Kittisak Meepoon Fact checked by:Thailand Medical News Team Dec 02, 2025 3 months, 4 days, 11 hours, 39 minutes ago
Medical News: Growing Evidence That COVID 19 Can Directly Cause Pain
A new study by Brazilian scientists from the Federal University of Alfenas, the Federal University of Ouro Preto, the Federal University of Minas Gerais, Unesp Institute of Chemistry Araraquara Campus, Brasil University Descalvado, the Federal University of Northern Tocantins and the Insect Molecular Biology Laboratory of the Federal University of Alfenas reveals that tiny fragments from the SARS-CoV-2 spike protein can directly activate pain pathways in the spinal cord. This
Medical News report highlights disturbing findings showing that even isolated spike peptides can stimulate pain receptors and immune cells inside the central nervous system, helping explain why millions of people with COVID-19 and Long COVID continue to suffer unexplained body aches nerve pain and persistent discomfort.
Study shows SARS-CoV-2 spike fragments can directly activate spinal pain pathways
How Spike Protein Pieces Trigger Pain Signals
Researchers tested three synthetic spike protein fragments called PSPD2001 PSPD2002 and PSPD2003 by injecting them into the spinal canal of laboratory mice. All three peptides reduced the mechanical pain threshold within one to seven hours indicating a strong pain inducing effect. The team then discovered that these spike fragments activate a key immune receptor known as TLR4 which sits on cells inside the spinal cord. When mice were pretreated with a TLR4 blocking compound the pain response disappeared completely. Even more striking TLR4 knockout mice showed no pain reaction at all confirming that this receptor is essential for the spike peptide pain mechanism.
Microglial Cells and Inflammatory Molecules Intensify Pain
The study found that spinal microglia immune cells of the central nervous system rapidly activated after exposure to the spike fragment PSPD2003. These activated microglia then produced inflammatory molecules including TNF alpha and IL 6 both known to amplify pain sensations. Imaging studies showed a sharp increase in microglial markers while molecular tests confirmed that PSPD2003 significantly increased TLR4 gene expression. The findings also revealed that two major inflammatory signaling routes the p38 MAPK pathway and NF kappaB pathway are switched on by the spike peptide further enhancing the pain response.
What The Findings Mean for COVID-19 and Long COVID
These results offer a clear biological explanation for why so many people infected with the virus report severe muscle pain headaches nerve discomfort and lingering pain syndromes even after the acute infection ends. The research strongly suggests that fragments of the spike protein can directly interact with the spine activate immune cells and unleash inflammatory pain pathways. This insight could help guide future treatments aimed at blocking TLR4 related inflammation and may lead to therapies that reduce long term COVID related pain. The conclusions also reinforce that the effects of SARS-CoV-2 extend far beyond the lungs as the virus and its protein fragments can influence sensitive neurological systems linked to chron
ic pain persistence.
The study findings were published on a preprint server and are currently being peer reviewed.
https://www.biorxiv.org/content/10.1101/2025.12.01.691535v1
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Read Also:
https://www.thailandmedical.news/articles/coronavirus
https://www.thailandmedical.news/articles/long-covid
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