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How coronavirus hijacks human cells and takes over our genes is turned on by our immune system

The new coronavirus ‘hijacks’ our body’s cells by blocking certain genes that fight infection, a new study suggests.

Viruses, such as the flu, usually interfere with two sets of genes: one that prevents viruses from multiplying and the other that sends immune cells to the site of infection to kill viruses.

But researchers found that SARS-CoV-2 behaves differently, inhibiting the genes that prevent the virus from copying itself, but causing the genes that immune cells need to behave normally.

This causes the virus to multiply and an overproduction of immune cells to flood the lungs and other organs, leading to irreversible inflammation.

The team at the Icahn School of Medicine at Mount Sinai in New York City says that treating patients in the early stages of the disease should focus on repairing the path blocked by the coronavirus rather than inflammation.

A new study found that coronavirus blocks interferons, genes that usually stop the virus from replicating, but allows other genes to go to the site of infection. Depicted: RNA (green) from coronavirus taking over an infected cell

A new study found that coronavirus blocks interferons, genes that normally stop the virus from replicating, but still allow other genes to go to the site of infection. Depicted: RNA (green) from coronavirus taking over an infected cell

This overproduction of immune cells leads to over-inflammation and causes dangerous cytokine storms, in which the body attacks its own tissues. Pictured: Nurse Katie Canina cares for a patient in ICU's Special Pathogens Unit at Brigham and Women's Hospital in Boston, Massachusetts, April 27

This overproduction of immune cells leads to over-inflammation and causes dangerous cytokine storms, in which the body attacks its own tissues. Pictured: Nurse Katie Canina cares for a patient in ICU's Special Pathogens Unit at Brigham and Women's Hospital in Boston, Massachusetts, April 27

This overproduction of immune cells leads to over-inflammation and causes dangerous cytokine storms, in which the body attacks its own tissues. Pictured: Nurse Katie Canina cares for a patient in ICU’s Special Pathogens Unit at Brigham and Women’s Hospital in Boston, Massachusetts, April 27

Dr. Benjamin tenOever, a virologist and microbiology professor at the Icahn School of Medicine, told DailyMail.com that an infected cell “has two jobs to do.”

“One task is to tell all the cells around you to strengthen … and the second task is to recruit the more professional immune cells to that site of infection,” he said.

Normally, our body’s cells have two groups of virus-fighting genes: interferons and chemokines.

Interferons are signaling proteins released by infected cells and are named for their ability to “disrupt” the virus’s ability to replicate itself.

Chemokines are small molecules that cause immune cells to go to the site of an infection so that they can attack and destroy the virus.

According to tenOever, the first set of genes controls virus replication for about seven to 10 days, so the second set has enough time to attack immune cells.

He calls interferons the ‘call-to-arms’ genes and chemokines the ‘call-for-amplification’ genes.

“The vast majority of viruses you encounter in nature are easily neutralized and destroyed by these systems,” said tenOever.

“Even the very first defense, the ‘call to arms’, is often enough to completely stop replication and neutralize the infection without even generating the second response.”

But unlike 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 Cellthe 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 replication of the virus – and a great introduction of the ‘call-for-amplification’ genes.

“A combination of the two is a bad combination,” said tenOever.

When they looked at lung cells from two COVID-19 patients who died, they found the exact same response.

‘In fact, people contract the disease, SARS-CoV-2 gets into the lungs and it starts to multiply and, at that site of replication, those cells that are infected cannot properly spread the word about their infection, causing it to can basically brood in the lungs, “said TenOever.

This means that the virus replicates because there aren’t many interferons, but those cells still require amplification.

So different types of immune system cells – neutrophils, macrophages and lymphocytes – arrive to get the job done, but by the time they arrive, there’s nothing controlling that virus.

“That virus has continued to multiply and spread, it is getting higher in the lungs, but they call for reinforcement,” said tenOever.

Now the lungs have immune cells like macrophages and neutrophils, which leads to inflammation that causes more inflammation. Essentially, the immune system turns against itself.

This likely leads to cytokine storms, which occur when the body attacks its own cells and tissues rather than just fighting the virus.

TenOever says the way this virus behaves is ‘nothing I’ve seen in 20 years’ of studying how cells respond to viral infections

TenOever says there are two ways to treat patients.

The first group consists of people who are just developing symptoms and have tested positive.

They can be given medicines that cause the missing call-to-arms genes so that the virus can act more like the flu.

“They can try treatments that restore the path blocked by the virus,” he said.

For those who are hospitalized and intubated it is already too late for this treatment, so they would benefit more from classes of drugs called interleukin-6 and interleukin-1 inhibitors.

These can help reduce cytokine storms and reduce inflammation throughout the body.

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