IS THIS the reason Delta is so contagious? Researchers find little known mutation on part of the Covid variant

A mutation on the Delta variant flown under the radar may explain why it is more than twice as contagious as previous strains.

Researchers tracking the Covid mutant have so far focused their attention on changes in the virus’ tip protein, which it uses to infect cells.

It was believed that these changes made it easier for Delta to spread between humans and more difficult for their immune systems to recognize and defend against.

Now, researchers believe that a conspicuous mutation that alters the structural body of the virus may have played a key role in making the strain world-dominant.

Their study found that R203M – which is unique to Delta – allows the virus to inject up to 10 times more of its genetic code into host cells than older versions of the virus.

When Covid enters the body, it programs healthy cells to release more viral particles, which in turn infect more cells and thus help it multiply.

Experts told MailOnline that the breakthrough may explain why people infected with Delta have a much higher viral load than those with earlier versions of the virus.

IS THIS the reason Delta is so contagious?  Researchers find little known mutation on part of the Covid variant

Researchers tracking the Covid mutant have so far focused their attention on changes in the virus’ tip protein, which it uses to infect cells. Now, researchers believe that an inconspicuous mutation that alters the virus’ N-protein may have played a key role in making the strain world-dominant.

In the latest study, researchers at the University of California adjusted a fake version of the original Covid virus to include the R203M mutation.

They then monitored how the modified strain interacted with lung cells in a laboratory and compared it to the original virus.

The team – led by Nobel Prize winner Professor Jennifer Doudna – was ‘surprised’ to find R203M deposited 10 times more mRNA than the older virus.

Patients with mutant Covid variant ‘have a viral load 300 times higher than those with original virus’

Humans infected with the Delta Covid variant have a viral load 300 times higher than those with the original version of the virus, a South Korean study has found.

The viral load – the amount of virus in a person’s blood – is highest in Delta patients when they first start showing symptoms.

However, it gradually drops to levels on a par with other variants 10 days after the peak of infection, according to the Korea Disease Control and Prevention Agency.

The researchers stressed that this “does not mean that Delta is 300 times more contagious” than the virus that emerged in Wuhan in 2019.

A higher amount of virus increases the chance of an infected person transmitting it to others.

The Delta variant, first identified in India, is behind almost every Covid infection in the UK and has become the world-dominant strain.

To bolster their results, they then constructed a real coronavirus to include R203M, which they said made it 51 times more contagious than the original virus.

Professor Lawrence Young, who was not involved in the study, said it confirmed a growing suspicion that there was more to Delta’s virulence than peak mutations.

The virologist from Warwick University told MailOnline that while peak protein changes help unlock cells, ‘R203M enhances the fusion process, whereby it enters them’.

R203M modifies Covid’s nucleocapsid (N), a protein envelope that surrounds its genetic information or genome, and is hidden away inside the virus.

The N protein plays a key role in stabilizing and releasing the genetic material of the virus as it enters the body.

Professor Lawrence told MailOnline that the process was ‘a bit like packing candy’.

‘I would describe the effect of the Delta N protein as an enhancement of the process by which the virus genome is wrapped in virus particles.

‘This increases the efficiency of virus replication – this results in more viruses being produced and transmitted.’

It is different from the nail protein, which protrudes from the surface and binds to cells.

Dr. Simon Clarke, a microbiologist at Reading University who was not involved in the research, described the result as ‘really interesting’.

“When the virus infects cells, it must get all of its genetic material into the cell, even 99 percent is not enough.

Think of it as getting the drawings for a car, but lacking key components that would make the car run.

‘R203M seems to make this process more efficient and faster in Delta.’

Dr. Clarke said that although R203M was ‘definitely important’, mutations in the nail protein still played a key role in Delta’s increased infectivity.

He said this was clear because vaccines – which target the nail protein – were made less effective against the variant.

‘I do not see how it [R203M] could explain less sensitivity of vaccines, so it tells us that we need to look at other things as well as the tip protein. ‘

The study, published in the journal Science, also looked at other variants that have changes in their N-proteins, and found that they were also better at infecting cells.

The alpha or Kent variant deposited seven and a half times more genetic code than the original virus, while that for Gamma, formally the Brazilian variant, was 4.2 times.

Professor Lawrence urged vaccine manufacturers to take the results into account while developing the next generation of Covid jabs.

He said: “It underscores the need to consider the use of second-generation vaccines that contain the N protein along with the tip and perhaps other viral proteins.”

‘It has always been clear that other changes in virus variants would contribute to increased’ virus fitness’.

“But these have been under-explored because of the disproportionate focus on spike because it is the current main vaccine target.”

Dr. Clarke said it was also ‘conceivable’ that an antiviral drug could also be designed to target the location of the mutation.

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