Trained Immunity of Foamy Macrophages: Key Role of HERV-K102 Particles
(submitted for Publication September 8, 2025)
In recent years it has become evident that trained immunity (TI) which involves epigenetic changes to the human genome opening up the DNA for easy access to innate immunity effectors does not necessarily have to involve pro-inflammatory genes. Moreover it is unclear how heterologous protection against a wide variety of pathogens, tumors and even chronic illness could be achieved by “foamy macrophages” especially since they undergo apoptosis when they trigger “trained immunity”. (In other words, how does a cell that no longer exists protect?)
If you have wondered about these odd nuances of TI, you are NOT ALONE.
Here is a 52 page manuscript recently submitted on September 8, 2025 with 112 refs, 9303 words, 7 Figures, 1 Table and 1 Supplemental Table that explains how HERV-K102 protector particles produced in M1-like macrophages (see A above) undergo cell lysis to release the HERV-K102 particles which help protect by any and all of the following:
particles may be oncolytic or may cause lysis of pathogen infected cells but instead merely integrates in normal cells (a process called arming) which amplifies the TI response in anticipation of the next time (recall)
particles induce antibodies to HERV-K102 envelope expressed on tumors and pathogen infested cells and these anti HERV-K102 envelope antibodies may also be neutralizing such as for enveloped RNA viruses (meaning when the virions bud from the surface of cells they pick up HERV-K102 envelope ie., SARS-CoV-2 and HIV-1 are both pandemic ‘enveloped’ RNA viruses and in theory can be cleared and/or inactivated by the antibodies to HERV-K102 envelope )
particles induce innate T cells (some are CD8+, some are gamma delta T cells, and various others) that are cytotoxic and recognize HERV-K102 envelope on the cell surface of cells such as HIV-1 infected cells and tumors of different types (for induction of the gamma delta T cells this is apparently via the cGAS-STING pathway)
through a variety of pattern recognition receptors for HERV-K HML-2 RNA this spreads the protector interferon response throughout the body (cGAS-STING that recognizes the cDNA genomes in HERV-K102 particles is very important when facing emerging RNA viruses meaning the RNA viruses shut down the recognition of foreign RNA so HERV-K102 with its cDNA genomes triggers the interferon antiviral pathways via alternative or backup pathways)
new evidence proposes that HERV-K102 particles shed from the sebocytes (foamy M1-like macrophages) in the upper respiratory tract (URT) may spread herd immunity (consisting of the protector interferon response and the HERV-K102 protector system)
after dose 1 of the Pfizer-BioNTech spike mRNA shot, HERV-K102 may be shed from the URT to the unvaccinated improving both COVID-19 and non-COVID-19 death rates, but with the second dose in the vaccinated the protection turns into a bioweapon, and where for each dose the herd immunity against non-COVID-19 diminishes in the unvaccinated (see Table 1 in the attached and below ) due to the commandeering of the protector HERV-K102 particles by the Pfizer-BioNTech LNPs (see Image 1 below)
Image 1. Only the Pfizer-BioNTech shot can lead to shedding causing death because only Process 2 used by Pfizer-BioNTech generates the spike protein (+/-endotoxin in E. coli) that is thought to cover the LNPs for their targeting to macrophages including the sebocytes in the Upper Respiratory Tract.
DIABOLICAL! Shedding makes much more sense now. Thank You, Dr. Laderoute