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Look at the answer to this question!
What part of the Pfizer Covid vaccine?

The unexpected molecular mimicry associated with the vaccine-expressed SARS-CoV-2 spike protein affects several major organ systems. While the primary identified mechanisms of mimicry involve surface receptor interference or autoantibodies attacking structural and signaling proteins, mitochondrial dysfunction can occur as a secondary downstream consequence of these primary insults.
Heart (Cardiovascular System)
Primary Mechanism: Autoantibody Attack (Structural Mimicry).
How it is affected: The immune system generates antibodies targeting the ⁠ELDKY⁠ sequence on the spike protein, which cross-reacts with alpha-tropomyosin, a structural protein highly concentrated in cardiac muscle. This can cause localized inflammation of the heart muscle or surrounding sac.
Mitochondrial Involvement: Secondary. The primary driver is autoimmune-mediated tissue inflammation (myocarditis/pericarditis). However, because cardiac myocytes depend heavily on mitochondria for energy, the resulting local inflammatory stress and altered calcium handling can subsequently induce secondary mitochondrial stress and energetic "brownouts."
Brain (Central Nervous System)
Primary Mechanism: Ion Channel Dysregulation (Signaling Mimicry).
How it is affected: Anti-spike antibodies can cross-react with the ⁠EPLDVL⁠ motif on the human UNC-80 protein, a core component of the NALCN leak sodium channel complex. This channel controls baseline electrical excitability in neurons, and its disruption can alter neurological signaling.
Mitochondrial Involvement: Indirect/Secondary. The primary mechanism disrupts the electrical firing thresholds of neurons. If severe enough, chronic neurological cellular stress or altered calcium influx through dysfunctional channels can overburden the neuron’s mitochondria, leading to localized metabolic strain.
Kidneys and Vascular System
Primary Mechanism: Receptor Blockade & Idiotypic Networks (Conformational Mimicry).
How it is affected: Anti-idiotypic antibodies (antibodies formed against the anti-spike antibodies) can mirror the shape of the spike protein itself, binding to and dysregulating ACE2 receptors. ACE2 is highly expressed on the vascular endothelium (blood vessel linings) and the tubular epithelial cells of the kidneys. Blocking or downregulating ACE2 disrupts the renin-angiotensin-aldosterone system (RAAS), promoting local vasoconstriction, fluid retention, and microvascular inflammation.
Mitochondrial Involvement: Indirect. The primary breakdown happens at the cell surface receptor level. However, the kidneys are among the most mitochondria-dense organs in the body; when ACE2 dysregulation triggers localized vascular hypoxia (low oxygen) and inflammatory cytokine cascades, the renal tubule mitochondria suffer downstream oxidative damage, impairing cellular bioenergetics.
Blood (HematOLOGIC System)
Primary Mechanism: Autoantibody Destruction (Hormonal Mimicry).
How it is affected: The ⁠TQLPP⁠ motif mimics human thrombopoietin (TPO), the primary hormone driving platelet production. Cross-reactive antibodies can bind native TPO or its signaling pathways, occasionally resulting in temporary platelet drops (thrombocytopenia).
Mitochondrial Involvement: Little to none. This is an extracellular, antibody-mediated clearance or inhibition mechanism that bypasses cellular metabolic machinery.

In mRNA vaccines like the Pfizer-BioNTech (BNT162b2) vaccine, the specific component identified as the source of unexpected molecular mimicry is the SARS-CoV-2 Spike (S) Glycoprotein (Arévalo-Cortés et al., 2024; Kanduc & Shoenfeld, 2020).
Because the vaccine works by introducing mRNA that instructs host cells to express the full-length spike protein to trigger a protective immune response, any structural or sequential overlapping between the spike and native human proteins can inadvertently cause the immune system to create cross-reactive autoantibodies (Mizuno et al., 2024; Safary et al., 2023).
Immunoinformatic and biochemical screens have mapped unexpected peptide commonalities (such as 5-mer to 7-mer amino acid sequences) shared between the viral spike protein and critical human tissues (Kanduc & Shoenfeld, 2020; Mizuno et al., 2024; Nunez-Castilla et al., 2021). When the immune system creates antibodies against these specific spike motifs, those antibodies can misidentify and target human structures, potentially triggering transient autoimmune responses (Arévalo-Cortés et al., 2024; Nunez-Castilla et al., 2021).
Observed Cross-Reactive Connections
The following diagrammatic list maps the specific regions (motifs) within the vaccine-expressed Spike protein to the human target structures, using both their common names and specific scientific names.
Affected Structures and Clinical Implications
1. Thrombopoietin
Peptide Motif: ⁠TQLPP⁠ (Nunez-Castilla et al., 2021).
Common Name: Thrombopoietin (TPO).
Specific Structural Name: Human Thrombopoietin Glycoprotein.
Mechanism: The ⁠TQLPP⁠ motif in the spike protein shares highly similar antibody-binding properties with human TPO (Nunez-Castilla et al., 2021). Cross-reactive antibodies generated by the vaccine may target native TPO, which is the primary hormone regulating platelet production in bone marrow, potentially contributing to rare cases of thrombocytopenia (low platelet counts) (Nunez-Castilla et al., 2021).
2. Protein Kinase G 1
Peptide Motif: ⁠ELDKY⁠ (Nunez-Castilla et al., 2021).
Common Name: PRKG1.
Specific Structural Name: cGMP-dependent protein kinase 1.
Mechanism: The ⁠ELDKY⁠ motif is embedded in both the viral spike and several human regulatory proteins (Nunez-Castilla et al., 2021). PRKG1 is essential for smooth muscle relaxation, calcium regulation, and platelet activation inhibition. Autoantibody cross-reactivity here is studied in connection with rare blood-clotting or vascular tone anomalies (Nunez-Castilla et al., 2021).
3. Tropomyosin
Peptide Motif: ⁠ELDKY⁠ (Nunez-Castilla et al., 2021).
Common Name: Tropomyosin.
Specific Structural Name: Striated Muscle Alpha-Tropomyosin Chain.
Mechanism: This structural protein is highly concentrated in cardiac and skeletal muscle tissue. Molecular mimicry between the spike protein and tropomyosin is one of several hypothesized pathways being investigated regarding rare post-vaccine cardiovascular events like myocarditis or pericarditis in susceptible individuals (Bozkurt et al., 2021; Fanti, 2026; Nunez-Castilla et al., 2021).
4. UNC-80 Homolog
Peptide Motif: ⁠EPLDVL⁠ (Mizuno et al., 2024).
Common Name: UNC-80 Protein.
Specific Structural Name: Unc-80 Homolog (NALCN Channel Complex Subunit).
Mechanism: In vitro testing has shown that antibodies raised against specific constituent sequences of the spike protein possess high cross-reactive affinity to the ⁠EPLDVL⁠ peptide sequence inside the human UNC-80 protein (Mizuno et al., 2024). UNC-80 acts as a core component of the leak sodium channel complex, which controls baseline electrical excitability in the central nervous system.
5. Angiotensin-Converting Enzyme 2
Peptide Motif: Structural/Conformational Binding Region.
Common Name: ACE2 Receptor.
Specific Structural Name: Angiotensin-Converting Enzyme 2 (Cell Surface Receptor).
Mechanism: Beyond short linear sequences, the overall shape of the spike protein interacts intimately with the ACE2 receptor to facilitate cellular instruction (Devaux & Camoin-Jau, 2023; Mizuno et al., 2024). The presentation of this massive structural block can cause anti-idiotypic networks (antibodies created against the primary antibodies) to mimic the shape of the spike itself, leading to a transient block or dysregulation of native ACE2 pathways and altering local vascular balance (Devaux & Camoin-Jau, 2023; Guo et al., 2023).
References
Arévalo-Cortés, A., Rodriguez-Pinto, D., & Aguilar-Ayala, L. (2024). Evidence for molecular mimicry between SARS-CoV-2 and human antigens: Implications for autoimmunity in COVID-19. Autoimmune Diseases, 2024, Article 8359683. https://doi.org/10.1155/2024/8359683
Cited by: 28
Balbona, E. J., Neuenschwander, J., Margulis, J., & Seneff, S. (2024). Potential association of Covid-19 mRNA vaccination and infections with the antiphospholipid antibody syndrome. Medical Research Archives, 12(11). https://doi.org/10.18103/mra.v12i11.6049
Cited by: 0
Bozkurt, B., Kamat, I., & Hotez, P. J. (2021). Myocarditis with COVID-19 mRNA vaccines. Circulation, 144(6), 471-484. https://doi.org/10.1161/circulationaha.121.056135
Cited by: 1054
Devaux, C. A., & Camoin-Jau, L. (2023). Molecular mimicry of the viral spike in the SARS-CoV-2 vaccine possibly triggers transient dysregulation of ACE2, leading to vascular and coagulation dysfunction similar to SARS-CoV-2 infection. Viruses, 15(5), 1045. https://doi.org/10.3390/v15051045
Cited by: 39
Fanti, S. (2026). Combined adaptive immune mechanisms mediate cardiac injury after COVID-19 vaccination. Circulation. https://doi.org/10.1161/CIRCULATIONAHA.125.074644
Cited by: 7
Guo, M., Liu, X., & Chen, X. (2023). Insights into new-onset autoimmune diseases after COVID-19 vaccination. Autoimmunity Reviews, 22(7), 103340. https://doi.org/10.1016/j.autrev.2023.103340
Cited by: 127
Kanduc, D., & Shoenfeld, Y. (2020). Molecular mimicry between SARS-CoV-2 spike glycoprotein and mammalian proteomes: Implications for the vaccine. Immunologic Research, 68(5), 310-313. https://doi.org/10.1007/s12026-020-09152-6
Cited by: 339
Karami Fath, M., Jahangiri, A., Ganji, M., Sefid, F., Payandeh, Z., Hashemi, Z. S., Pourzardosht, N., Hessami, A., Mard-Soltani, M., Zakeri, A., Rahbar, M. R., & Khalili, S. (2021). SARS-CoV-2 proteome harbors peptides which are able to trigger autoimmunity responses: Implications for infection, vaccination, and population coverage. Frontiers in Immunology, 12, Article 705772. https://doi.org/10.3389/fimmu.2021.705772
Cited by: 44
Mizuno, Y., Nakasone, W., Nakamura, M., & Otaki, J. M. (2024). In silico and in vitro evaluation of the molecular mimicry of the SARS-CoV-2 spike protein by common short constituent sequences (cSCSs) in the human proteome: Toward safer epitope design for vaccine development. Vaccines, 12(5), 539. https://doi.org/10.3390/vaccines12050539
Cited by: 9
Nunez-Castilla, J., Stebliankin, V., Baral, P., Balbin, C. A., Sobhan, M., Cickovski, T., Mondal, A. M., Narasimhan, G., Chapagain, P., Mathee, K., & Siltberg-Liberles, J. (2021). Potential autoimmunity resulting from molecular mimicry between SARS-CoV-2 Spike and human proteins. bioRxiv. https://doi.org/10.1101/2021.08.10.455737
Cited by: 115
Safary, A., Akbarzadeh-Khiavi, M., Barar, J., & Omidi, Y. (2023). SARS-CoV-2 vaccine-triggered autoimmunity: Molecular mimicry and/or bystander activation of the immune system. BioImpacts, 13(4), 269-273. https://doi.org/10.34172/bi.2023.27494
Cited by: 16

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