How does the coronavirus “open the gates” to infection? Scientists have discovered the “second key”

It has been 17 years since the SARS-CoV coronavirus threatened an outbreak of a global pandemic. Then the worst was avoided. This time we were not so lucky. What makes SARS-CoV-2 so much more contagious than its predecessor? Scientists have just discovered the second “key” through which it enters the cells of our body. It was described in the scientific journal Science, and the article also appeared on sciencealert.com.

1. The first “key” to open the door to our cells by the coronavirus is a receptor called ACE2
2. The second “key” that SARS-CoV-2 uses is the neuropilin-1 protein – it is “abundant” in the nerve tissues of the nasal cavity
3. Scientists: If You Think of ACE2 as a Door Lock, Neuropilin-1 Could Be a Virus Directing to Your Door
4. Many imagine that the discovery could be the starting point for the development of new antiviral drugs based on blocking cell receptors
5. For more up-to-date information on the coronavirus epidemic, visit the TvoiLokony home page

SARS-CoV-2 is a very contagious pathogen (although “it is far from infectious to viruses that have long been known to mankind, such as the measles or chicken pox viruses” – after patient.gov.pl). As Science points out, the related SARS-CoV, which caused the epidemic in 2002-2003 (mainly in Asia), resulted in significantly fewer victims – in 2002 and 2003 more than 8 people fell ill with SARS, 096 of them died. Responsible for the current pandemic, SARS-CoV-774 has already infected more than 2 million people, over 42 million have lost their lives.

1. Coverage of the COVID-19 coronavirus [MAP]

What makes it easier for the coronavirus to enter our cells? The first «key»

Scientists from the Technical University of Munich (Germany) and the University of Helsinki (Finland) have discovered another ‘key’. It is the protein neuropilin-1 – a receptor active in neurons that gives the new coronavirus an advantage in infecting our tissues.

Recall that the first is a receptor called angiotensin converting enzyme 2 (ACE2). Recently, scientists at the Oak Ridge National Laboratory in Tennessee found that it helps the coronavirus to bind to the surface of cells (while an enzyme called serine transmembrane protease type II / TMPRSS2 opens the ‘door’ to the cell). Subsequently, the coronavirus penetrates deep into the body, attacking cells in places with the same receptors. This mode of action of the virus explains the damage observed in many patients, including heart or kidneys – these are where ACE-2 receptors are found.

After entering cells, the coronavirus has been found to stimulate the body to produce more ACE-2 receptors in places where they are normally present in small amounts, e.g. in the lungs. This process opens the door to infection, allowing it to multiply rapidly and send an army of pathogens to infect other bodies.

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How SARS-CoV-2 opens the door of infection. A new discovery – the second “key”

The second “key” that SARS-CoV-2 uses to infect our cells, the already mentioned neuropilin-1 receptor, is “abundant” in the nerve tissues of the nasal cavity. Typically, this protein plays a role in the formation of new capillaries. It turns out, however, that it can also help the coronavirus to bind to the surface of our cells.

“ The starting point of our study was the question of why SARS-CoV, the coronavirus that led to a much smaller epidemic in 2003, and SARS-CoV-2 are different in terms of infectivity, even though they use the same major receptor – ACE2, ” said the recipient participation in the study by Ravi Ojha, virologist at the University of Helsinki.

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Scientists concluded that, compared to its older “relative”, SARS-CoV-2 has an additional tool to facilitate cell penetration. But what exactly was this mechanism?

After consulting with scientists from different countries, German and Finnish scientists focused on neuropilin-1. Electron microscopy of the surface spikes / projections covering SARS-CoV-2 indicated a possible association with this receptor. Let us remind you that the protrusions forming the characteristic “crown” of the virus condition the recognition of receptors on the surface of the host cell and the penetration of the virus into its interior.

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To confirm their assumptions, scientists used antibodies specially selected to block access to neuropilin-1. They have been tested on «pseudoviruses» containing SARS-CoV-2 proteins. As it turned out? The «pseudoviruses» found it much more difficult to get inside the cell when neuropilin-1 was blocked.

«Neuropilin-1 drives the virus to the door of our cell»

“If you think of ACE2 as a door lock to a cell, then neuropilin-1 could be a factor driving the virus to the door,” explains one of the scientists involved in the study, explaining the way SARS-CoV-2 enters cells.

Since neuropilin-1 is abundant in the nerve tissues of the nasal cavity, we can imagine such a situation: when an aerosol infected with SARS-CoV-2 gets into the nose, the coronavirus can comfortably walk on the red carpet, which will lead it directly to the interior of our cells – describe scholars.

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This discovery will help explain why SARS-CoV-2 infections can be destructive to brain function? According to scientists, it contributes to further research.

However, many already imagine that the findings described above could be the starting point for the development of new antiviral drugs based on blocking cell receptors. “Our laboratory is currently testing the action of new molecules that we have specifically designed to break the link between the virus and neuropilin,” says Giuseppe Balistreri, a virologist at the University of Helsinki. “The preliminary results are very promising,” he emphasizes.

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