Nikhil Prasad Fact checked by:Thailand Medical News Team Mar 13, 2025 5 hours, 41 minutes ago
Medical News: A new study has uncovered how COVID-19 can directly harm the nervous system, shedding light on why some patients experience persistent neurological symptoms. Researchers from The University of Hong Kong and Western University of Health Sciences in the United States have found that the SARS-CoV-2 virus can infect sensory nerve cells, triggering a destructive process known as axonal degeneration. This process is driven by the activation of a protein called transient receptor potential vanilloid 1 (TRPV1), which plays a key role in nerve function and pain sensation.
COVID-19 is Damaging Nerve Cells Via TRPV1 Activation
This
Medical News report delves into the study’s findings, highlighting the ways in which COVID-19 affects sensory neurons and discussing potential treatments that could help prevent long-term neurological complications.
How COVID-19 Infects Sensory Neurons
The study focused on peripheral sensory neurons, which are responsible for transmitting signals such as pain, temperature, and touch from the body to the brain. Using advanced stem cell technology, the researchers generated these neurons from human-induced pluripotent stem cells (iPSCs) and exposed them to the Omicron BA.5 variant of SARS-CoV-2.
Their findings revealed that the virus upregulated the expression of the angiotensin-converting enzyme 2 (ACE2) receptor in these neurons, making them more susceptible to infection. Once inside the neurons, the virus caused an increase in TRPV1 expression, leading to a cascade of harmful events. TRPV1, which is normally involved in pain perception and temperature regulation, became overactive, resulting in axonal degeneration - where nerve fibers break down and lose their ability to function properly.
TRPV1 Activation and Its Devastating Effects
The researchers used single-nucleus RNA sequencing to analyze the genetic response of neurons to the virus. They discovered that exposure to SARS-CoV-2 led to increased activity in pathways involved in inflammation, virus receptor activity, and axonal damage. The virus not only infected sensory neurons directly but also promoted the movement of TRPV1 from the nucleus to the cytoplasm, where it contributed to nerve damage.
A particularly alarming finding was that even neurons that were not directly infected by the virus still suffered damage due to increased TRPV1 activity. This suggests that the virus can indirectly harm surrounding nerve cells, potentially explaining the widespread neurological symptoms observed in COVID-19 patients, such as loss of smell, chronic pain, and cognitive dysfunction.
A Potential Treatment: Blocking TRPV1
One of the most promising aspects of the study was the discovery that blocking TRPV1 activation could protect nerve cells from damage. The researchers tested a TRPV1 inhibitor called capsazepine, which significantly reduced axonal degeneration in infected neurons. This suggests that drugs targeting TRPV1 could be used as a potential treatment to prevent long-term nerve damage in COVID-19 pat
ients.
Additionally, the study explored the effects of a mutated version of the virus with a deletion in its spike protein. This weakened strain showed reduced ability to activate TRPV1 and caused less nerve damage compared to the fully intact Omicron BA.5 variant. These findings highlight the role of TRPV1 in COVID-19-related nerve damage and suggest that targeting this protein could be a viable therapeutic strategy.
The Broader Implications
This research provides valuable insights into the neurological effects of COVID-19 and offers hope for new treatments. Neurological symptoms are among the most commonly reported complications of both acute COVID-19 and long COVID, affecting millions of people worldwide. Understanding how the virus interacts with sensory neurons could lead to better treatments for conditions such as post-viral neuropathy and persistent pain syndromes.
The study also raises important questions about the role of TRPV1 in other viral infections. Previous research has shown that respiratory viruses such as the flu and RSV can also activate TRPV1, suggesting that this pathway may be a common target for viral-induced nerve damage. Further research is needed to explore whether TRPV1 inhibitors could be used more broadly to treat nerve damage caused by different viruses.
Conclusion
The findings from this study provide strong evidence that SARS-CoV-2 can directly infect sensory neurons and trigger nerve damage through TRPV1 activation. This process contributes to the neurological symptoms seen in many COVID-19 patients, including chronic pain, loss of smell, and cognitive issues. The discovery that blocking TRPV1 can prevent nerve damage offers a promising new avenue for treatment, potentially helping to mitigate the long-term effects of COVID-19. Future research will be essential to develop targeted therapies that can protect the nervous system from viral infections and prevent long-term neurological complications.
The study findings were published on a preprint server and are currently being peer reviewed.
https://www.biorxiv.org/content/10.1101/2025.03.06.641885v1
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