COVID-19 Spike Protein Mimicry Turns 9 Key Human Proteins into Autoimmune Targets
Nikhil Prasad Fact checked by:Thailand Medical News Team Sep 11, 2025 4 hours, 19 minutes ago
Medical News: How the Virus Tricks the Immune System
Researchers from the SB RAS Institute of Chemical Biology and Fundamental Medicine in Novosibirsk, Russia, the SRF “SKIF” in Koltsovo, Russia, and the Department of Natural Sciences at Novosibirsk State University have discovered that the SARS-CoV-2 spike protein carries dangerous similarities to human proteins. When the body launches an immune response against the virus, it may also attack these human proteins by mistake. This
Medical News report highlights that this form of molecular mimicry could explain why COVID-19 and long COVID are often linked to serious autoimmune diseases.
COVID-19 Spike Protein Mimicry Turns 9 Key Human into Autoimmune Targets
The 9 Key Proteins and Their Impact
The study identified nine human proteins—DAAM2, CHL1, HAVR2/TIM3, FSTL1, FHOD3, MYO18A, EMILIN3, LAMP1, and αENaC—that share sequences with the coronavirus spike. Each of these proteins plays a vital role in the body, and damage to them could have serious effects:
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DAAM2 and CHL1 – Both are linked to the nervous system. Autoantibodies against them could contribute to brain fog, memory loss, and neurological problems seen in long COVID.
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HAVR2/TIM3 – An immune checkpoint protein. If targeted, it may disrupt immune balance, increasing risks of autoimmune disorders and chronic inflammation.
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FSTL1 – Involved in cell growth and immune regulation. Attacks on this protein could worsen tissue damage and immune dysregulation.
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FHOD3 – Found in heart muscle. Autoimmunity here may lead to myocarditis, heart rhythm problems, or long-term heart damage.
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MYO18A – Important in immune cell regulation. Antibodies against it could fuel inflammation and weaken immune tolerance.
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EMILIN3 – Linked to connective tissue and TGF-β signaling. Problems with this protein may explain muscle weakness and exercise intolerance in long COVID.
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LAMP1 – Crucial for lysosome function and antigen processing. If attacked, viral clearance could be disrupted, and immune system errors might increase.
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αENaC – A sodium channel important for lung fluid balance and taste perception. Attacking this protein may cause breathing problems, swelling in the lungs, and loss of taste or smell.
The Role of Genetic Factors
The researchers also found that certain immune gene variants, known as HLA class II alleles, make some people more prone to this cross-reactivity. For example, HLA-DRB104:01 and HLA-DRB115:01 were highlighted as increasing susceptibility to autoimmune responses. This genetic factor may explain why some individuals develop severe autoimmune conditions
after COVID while others do not.
Why This Matters
The findings suggest that COVID-19 is not only a respiratory disease but also a possible trigger for long-term autoimmune problems. By hijacking these 9 key proteins, the virus may spark conditions ranging from neurological impairment to cardiovascular issues, chronic fatigue, and loss of immune tolerance. The research also warns that vaccine designs must carefully avoid viral fragments that resemble human proteins to reduce autoimmune risks.
Final Thoughts
This study provides strong computational evidence that SARS-CoV-2 may set off autoimmunity by imitating 9 key proteins essential to human health. The work helps explain why so many COVID survivors experience lingering and varied symptoms. While more experimental confirmation is needed, the findings open new doors for understanding long COVID and developing safer treatments.
The study findings were published in the peer reviewed International Journal of Molecular Sciences.
https://www.mdpi.com/1422-0067/26/18/8793
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Read Also:
https://www.thailandmedical.news/news/list-of-86-of-167-autoantibodies-that-covid-19-infections-and-vaccines-induces-in-the-human-host-part1
https://www.thailandmedical.news/news/mysterious-autoantibodies-behind-long-covid-symptoms-identified
https://www.thailandmedical.news/news/covid-19-induced-anti-ganglioside-autoantibodies-is-causing-neuropathy-in-many
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