimally between pH 6-6.5, releasing FcRn at pH 7. But it also translocates IgG across cell membranes, and is likely why plasmapheresis works to lower HLA (and other autoimmune) antibody titers. This was as much a forensic investigation as it was research. There is so much more when you dive into the innate and adaptive immune responses. Particularly when you start to look at aluminum adjuvants. They are not taken out of the body. They are phagocytosed by macrophages and dendritic cells and can remain there for years with the antigen. They also stimulate the production of DAMPs, cause cell necrosis and apoptosis (which would free exosomes containing modified superinfecting viral antigens).
Following the study of HLA being allegedly immunogenic (Ferrone et al in my previous post), Oh et al (1975) used "soluble HLA antigen" (which could not be distinguished from exosomes carrying viral components) to isolate HLA. The immunogenic substance was contaminated with molecular weight proteins much higher than HLA, and ceruloplasmin (CP) was noted as the primary contaminant. CP is essential for copper homeostasis under hypoxia/ischemia. Just so happens that copper agglomerates SUMO2 whichever all over these viral envelope proteins, particularly EBV gp350. The only viral envelope protein to have more SUMO2 and glycosylation binding sequnces is the SARS-CoV-2 spike protein. And nobody but me recognized that. SUMO2/3 is a major player which was first identified on H1N1 NS protein, a collaboration between China and the US in a 2011 study. SUMO modifies NS1 to shut down interferon production. Now I'm not propagating conspiracy here, just pointing out data to show how SUMO can change protein function. In a darker place, it would be ideal to conceal alternative motives, especially considering the association with HLA diseases. Furin cleavage site? Good distraction.
Jenn, I appreciate your dialogue and observations. With my first grandson just arriving last month, and son and daughter-in-law being artists, I felt compelled to give them some advice. My background is in transplant compatibility testing. Stay with me, this is relevant to the discussion. Ten years ago, I made a serendipitous discovery that shocked me and pushed me to research the literature. This ultimately led to dissent from mainstream theory that transplants are rejected by mismatched organs. I discovered through my research that this is only a consequence of viral superinfection complicated by stress (which can come in many forms).
While different vaccines have slightly different mechanisms of action, most have the capacity for a viral envelope protein to be stored in the nucleus due to a post-translational protein modification called SUMO2/3. I found that this can alter the structure of the viral protein and the way it is recognized by the immune system. It can also provide it with new and unknown functions. Bottom line, it lays the groundwork for an allo (in the case of transplants) or auto (in the case of autoimmunity) immune response.
With that being said, I just published the in silico evidence last month. The autoimmune component was not part of the paper.
I am not anti-vax. However, based on my experience and data, I now lean in favor of vaccine hesitancy because we are introducing an element that is not natural, tricked our immune system into seeing danger and responding to it, all in hopes of staving off a disease with a low frequency of consequences. I still have more work to do, and this is an uphill battle as you can imagine. But the combination of EBV reactivation by stress, compounded by the introduction of a second virus, may be a recipe for chronic suffering down the road depending on one's exposure, genetic makeup and stress levels (diet and general health play a role obviously).
If I had to do it all over again, I would be far more hesitant knowing what I know about the immune response that can be activated with these components at present. Am I saying that vaccines can cause disease? I cannot rule this out right now, because the confounding variables I have encountered are not accounted for in the vaccine studies I have reviewed. Am I saying that they can cause organ transplant rejection? Highly likely, especially influenza. But you will not read that in any study including mine (TBD). The literature and at least the data I've been exposed to support my hesitancy. To be fair, I do not advocate mainstream views but rather a dissenting viewpoint. I am trying to get funding to continue my investigation.
Not sure this helps. But until the variables are addressed, I will not be taking or advocating for anyone to be vaccinated. I don't like numbers involving death any more than anyone else. But is chronic suffering any worse in the long term? If I am able to prove that adjuvants and certain live-attenuated or killed vaccines or VLPs or mRNA can provide the necessary components for disease, why would I expose anyone to them intentionally? Wouldn't it be smarter to isolate until I'm no longer able to spread? Concentration is the key to disease. Vaccines concentrate viral components.
The problem, as I see it, is as much an obstacle by the scientific community as it is in the anti-vax community. This is why neither trust the other.
For what it's worth, those are my observations. I can overwhelm you with studies to provide you with evidence, but I don't think that will help right now until more work is done.
Best regards.
Steve Heron, Master of Clinical Immunology, CHS
Thanks Steve for sharing your thoughts. Can you share some links to the research you mention? I'm aware of the danger of of latent herpesviruses like CMV in transplantation but have not seen any evidence around the potential mechanisms you mention.
As an adult living with long covid for the past 5 1/2 years, I can tell you that for the first 3yrs I wish I had died. Each moment was agony in physical suffering. It is isolating and takes a toll on the whole family. I now live the best life I can as a disabled person. (Prior to long covid I was an endurance runner & at the top of my career. I was fit AF. ) I can no longer work or do more than one activity a day. I cannot imagine the loss of this much health as a child & having to struggle with these issues the rest of their lives. The devastation is not only to the child, their family, and their friends, but to our community and future loss of what they could have contributed.
I strongly feel that we need to continue to improve the vaccines as we learn more about the virus. But vaccines are not enough. Society quickly moved away from isolating when sick due to pressure to influence the WHO’s & CDC’s recommendations despite them knowing Covid is Airborne. Work places went back to sick shaming when taking time off & schools punish kids for their absenteeism. Masks are now political when they are personal protective equipment (PPE). It is frustrating that health care providers rarely role model masking themselves. I have experienced them getting upset when asked to mask because my immune system is vulnerable. It is really scary to see so little masks in health care settings (and in public) when Covid spikes seasonally. We need more discussion about airborne transmission and the need for multi pronged approach based on science.
PS- surgical or cloth masks are not as protective as N95s & need to be fitted to your face.
All medical decisions are risk-benefit analyses. All medical decisions are prone to error. Your/our job is to choose on which side you want to err, since none of us make perfect decisions. A certain percentage of folks operated on for appendicitis will and should have normal appendices. Otherwise people will wind up with ruptured appendices too often. Which do you prefer? Get it?
I think the issue is that most people are making these decisions without knowing all of the risks and facts about Covid. I continue to meet people with newly diagnosed long covid saying they didn’t know that could happen. Most people think it is just like getting the flu and only vulnerable populations could have serious harm. (Side bar- it is also extremely disturbing how cavalier people are about protecting the vulnerable population as if their lives are expendable, but I digress). I’m not saying the vaccine is for everyone, but people could make different choices (stay home when sick, test, mask, ask known sick people to not attend a function, make a meeting virtual instead of in person, not travel when sick, etc) if they knew the real risks.
Let me start with my work, because it is the only known challenge to the narrative that I am aware of. Https://doi.org/10.1016/j.trim.2025.102197. In the discussion, I review the inconsistencies in the literature as a basis for my hypothesis. I don't know of any wet work that has been done to demonstrate superinfection in the context of disease, but here is an in silico study. Https://doi.org/10.1016/j.jtbi.2019.01.011. This study was my 2nd clue into identifying vaccines having the potential to cause transplant rejection. Doi.org/j.1600-6143.2011.03604.x. In case the doi is wrong, Katerinis et al De novo anti-HLA antibody after pandemic H1N1 and seasonal influenza immunization in kidney transplant recipients. AJT. 2911;11:1727-1733. In the same journal, another article immediately challenges the premise. Of course, at least one of the authors challenging the concept has a COI with pharma. I've been communicating with Dr. Mustafa who is interested in the concept of vaccines causing organ rejection. After he published this paper (Front. Immunol. Doi: 10.3389/fimmu.2025.156377) I ran an analysis using the algorithm I created. The patient's antibodies were most likely from the influenza vaccine and EBV reactivation and were a memory response exacerbated by the adjuvants in the RZV and PCV13 vaccines. Until you have enough data to tease these things apart, you can't unravel the patterns. There is way too much noise among adult transplant recipients to see this. It requires a pediatric population where there are no interfering pregnancies, transfusions or prior transplants (the old paradigm of sensitization), and shots or infections are staggered. The seminal study for determining that HLA were immunogenic took place in 1975 using a rabbit model injected with human lymphocytes. A negative control (1 of 4) made the same antibodies and it was blown off as being xenoantibody. Just so happens that rabbits are a great conduit for HSV-1. When you put HSV-1 gB together with EBV gp350, you come up with the same HLA antibody specificity as the lymphocytes that were injected into all the positive controls. No one ever challenged this study (Ferrone et al. Tissue Antigens 1975;5:41-7). And HLA Class 2 were never tested for immunogenicity. That's a problem, because the neonatal Fc receptor is important to antigen presentation and appears identical to HLA Class 1 in structure and sharing Ɓ2M, which requires an acidic pH to function (lysosome and ischemia/reperfusion injury).The problems go on and on. It starts in 1957 with Peter Medawar publishing an article (Ann. The New York Acad Sci. 1957;68(2):255-267) where he identified that the immunogenic subcellular particle causing transplanted skin rejections is a virus-like particle that is isolated from the cell nucleus derived from regional lymph nodes-susceptile to ischemia/reperfusion injury. HLA have NEVER been found in the cell nucleus. IR is a breeding ground for glycolysis and SUMOylation. Together, under stress, these post-translational protein modifications may induce the formation of viral neoepitopes. The immune system cannot distinguish one virus from another in the same lymph node, and therefore may make a lower affinity, higher avidity response to combat both simultaneously. Neither can be detected at this level. EBV upregulates hyaluronic acid which is incorporated into exosomes and can be oxidized under stress or ROS to become a DAMP (danger associated molecular pattern). Shall I go on? You can see more on my LinkedIn series, TidbiTs of Transplant Rejection, where I give some practical examples of problems with data analysis (from memory since I have to be careful legally). My audience appears to be dwindling, so I'm not sure how long I will continue that endeavor. I guess it's too complicated to comprehend and too overwhelming to consider after considering everything we were taught might be skewed, or wrong. Trying to get funding to continue the work as we speak. Hope that helps. Best regards.
I just realized I did not follow-through in order with a few points. The FcRn was not discovered until 10 years after HLA, and Ɓ2M is a much better indicator of kidney function than GFR. No one has ever determined whether the Ɓ2M in urine comes from FcRn or HLA Class I. It has always been assumed that it is from HLA. While there is room for argument here, without data this is a blind spot. Because of the pH dissociation with FcRn vs peptide loss determing dissociation from HLA, it seems more likely that FcRn is the more likely candidate providing the Ɓ2M. Stress and IR injury induce pH changes in localized tissue. FcRn is upregulated under cell stress and functions optimally between pH 6-6.5, releasing FcRn at pH 7. But it also translocates IgG across cell membranes, and is likely why plasmapheresis works to lower HLA (and other autoimmune) antibody titers. This was as much a forensic investigation as it was research. There is so much more when you dive into the innate and adaptive immune responses. Particularly when you start to look at aluminum adjuvants. They are not taken out of the body. They are phagocytosed by macrophages and dendritic cells and can remain there for years with the antigen. They also stimulate the production of DAMPs, cause cell necrosis and apoptosis (which would free exosomes containing modified superinfecting viral antigens).
Following the study of HLA being allegedly immunogenic (Ferrone et al in my previous post), Oh et al (1975) used "soluble HLA antigen" (which could not be distinguished from exosomes carrying viral components) to isolate HLA. The immunogenic substance was contaminated with molecular weight proteins much higher than HLA, and ceruloplasmin (CP) was noted as the primary contaminant. CP is essential for copper homeostasis under hypoxia/ischemia. Just so happens that copper agglomerates SUMO2 whichever all over these viral envelope proteins, particularly EBV gp350. The only viral envelope protein to have more SUMO2 and glycosylation binding sequnces is the SARS-CoV-2 spike protein. And nobody but me recognized that. SUMO2/3 is a major player which was first identified on H1N1 NS protein, a collaboration between China and the US in a 2011 study. SUMO modifies NS1 to shut down interferon production. Now I'm not propagating conspiracy here, just pointing out data to show how SUMO can change protein function. In a darker place, it would be ideal to conceal alternative motives, especially considering the association with HLA diseases. Furin cleavage site? Good distraction.
Many thanks, I will read throught this.