A NEW study has claimed that the novel coronavirus “hijacks our body’s cells”, with one shocked scientist saying he’s seen nothing like this in 20 years of studying viral infections.
The study suggests the virus works by blocking certain genes that fight against infections. Viruses, such as the flu, usually interfere with two sets of genes: one that prevents viruses from replicating and the other that sends immune cells to the infection site to kill viruses. However, researchers found coronavirus behaves differently.
The coronavirus is said to work by inhibiting the genes that stop the virus from copying itself but allowing the genes that call for immune cells to behave normally.
This causes the virus to multiply and an overproduction of immune cells to flood the lungs and other organs, which leads to unmitigated inflammation.
The team, from the Icahn School of Medicine at Mount Sinai in New York City, have even suggested a treatment method based on the findings.
They say treatment for patients in the early stages of the disease should be focused on restoring the pathway being blocked by coronavirus rather than focusing on inflammation.
Dr Benjamin tenOever, a virologist and professor of microbiology at the Icahn School of Medicine, told The Daily Mail that an infected cell has “two jobs to do”.
“One job is to tell all the cells around you to fortify…and the second job is to recruit the more professional immune cells to that site of infection,” he said.
Typically, our body’s cells have two groups of virus-fighting genes: interferons and chemokines.
Interferons are signalling proteins released by infected cells that “interfere” with the virus’s ability to multiply itself.
Chemokines are small molecules that call for immune cells to go the site of an infection so they can target and destroy the virus.
According to tenOever, the first set of genes control virus replication for about seven to 10 days.
This means the second set has enough time to get immune cells to attack.
He refers to interferons as the “call-to-arms” genes and to chemokines as the “call-for-reinforcement” genes.
“The vast majority of viruses that you encounter in nature are readily neutralised and destroyed by these systems,’ tenOever said.
“Even the very first defence, the ‘call-to-arms,’ is often enough to completely stop replication and neutralise the infection without even generating the second response.”
But, unlike the flu or Severe Acute Respiratory Syndrome (SARS), the coronavirus blocks one set of genes and activates the other.
For the study, published in the journal Cell, the team looked at healthy human lung cells and an animal model in ferrets.
They found a very mild response from the ‘call-to-arms’ genes – which block the virus’s replication – and a large introduction of the ‘call-for-reinforcement’ genes.
“A combination of these two is a bad combination,” said tenOever.
When they looked at lung cells from two COVID-19 patients that died, they found the exact same response.
“Basically people are contracting the disease, SARS-CoV-2 enters the lungs and it begins to replicate and, at that site of replication, those cells that are infected, they don’t do a good job of spreading the word about their infection which allows it to essentially fester in the lungs,” tenOever said.
“That virus has continued to replicate and continue to spread, getting to higher and higher numbers in the lungs, but they’re calling for reinforcements.”
Now, the lungs have immune cells are attacking each other, meaning the immune system is turning against itself.
This is likely what leads to cytokine storms, which occur when the body attacks its own cells and tissues instead of just fighting off the virus.
TenOever says the way this virus behaves is “nothing like I’ve seen in 20 years” of studying how cells respond to viral infections.
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