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Why can people infected with SARS-CoV-2 spread the disease without knowing they are infected? Pharmacology professor Rajesh Khanna and his team at the University of Arizona found that one possible reason is that the coronavirus can alleviate or block the sensation of pain. These findings have not been reviewed and require confirmation in clinical trials. But what are the consequences of these suspicions?

  1. Research by Rajesh Khanna and his team (not yet reviewed) indicates a new possible way the coronavirus infects cells, which affects our nervous system
  2. The pharmacologist and his team studied the protein neuropilin-1 and its relationship to pain sensation. It has been established that when combined with another protein – VEGF-A (called vascular endothelial growth factor), it can trigger pain signals
  3. In people infected with SARS-CoV-2, the activity of neuropilin-1 is higher than in healthy people. Despite this, COVID-19 patients did not experience increased pain
  4. Rajesh Khanna: In vitro studies using nerve cells have shown that when coronavirus spikes bind to neuropilin-1, the excitability of pain neurons is suppressed. This suggests that in a living organism we would be dealing with pain relief
  5. You can find more up-to-date information on the TvoiLokony home page

«Imagine you have contracted a deadly virus that makes you immune to pain. By the time you know you’re infected, it’s too late – you have spread the virus in the environment »- this is how Rajesh Khanna begins his article on the link between pain and SARS-CoV-2, which appeared in The Conversation – reprinted by sciencealert ( the full description of the study is to be published in the peer-reviewed medical monthly Pain).

“Recent findings in my lab suggest that this scenario may be one of the reasons why people infected with SARS-CoV-2 may spread the disease without knowing it,” explains the scientist from the University of Arizona.

Research by his team (not yet reviewed) indicates a new way the coronavirus infects cells, which affects our nervous system. What is it actually about? Let’s start from the beginning.

How does the coronavirus attack our cells? Scientists have discovered a new possible way

Most of the scientific work to date has investigated or based on the mechanism of SARS-CoV-2 entry into cells using ACE-2 proteins (receptors that allow the coronavirus to enter the cell interior). How is it done?

Scientists at the Oak Ridge National Laboratory in Tennessee have found that the virus infects humans through ACE-2 receptors in the nose. Then it penetrates deep into the body, attacking cells in places with the same receptors. This mode of action of the virus explains the heart and kidney damage and abdominal pain observed in many patients. Because it is in the intestines, kidneys and heart that ACE-2 receptors are found.

  1. The coronavirus affects not only the lungs. It affects all organs

Once the coronavirus enters cells, it causes the body to produce more ACE-2 receptors in places where they are normally present in small amounts, such as in the lungs. This process opens the door to infection, allowing it to multiply rapidly and send an army of pathogens to infect other organs.

  1. More in the article “How does the coronavirus attack the body and” opens the door to infection? “

Researchers led by Rajesh Khann found that cells could possibly be infected in other ways as well.

Coronavirus relieves pain?

Rajesha Khanna studies how proteins in cells trigger pain signals that are then passed on to the brain.

“When these proteins are active, nerve cells” talk to each other, “the scientist explains. “When dealing with chronic pain, this conversation is deafening,” she adds. By studying changes in the excitability of nerve cells and their causes, it is possible to discover the sources of chronic pain and develop ways to control it (Dr. Khanna’s laboratory is working on alternative pain treatments).

But what does this have to do with COVID-19? It all started with two versions of scientific reports that appeared on BioRxiv – this is a publicly accessible repository of preprints (i.e., preliminary versions of scientific publications) for the life sciences. These works suggested that the SARS-CoV-2 spikes that make up the characteristic crown bind to a protein called neuropilin-1 (remember that thanks to these “spikes”, the virus recognizes receptors on the surface of the host cell and by binding to them, it penetrates into its interior).

The pharmacologist and his team have been studying the neuropilin-1 protein and its relationship to pain sensation over the past year. It has been established that in combination with another protein – VEGF-A (called vascular endothelial growth factor), it can trigger pain signals. These are transmitted through the spinal cord to the higher centers of the brain, causing a sensation of pain.

  1. How does COVID-19 damage the brain?

It has also been established that in people infected with SARS-CoV-2, the activity of neuropilin-1 is higher than in healthy people. Despite this, COVID-19 patients did not experience increased pain.

– In vitro studies carried out in my laboratory using nerve cells, we have shown that when coronavirus spikes bind to neuropilin-1, the excitability of pain neurons is suppressed, which leads to a reduction in pain sensitivity. This suggests that in a living organism we would be dealing with pain relief.

What are the conclusions of this? According to the pharmacologist, scientists are facing two pathways: blocking neuropilin-1 to limit the entry of SARS-CoV-2 into cells, and blocking neuropilin-1 to block pain.

If the discovery that the novel coronavirus attacks cells via a pain-related protein is confirmed in humans, it could give rise to new drugs to fight COVID-19, says Rajesh Khanna.

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  1. Surprising Discovery: Stroke May Be the First Sign of COVID-19. With whom?
  2. Have we treated COVID-19 poorly so far? British scientists recommend an individual approach to each case
  3. Virologist: We have a second or even third wave of coronavirus infections

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