Recently, there have been an increasing number of clinical studies and reports indicating that mass vaccination campaigns during a pandemic and repeated administration of vaccine doses are associated with the development of antibody-dependent enhancement, which represents the mild end of induced immunodeficiency. The severe end of induced immunodeficiency is the development of a form of Acquired Immunodeficiency Syndrome without an actual infection by HIV, and the disease could also be regarded as an immunological hurricane, especially for people with comorbidities.

The following is a warning from Dr. Luc Montagnier, a researcher who won the Nobel Prize in Medicine or Physiology for discovering the HIV virus in 2008:

For those of you who have taken the third dose, go and take an AIDS test. The results may surprise you. Then, sue your government.

Well, imagine what happened days after the Winner of the Nobel Prize gave his warning? Scientists discovered a more virulent HIV variant in the Netherlands, a country that happens to have Green Passes implemented and a high rate of a COVID-19 booster intake. Many people would regard this as a mere coincidence, but is it one? Let’s find out.

Researchers could not create a single effective vaccine dose against SARS-CoV-1, MERS-CoV, Dengue Virus 2 and Respiratory Syncytial Virus. In all cases, the results led to the development of antibody-dependent enhancement, which is characterised by suboptimal antibodies that rather than killing the virus, help it infect more host cells. This is because näive antibodies are outcompeted by vaccinal antibodies, which are not fully adapted to the nature of the virus, according to recent research by Dr. Geert Vanden Bossche. Children, whose innate immune systems are more sensitive to viral infection, experienced antibody-dependent enhancement after a clinical trial in vaccinology to prevent the onset of infectious disease by Dengue Virus 2. Imagine that a mass vaccination policy involving two or three doses is implemented around the world against a virus that is a relative to Dengue Virus 2 and that also likely has segments from the HIV-1 virus in around 1% of its genome. The reverse transcription of a visible number of nucleotides from both the SARS-CoV-2 and the HIV-1 genomes led to their integration into the coding DNA of host cells and this is abnormal, given that nucleotides from viral RNAs are very rarely reverse transcribed and integrated into the host cell’s DNA, and when this happens, they are almost always inserted into the non-coding DNA.

Moreover, there are a number of commonalities in pathophysiology and therapy between COVID-19 and AIDS. An example is the repurposing of the lopinavir, ritonavir and darunavir antiretroviral drugs for COVID-19 therapy. Another example is the interaction of both SARS-CoV-2 and HIV-1 with the AIP4 protein, which is implicated in inflammation, and both interactions led to lower signalling rates of interferons. Interestingly, people with significant comorbidities are pronouncedly more likely to develop complications due to cytokine depletion and the development of a cytokine storm in the case of infection by SARS-CoV-2 and HIV-1. With regards to the pathogenesis by the SARS-CoV-2, there is a viral protein known as the spike protein, which induces hyper-inflammatory processes through Toll-Like Receptor 4 signalling in macrophages (a kind of antigen-presenting cells), weakens genes implicated in DNA repair and antibody gene rearrangement, potentially making people more vulnerable to mutations and causing the formation of weaker antibodies, and acts as a superantigen, potentially causing a magnitude of pathological and immunological damages similar to pathogenic super-bacteria (pathogens that are antibiotic resistant).

Moreover, the S1 subunit and the active trimer of the spike protein are also capable of disrupting the activity of mitochondria in brain endothelial cells and likewise, have implications upon metabolism (Eun Seon Kim et al, 2021) and the 674-685 fragment of the protein was shown to prevent mitochondria from synthesising cytochrome c, which is responsible for inducing apoptosis of infected cells (Olena Kalashnik, 2021). We believe that the spike protein causes more infected cells not to undergo apoptosis if the virus and the spike protein spread to tissues in various sites of the host organism. The spike protein produced by the vaccinal mRNA is not less toxic, but only more immunogenic, meaning that there is a higher immune sensitivity against it than against the viral spike protein, and researchers induced two Proline amino acid substitutions in the S2 subunit of the spike protein so that it became more immunogenic. The amino acid substitutions were induced to keep the spike protein in a pre-fusion conformation, but it is not fully certain that the stabilised spike protein will remain that way. The receptor-binding domain of the vaccinal spike protein is intact, meaning that it is as capable of binding to the ACE2 receptors of host cells as the viral spike protein (Timothy P. Riley et al, 2021). Likewise, risks are not really decreased because an increased immune sensitivity could also mean a higher susceptibility for hyper-inflammatory immune responses, especially in people with one or more comorbidities.

The following is a video of a team of scientists who decided to add an HIV protein to the spike protein-based vaccines in order to stabilise the vaccinal protein.

trim.E6C0394B-4028-49EA-98EB-E5BB7CC669B8

The problem is that such an addition would only increase the number of nucleotides that will be reverse transcribed by HIV/LINE-1 Reverse Transcriptases and integrated into the coding DNA of host cells, and it will possibly make the spike protein even more toxic. So, will diverse scientific teams continue to play Mother Nature in the name of helping mankind fight against a virus with a mortality rate lower than 1%, or will such teams come back to their senses and do their required full and careful research before making complicated decisions?

Therefore, are there risks of induced immunodeficiencies, particularly in people with significant underlying health conditions? The data suggests so, and I believe there needs to be a massive independent research-based mobilisation to find wise and firm ways of mitigation of future immunodeficiency syndromes. This is not to induce unnecessary fear, but to tell the truth. This is the question of the pandemic: have the zealous health overlords played Mother Nature? This is a perfidious problem that very likely will take a longer time for its full effects to appear. We know that the Omicron variant is more capable of camouflaging itself and impairing key antiviral cytokine responses as well, so the problem involves two planes here. This is the time for unprecedented action and seriousness, and firm action from the people will allow the good scientists and doctors to come up with great solutions before there is too much harm done to immunology and health. Whilst AIDS is the disease of the 21st century, the truth is that developing cytokine and natural killer cell-based therapies and vaccines (natural immunity-based and non-pathogenic) may represent the treatment of the 21st century. Likewise, there is hope and it all depends on how much solidarity each one of us has to spread the truth like light and turn the situation around.

Reference list

1. Tarasova O, Ivanov S, Filimonov DA, Poroikov V. Data and Text Mining Help Identify Key Proteins Involved in the Molecular Mechanisms Shared by SARS-CoV-2 and HIV-1. Molecules. 2020; 25(12):2944. https://doi.org/10.3390/molecules25122944
2. Uncanny similarity of unique inserts in the 2019-nCoV spike protein to HIV-1 gp120 and Gag Prashant Pradhan, Ashutosh Kumar Pandey, Akhilesh Mishra, Parul Gupta, Praveen Kumar Tripathi, Manoj Balakrishnan Menon, James Gomes, Perumal Vivekanandan, Bishwajit Kundu bioRxiv 2020.01.30.927871; doi: https://doi.org/10.1101/2020.01.30.927871
3. Arvin, A. M., Fink, K., Schmid, M. A., Cathcart, A., Spreafico, R., Havenar-Daughton, C., Lanzavecchia, A., Corti, D., & Virgin, H. W. (2020). A perspective on potential antibody-dependent enhancement of SARS-CoV-2. Nature, 584(7821), 353–363. https://doi.org/10.1038/s41586-020-2538-8
4. Halstead S. B. (2021). Vaccine-Associated Enhanced Viral Disease: Implications for Viral Vaccine Development. BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy, 35(5), 505–515. https://doi.org/10.1007/s40259-021-00495-6
5. Ken Shirato and Takako Kizaki (2021), SARS-CoV-2 spike protein S1 subunit induces pro-inflammatory responses via toll-like receptor 4 signaling in murine and human macrophages, Heliyon 7 e06187, pp 2-9, doi: https://doi.org/10.1016/j.heliyon.2021.e06187
6. Jafarzadeh, A., Chauhan, P., Saha, B., Jafarzadeh, S., & Nemati, M. (2020). Contribution of monocytes and macrophages to the local tissue inflammation and cytokine storm in COVID-19: Lessons from SARS and MERS, and potential therapeutic interventions. Life sciences, 257, 118102. https://doi.org/10.1016/j.lfs.2020.118102
7. Mary Hongying Cheng, She Zhang, Rebecca A. Porritt, Magali Noval Rivas, Lisa Paschold, Edith Willscher, Mascha Binder, Mosche Arditi and Ivet Bahar (2020), Superantigenic character of an insert unique to SARS-CoV-2 spike supported by skewed TCR repertoire in patients with hyperinflammation, Proceedings of the National Academy of Sciences of the United States of America, 117(41), pp 25254-25262, doi: https://doi.org/10.1073/pnas.2010722117
8. Kim, E. S., Jeon, M. T., Kim, K. S., Lee, S., Kim, S., & Kim, D. G. (2021). Spike Proteins of SARS-CoV-2 Induce Pathological Changes in Molecular Delivery and Metabolic Function in the Brain Endothelial Cells. Viruses, 13(10), 2021. https://doi.org/10.3390/v13102021
9. Kalashnyk, O., Lykhmus, O., Izmailov, M., Koval, L., Komisarenko, S., & Skok, M. (2021). SARS-Cov-2 spike protein fragment 674-685 protects mitochondria from releasing cytochrome c in response to apoptogenic influence. Biochemical and biophysical research communications, 561, 14–18. https://doi.org/10.1016/j.bbrc.2021.05.018
10. Kirchdoerfer, R. N., Wang, N., Pallesen, J., Wrapp, D., Turner, H. L., Cottrell, C. A., Corbett, K. S., Graham, B. S., McLellan, J. S., & Ward, A. B. (2018). Stabilized coronavirus spikes are resistant to conformational changes induced by receptor recognition or proteolysis. Scientific reports, 8(1), 15701. https://doi.org/10.1038/s41598-018-34171-7
11. Timothy P. Riley, Hui-Ting Chou, Ruozhen Hu, Krzysztof P. Bzymek, Ana R. Correia, Alexander C. Partin, Danqing Li, Danyang Gong, Zhulun Wang, Xinchao Yu, Paolo Manzanillo and Fernando Garces (2021), Enhancing the Prefusion Conformational Stability of SARS-CoV-2 Spike Protein Through Structure-Guided Design, Frontiers in Immunology, doi: https://doi.org/10.3389/fimmu.2021.660198