Dr. Fauci... You have replied to my letter of May 6, 2020 ... a little too late
"Exploiting the Newly Identified HERV-K102 Protector Foamy Retrovirus Unique to Humans for Protection Against COVID-19 Severity"
A 15 page letter to Dr. Anthony Fauci, Dr. Hugh Auchincloss, Dr. John J. McGowen and Dr. H. Clifford Lane was sent on May 6, 2020 explaining how to exploit the human endogenous retrovirus K102 (HERV-K102) to “save lives” and “end the pandemic sooner”. The title of this letter was "Exploiting the Newly Identified HERV-K102 Protector Foamy Retrovirus Unique to Humans for Protection Against COVID-19 Severity."
Today I got my reply, and it seems Dr. Fauci is saying “yup, you were right, we should have explored and tested the novel VIRUS ANTI-VIRUS, HERV-K102 trained (innate) immunity protector system, just like you said.”
Just like fighting fire with fire, HERV-K102 a protector non-pathogenic foamy retrovirus is replication competent (Laderoute MP et al, 2007; 2015), so it actually is a virus anti-virus response.
Moreover, the released particles also appears to mediate an autologous innate immunity vaccination process activating innate T cell and B-cell responses to HERV-K102 envelope.
The HERV-K102 Protection System involves the HERV-K102 particles (1, kills virus infected cells)
and
the innate T cells (2) and antibodies from B cells (3) all which kill virus infected cells.
HOWEVER, since HERV-K102 envelope becomes expressed on virally infected cells, virus that bud through the cell’s surface, the so-called ‘enveloped RNA viruses’ pick up the HERV-K102 envelope and express this envelope on their virions.
This means the antibodies to HERV-K102 Envelope can neutralize and clear SARS-CoV-2 virions (4).
Interestingly, the HERV-K102 envelope peptides described in our 2007 paper and used to test for antibody in patients with various viral infections including HIV-1 patients were selected based on their likelihood for being cryptic in the particles but fully accessible in the HERV-K102 envelope that is expressed at the cell surface of the virally infected cells and also found on the SARS-CoV-2 virions.
About 75 % of the HIV-1 patients had strong antibody levels to the two cryptic peptides ML4 and ML5. About 75 % of the HIV-1 patients had low but demonstrable HERV-K102 particles in plasma. Altogether about 96% of HIV-1 patients had particles and/or antibodies to HERV-K102.
HIV-1 is also an RNA pandemic virus with no safe or effective ADAPTIVE IMMUNITY vaccine.
There are two forms of the HERV-K102 envelope as shown below.
The 3-D visualization offered by AlphaFold
[Jumper, J et al. Highly accurate protein structure prediction with AlphaFold. Nature (2021). and
Varadi, M et al. AlphaFold Protein Structure Database: massively expanding the structural coverage of protein-sequence space with high-accuracy models. Nucleic Acids Research (2021).]
seems consistent with our choice of the ML4 and ML5 peptides being cryptic on the HERV-K102 particles (the pol-env version) but accessible on the cell surface of virus infected cells and on SARS-CoV-2 “enveloped” particles (the envelope version) [Laderoute MP et al, 2007].
As shown in the left side below for the pol-env version thought to be particle associated, the ML5 peptide for HERV-K102 has a unique Cysteine (C) amino acid (1123) in the middle, which seems to be spatially close to the C 1042 which is in a disulfide bond with C1035. It is unclear what happens to the disulfide bond arrangement after cleavage of the surface unit from the transmembrane portion at arginine (R) /phenylalanine (F) involving R 1225 and F 1226. It is known this cleavage is an absolute requirement for FV particle infectivity. It is possible that upon cleavage that a conformation change hides this ML-5 epitope along with the ML-4 epitopes in particles. Therefore on the particles it is PROPOSED to be cryptic and unable to bind with the ML5 specific antibodies. In contrast, on the right for the envelope expressed on the membrane of virus infected cells, the distance is too far for C:C bonding so the ML5 site is accessible. A conformation difference caused by the presence or absence of the disulfide bond could also explain the access of the epitope to ML4 antibodies on the right but which remains cryptic in the particles on the left.
Thus, in theory, antibodies to the ML4 and ML5 peptides do not bind to particles (the P63135 pol-env), but only to envelope on the surface of virally infected cells or to HERV-K102 envelope on the SARS-CoV-2 virions (ie., the P61567 env).
NOTE that for the autologous innate vaccination process by the released HERV-K102 particles, somehow the interaction of the particles such as binding to heparan sulphate found on almost all cells, causes a conformational change in envelope opening access to the ML4 and ML5 epitopes to allow triggering of the innate T and B cells with receptors to HERV-K102 envelope. This also results in HERV-K102 entering the cells and activating the cGAS-STING double stranded DNA sensor triggering interferon and other responses [Guo Y et al, 2022]. In fact the spreading of the HERV-K102 particles to healthy cells where it is thought they just integrate into genomic DNA arms the cells 1) with more copies of HERV-K102 for a more rapid response in a epigenetically opened area, and 2) entry will trigger the interferon response by a novel mechanism cGAS-STING (cDNA) providing alternative backup to other modes of pattern recognition such as the TLRs. Many human pathogens delay the interferon response to their replicative advantage.
HERV-K102 particles have cDNA genomes [Laderoute MP et al, 2007] because they are protector foamy retroviruses and have a life-cycle opposite to orthoretroviruses. They enter cells with the double-stranded cDNA already reverse transcribed and ready for integration and would be able to replicate sooner than the orthoretroviruses. The orthoretroviruses which reverse transcribe upon entry and then integrate for replication are at a disadvantage against the protector foamy viruses.
That certain peptides of HML-2 envelope can trigger the release of cytokines from CD19 + B cells and CD4 and CD8 T cells was shown for PBMCs from ALS patients and normal healthy controls [Arru G et al, 2021]. Ditto for the demonstration of HML-2 envelope on these cells by flow cytometry. Thus, this corroborates the notion that the HERV-K102 envelope specific innate T and B cells (antibody) demonstrated in HIV-1 patients and in breast cancer patients are not disease causing but part of the normal innate immune protection system.
Finally, although normal healthy controls and ALS patients did have demonstrable antibody to HERV-K102 envelope, the % positive was higher for ALS patients (about 77% testing positive ) when compared with the normal healthy controls (about 18%) for these peptides.
Note that our serology (see above) for the cryptic HERV-K102 peptides were about 75 % in HIV-1 patients and 2% (marginal positives) in the normal healthy controls (interviewed to not have colds or flu or be on any medications at the time of blood draw).
So our strategically selected peptides and serology may hold more clinical significance as to how innate immunity involving HERV-K102 particles and INNATE NEUTRALIZING ANTIBODIES protect against pandemic RNA viruses.
So the issue with the adaptive immunity COVID-19 vaccines:
The problem with the adaptive immunity COVID-19 vaccines was that they strongly induced IgG antibodies and neutralizing antibodies to SPIKE protein after 2 or more doses, which led to infection of the protector LB-FMs by ADE which then transitioned the protector foamy macrophages from this :
into factory warehouses for SARS-CoV-2 (see below). NOTE that just having adequate levels of vitamin D3 protects against COVID-19 infection and severity [Chiodini I et al, 2021; Walsh JB et al., 2022]. Note that adequate vitamin D blocks the transition of the LB-FMs to LB+FMs [Oh J et al, 2009].
It has been estimated that at 50 ng/ml of vitamin D in blood that this would essentially prevent many if not most COVID-19 deaths [Borsch et al, 2021], all without the severe toxicity of the mRNA vaccines [Seneff S & Nigh G, 2022; Seneff S et al, 2022]. There would not be any hassle pertaining to delivery, administration and the need to gaslight the public on the safety and effectiveness. There would not be any need to mandate vaccination when serious adverse event reporting sometimes escaped the censorship or when neighbors came down with serious adverse events including death (in the fall of 2021).
SARS-CoV-2 infection via ADE into the WDR74 positive, lipid body negative foamy macrophages (LB-FMs) (which produce the protector HERV-K102 particles):
results in the loss of critical trained immunity needed to neutralize and clear the newly emerged pathogen (also with a loss in the amplification of the early interferon type 1 and 3 signal);
causes the induction of immunosenescence in macrophages (see below) which initiates and/or exacerbates chronic disease and causes the loss of immune surveillance against all pathogens and tumors; and
by conversion to LB+FMs, creates an immunologically-priviledged site for the replication and cell surface budding of the newly selected SARS-CoV-2 variants [Dias S et al, 2020] which in the URT are then transmitted to others.
That the HERV-K102 “trained (innate) immunity” protector system may offer sterilizing immunity to RNA pandemic viruses was shown in the data below for HIV-1 in the HIV-1 exposed seronegative cohort (HESN) [Laderoute et al, Open AIDs J, 2015]. Increased integration of HERV-K102 into genomic DNA isolated from plasma (at about 5-fold over normal healthy controls, p<0.0005), reflects previous very high replication levels of HERV-K102 in the commercial sex workers (CSW) associated with resistance to HIV-1 acquisition (notably related to the absence of IgG antibodies to HIV-1 envelope). In contrast, those who became infected with HIV-1 with anti-retroviral treatment (T) or not (NT) did not show any evidence of high HERV-K102 replication (separately or together).
So, the name of the game is HERV-K102 has to clear and/or neutralize SARS-CoV-2 BEFORE the spike specific IgG are produced or it is game over.
But the COVID-19 vaccines induced strong IgG to spike in the LRT and the URT. So the innate system was fighting the adaptive immune response. When the strength of the innate immunity waned by 6 months, the adaptive won placing the host at much higher risks of severity and/or death (associated with poorer vaccine effectiveness (VE) against infection, hospitalization, ICU admission and death).
The 2 dose adaptive immunity vaccines were the worst thing for patients and for halting the pandemic. Not only that but the mRNA vaccines were extremely toxic [Seneff S & Nigh G, 2022; Seneff S et al, 2022].
Here is the all-cause mortality data and the non-COVID mortality data from the ONS of the entire UK population which proves these points where MORTALITY RATE RATIOS ABOVE 1 INDICATE MORE DEATH IN THE EVER VACCINATED OVER THE NONVACCINATED.
Note that in February 2021 the protection observed (where the mortality rate ratios were under 1 ) related to innate immunity where 96% of the immunized at this time only had one dose of vaccine and thus, the majority here had no IgG to spike protein. (The UK and Canada decided to postpone the second dose so that more people could be protected with the first dose).
Summary and Conclusions
So in summary, Dr. Fauci, you should have investigated the HERV-K102 trained innate immunity protection system in the summer of 2020.
You could have saved lives and could have ended the pandemic by May 2021 (according to one estimate if adaptive immunity vaccines were not implemented [Kistler KE et al, 2022]).
If you had tested for HERV-K102 particle production, integration levels, and the innate neutralizing antibodies to HERV-K102 using the methods already available [Laderoute MP et al, AIDS 2007], you would have realized the true efficacy of ivermectin and HCQ. In fact the Defense Advanced Research Projects Agency (DARPA) recommended to you that you should employ ivermectin and HCQ should there ever be a pandemic (in part because a safe and effective adaptive immunity vaccine approach was deemed impossible). Why this advice was not heeded needs explanation.
If you had tested for HERV-K102 activation and requested the same of the vaccine manufacturers with follow-up over a year or more to observe the development of vaccine selected variants, you would have immediately known that your 2 dose COVID-19 vaccines were in fact, sabotaging critical innate host defenses by ADE. This was predicted and became a high level concern of experts (including yourself) based on the findings for SARS-CoV-1 and the lack of safe and effective vaccines. Indeed, an important meeting was convened the day after the pandemic was declared on March 11, 2020 concerning the potential issues of ADE with adaptive immunity vaccines to SARS-CoV-2 [Lambert P-H et al, Vaccine June 2020].
This we know from your representation at the March 12 and 13, 2020 meeting by Dr. Barney S Graham (Deputy Director of the NIH Vaccine Research Center who has a conflict of interest pertaining to patents on the coronavirus vaccines and monoclonal antibodies) on the “assessment of risk of disease enhancement with COVID-19 vaccines” involving the Coalition for Epidemic Preparedness Innovations (CEPI) and the Brighton Collaboration Safety Platform for Emergency Vaccines (SPEAC) [Lambert P-H et al, Vaccine June 2020].
In addition, members of the Brighton Collaboration, Program of the Task Force for Global Health (Decatur, GA, USA) involved with pandemic vaccine safety such as Dr. Robert T Chen whom I had the pressure of voluntarily working under from 2008 to 2015 on the Viral Vector Vaccine Safety Working Group [Chen RT et al, Vaccine, 2015; Klug B et al., Vaccine, 2016; Kochhar S et al, Vaccine 2019] and Dr. Cornelia L Dekker were also in attendance.
Interestingly, Dr. Ralph S Baric a highly acclaimed coronavirus expert studying coronavirus mechanisms of pathogenesis and treatments was also in attendance, who has a conflict of interest due to agreements (collaborations) which surprisingly were already signed with Moderna and Pfizer ie., prior to the declaration of the pandemic [Lambert P-H et al, 2020]. Dr. Baric is alleged to have created the SARS-CoV-2 pandemic virus with the Wuhan Institute of Virology with NIH funds which allegedly launched through an unintended lab leak, although we cannot be sure about the latter as to whether it was planned or not.
At the very least, you could have warned the public about keeping vitamin D levels elevated over 50 ng/ml, keeping a healthy weight, and avoiding alcohol and sugar to avoid the risk of insulin resistance and being hospitalized. You could have and should have followed the science. Was it that you were mistaken that you were the science which clouded your thinking?
Attaining at least 50 ng/mL 125 nmol/L circulating 25-hydroxyvitamin D was and remains the most important and urgently needed action needed to reduce transmission and severity of COVID-19.
Please see the research articles cited and discussed at: https://vitamindstopscovid.info/00-evi/ .
With levels lower than this the immune system's innate and adaptive responses become progressively weaker and the risk of wildly dysregulated, indiscriminate cell destroying, inflammatory responses increase.
Without proper vitamin D3 supplementation, or recent high levels of ultraviolet B radiation on unprotected, white, skin, most people have only 5 to 25 ng/mL circulating 25-hydroxyvitmain D. Neither vitamin D3 nor 25-hydroxyvitamin D (produced primarily in the liver, over a week or so, from vitamin D3) are hormones.
The kidneys can work fine (producing a very low level of circulating 1,25-dihydroxyvitamin D, which acts as a hormone, by which the kidneys and parathyroid gland regulate calcium-phosphate-bone metabolism) with 20 ng/mL 50 nmol/L, but immune cells need 50 ng/mL 125 nmol/L at least. The immune system is not affected by the very low, stable, level of hormonal 1,25-dihydroxyvitamin D. The immune system does not use hormonal signaling.
It is frequently stated that "vitamin D is a hormone", but this is incorrect. "Vitamin D" is a general term to refer to vitamin D3 cholecalciferol, 25-hydroxyvitamin D calcifediol (or "calcidiol") and 1,25-dihydroxyvitamin D - but they are three separate compounds with different roles.
For 70 kg 154 lb bodyweight without obesity, 0.125 mg (5000 IU) vitamin D3 a day, on average (up to 10 days between intakes is OK) will raise circulating 25-hydroxyvitamin D to at least 50 ng/mL over several months. Bolus (high, single dose) vitamin D3 (for 70 kg BW) such as 10 mg (400,000 IU) raises the level over 4 days or so, due to the delays in hydroxylation in the liver.
The most important and urgently needed treatment for all those who are infected with SARS-CoV-2 and whose 25-hydroxyvitamin D level is well below 50 ng/mL (most people, unless they have been supplementing vitamin D3 properly for a few months) is a single oral dose of calcifediol, which *is* 25-hydroxyvitamin D. This is more reliably absorbed than vitamin D3 (having two hydrophilic hydroxyl groups rather than one) and goes straight into circulation, raising the level safely over 50 ng/mL in 4 hours. 0.014 mg per kg bodyweight is sufficient. For 70 kg this is one milligram of calcifediol. https://nutritionmatters.substack.com/p/calcifediol-to-boost-25-hydroxyvitamin
The same is true for sepsis patients or anyone suffering a clinical emergency and so requiring proper immune system function as a matter of life and death.
If everyone had 50 ng/mL or more circulating 25-hydroxyvitamin D, there would be almost no sepsis, which killed 11 million people, worldwide, in 2017: https://www.thelancet.com/journals/lancet/article/PIIS0140-6736(19)32989-7.
Fauci is a Slytherin, and he himself once mentioned, when asked, that he took 6000 IU per day of vitamin-D, a perfectly reasonable dose. I suspect he checked levels, because it is not an off-the-shelf dose.