No Neutralizing Monoclonal Antibodies to Spike Protein Left: Time to Clone and Produce Humanized Innate Immunity Monoclonal Neutralizing Antibodies to HERV-K102 Envelope Protein
Figure 1. Virions of Enveloped RNA Viruses (those that bud through the cell surface membrane, like SARS-CoV-2) can be Neutralized and Cleared by HERV-K102 Envelope Antibodies When SARS-CoV-2 Virions Produced in Human Cells
The beauty of innate immune protection is that it doesn’t recognize virus-specific antigens … so it doesn’t matter what variant it is, and innate immunity doesn’t select for variants like the adaptive immunity vaccines and the spike specific neutralizing monoclonal antibodies [1].
These anti-HERV-K102 Env protector neutralizing antibodies are in the upper respiratory tract in COVID-19 patients protecting against severe disease [2]. They are produced during active viral infections along with protector HERV-K102 particles [3]. They are also there in post-viral syndromes like chronic fatigue syndrome (CFS) [2]. When under therapy that produces CFS remission, no HERV-K102 particles can be detected in blood; at 84 hours off therapy there are 2.55 x 10 (11) particles per ml of plasma (all cDNA) and acute insomnia sets in the first night followed by extreme fatigue and brain fog until therapy (hypericum) resumes [3].
The innate immunity monoclonal neutralizing antibodies to HERV-K102 envelope may be very useful therapies not only for RNA virus pandemics and pandemic preparedness but could be used in patients infected with other intracellular pathogens, and those with tumors [4, 5]. The cell surface expression of HERV-K102 Env is directly linked to the apoptosis machinery [4] so the isotype would not matter so much.
In cases where there may be apoptosis resistance such as by virus infection of cells or soluble spike protein activation (infection or vaccine consequences), be sure to use as cofactors, zinc, genistein, 7 keto-DHEA, and/or ivermectin and optimize the vitamin D3 levels for best results with the innate antibody.
It is not presently known if spike stimulation of cells via ACE2, BSG, or some other receptor would induce HERV-K102 envelope expression, so it is presently unknown if the innate monoclonal antibody to HERV-K102 Env would be useful for the treatment of patients with long COVID or COVID-19 vaccine injuries. However, secondary exposure of macrophages to spike protein does induce; trained immunity enhancers, IRF1 & NFKB1 (needed for HERV-K102 proviral genome expression), mediators of apoptosis resistance, and thus, likely also immunosenescence (which causes initiation and progression of chronic diseases) [6].
If spike stimulation does induce HERV-K102 Env expression at the cell surface, for the treatment of long COVID-19 or COVID-19 vaccine injury patients, those with neurological symptoms may present challenges [7,8]. Firstly, generally the blood brain barrier (BBB) prevents antibody crossing into the central nervous system while TNF-alpha, IL-1, IL-6 , IFN-gamma and IL-17A make the BBB more permeable [7]. Secondly, killing too many neurons may not be desirable, and one would probably want to use IgG4 isotypes to prevent too much inflammation/coagulation.
Even in sickness like SLE, the dominant isotype of antibodies to HERV-K102 Env are IgG1 and IgG2 where IgG2 in a complex with soluble HERV-K102 SU Env activates neutrophils for both antibody dependent neutrophil phagocytosis and also the formation of neutrophil extracellular traps (NET) [9].
REFERENCES
Jensen B, Luebke N, Feldt T, et al. Emergence of the E484K mutation in SARS-COV-2-infected immunocompromised patients treated with bamlanivimab in Germany. Lancet Reg Health Eur. 2021 Sep;8:100164. doi: 10.1016/j.lanepe.2021.100164.
Apostolou E, Rizwan M, Moustardas P, et al. Saliva antibody-fingerprint of reactivated latent viruses after mild/asymptomatic COVID-19 is unique in patients with myalgic-encephalomyelitis/chronic fatigue syndrome. Front Immunol. 2022 Oct 20;13:949787. doi: 10.3389/fimmu.2022.949787.
Laderoute MP, Giulivi A, Larocque L, et al. The replicative activity of human endogenous retrovirus K102 (HERV-K102) with HIV viremia. AIDS. 2007 Nov 30;21(18):2417-24.
Wang-Johanning F, Rycaj K, Plummer JB, Li M, Yin B, Frerich K, Garza JG, Shen J, Lin K, Yan P, Glynn SA, Dorsey TH, Hunt KK, Ambs S, Johanning GL. Immunotherapeutic potential of anti-human endogenous retrovirus-K envelope protein antibodies in targeting breast tumors. J Natl Cancer Inst. 2012 Feb 8;104(3):189-210. doi: 10.1093/jnci/djr540.
Wang-Johanning F, Radvanyi L, Rycaj K, Plummer JB, Yan P, Sastry KJ, Piyathilake CJ, Hunt KK, Johanning GL. Human endogenous retrovirus K triggers an antigen-specific immune response in breast cancer patients. Cancer Res. 2008 Jul 15;68(14):5869-77. doi: 10.1158/0008-5472.CAN-07-6838.
Laderoute MP. Controversies in the Immunology of the Adaptive Immunity COVID-19 Vaccines. pp149 with 255 refs [submitted]
Iwasaki A. Immune Regulation of Antibody Access to Neuronal Tissues. Trends Mol Med. 2017 Mar;23(3):227-245. doi: 10.1016/j.molmed.2017.01.004. Epub 2017 Feb 7.
Monje M, Iwasaki A. The neurobiology of long COVID. Neuron. 2022 Nov 2;110(21):3484-3496. doi: 10.1016/j.neuron.2022.10.006.
Tokuyama M, Gunn BM, Venkataraman A, Kong Y, Kang I, Rakib T, Townsend MJ, Costenbader KH, Alter G, Iwasaki A. Antibodies against human endogenous retrovirus K102 envelope activate neutrophils in systemic lupus erythematosus. J Exp Med. 2021 Jul 5;218(7):e20191766. doi: 10.1084/jem.20191766.
Tokuyama M, Gunn BM, Venkataraman A, Kong Y, Kang I, Rakib T, Townsend MJ, Costenbader KH, Alter G, Iwasaki A. Antibodies against human endogenous retrovirus K102 envelope activate neutrophils in systemic lupus erythematosus. J Exp Med. 2021 Jul 5;218(7):e20191766. doi: 10.1084/jem.20191766. Epub 2021 May 21. Also a sightly different preprint is available at https://doi.org/10.1101/776468 Sept 20, 2019. This paper claims most of the antibody to HERV-K102 is IgG2 with some IgG1.. The complex of soluble HERV-K102 Env (SU domain) with IgG2 antibody activates neutrophils via the FCGR3B (CD16b). SLE plasma (or purified IgG) and recombinant HERV-K102 SU Env form a complex which activates neutrophils: enhances antibody dependent neutrophil phagocytosis (shown by flow cytometry) and increases Neutrophil Extracellular Trap (NET) formation; shown by microscope for fluorescence following Hoeschst staining for extracellular DNA, citrullinated histone 3, and neutrophil elastase.
Compare President Trump's experience with the original monoclonal antibodies to Joe Biden's Paxlovid-induced rebound Covid.
As your title indicates, the original monoclonal antibodies are now ineffective against the Omicron-series variants' spike proteins. I believe that the Americans have "deauthorized" the original monoclonals and sent them for disposal. However, they should still have been useful against Vaxx injury from the initial injections which should have induced the original spikes (if we were confident that we knew what was truly in the vials.)
I can't get as deeply into the literature as you are able, but I haven't seen anything to suggest that such a treatment has been studied. The FLCCC website does not list this in their long covid or vaxx injury segments.