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On first inspection, mutations in the highly contagious delta covid variant don’t seem so worrying.
For starters, delta has fewer genetic changes than earlier versions of the coronavirus.
“When people saw that the epidemic in India was caused by the delta, they had no idea that it would be so bad or that it would overtake other variants,” said Trevor Bedford, evolutionary biologist at the Fred Hutchinson Cancer Research Center.
But those expectations were wrong.
Delta has retained some of the most successful mutations found in earlier variants, but also contains new genetic changes that allow it to spread twice as fast.
Delta is more dangerous in many ways. It has an incubation period of four days instead of six, which makes people contagious earlier. When the pandemic started, people spread the original coronavirus to an average of two or three people. Today, people infected with the delta infect an average of six people.
As of this week, the delta variant had caused at least 92% of new infections in the United States, according to covariants.org, a research company in Bern, Switzerland.
While the delta isn’t necessarily more deadly than the other variants, it can kill large numbers of people just because it infects a lot more, said Dr Eric Topol, founder and director of the Scripps Research Translational Institute.
Scientists have sequenced the delta mutations but are still trying to figure out their significance, said Angela Rasmussen, a virologist at the Vaccines and Infectious Diseases Organization at the University of Saskatchewan. “When we see the same mutations appear repeatedly and independently, it suggests that they are important,” Rasmussen said.
Scientists have the best understanding of mutations in the so-called spike protein – which protrudes from the surface of the virus like a bludgeon – and which have been studied most intensely because of its severe ramifications, Rasmussen said. The coronavirus uses the spike protein to enter human cells, and changes in the spike can help the virus escape antibodies.
Scientists believe that one of the most important areas of the peak is the receptor binding domain, the specific part of the protein that allows the virus to attach itself to a receptor on the surface of our cells, said Vaughn Cooper. , professor of microbiology and molecular biology. genetics at the University of Pittsburgh. Receptors are like sockets or docking stations that allow proteins to interact with the cell. Once the virus enters the cell, it can wreak havoc, hijacking the cell’s genetic machinery and turning it into a virus-making factory.
Disturbing mixture of Delta
The rapid spread of Delta is particularly surprising given that it lacks two mutations that made the earlier variants so frightening.
Delta lacks the peak N501Y mutation found in alpha, beta, and gamma variants, which allowed them to invade cells more successfully than the original virus. This mutation changed an amino acid – a building block of proteins – in the receptor binding domain.
Delta also doesn’t have the E484K mutation, which made the gamma variant so disturbing. This genetic change, sometimes called “Eek”, allows the virus to spread even among people who have been vaccinated.
(Scientists use the Greek alphabet to name the worrisome variants.)
“The ‘D’ in delta means ‘different’ and a ‘detour’ to a different genomic mutation path,” Topol said. “But that doesn’t mean ‘bad luck’,” he said, noting that existing covid vaccines remain primarily effective against the delta variant.
Vaccines protect people from covid by providing them with antibodies that attach to the spike protein, preventing the virus from entering cells. By drastically reducing the number of viruses that enter cells, vaccines can prevent people from developing serious illness and make them less infectious to others.
Delta shares mutations with other successful variants. Like all identified variants in circulation, delta contains a cutting edge mutation called D614G, sometimes known as “Doug,” which became ubiquitous last year.
Scientists believe that Doug increases the density of the spike protein on the surface of viral particles and makes it easier for the virus to enter cells.
Delta also has a spike mutation called P681R, which closely resembles a mutation in the alpha variant that appears to produce higher viral loads in patients, Cooper said. People infected with the delta have 1,000 times more virus in their airways, making them more likely to spread the virus when they sneeze, cough or talk.
The P681R mutation, also found in the kappa variant, is located at the start of a part of the genome called the furin cleavage site, Cooper said.
Furin is a naturally occurring human enzyme that is hijacked by the coronavirus, which uses it to cut the spike protein into the optimal shape to enter the cell, Rasmussen said. The new mutation makes this sculpture more effective, said Rasmussen.
Another delta mutation – also found in kappa and epsilon – is called L452R. The experiments suggest that this mutation, which also affects the receptor binding domain, works to prevent antibodies from neutralizing the virus, Cooper said.
These changes seem to be more formidable in a team than alone.
The genetic changes “certainly do something, but why this combination makes the delta variant more suitable is not entirely clear,” Bedford said. “Putting them together seems important. “
Delta also developed genetic changes not seen in other variants.
One such peak mutation is called D950N. “It could be unique,” Cooper said. “You don’t see that anywhere else. “
The D950N mutation is different from other mutations because it is located outside the receptor binding domain in an area of the coronavirus genome that helps the virus fuse with human cells, Cooper said. Fusion with human cells allows the coronavirus to dump its genetic material into these cells.
This mutation could affect the types of cells that the virus infects, potentially allowing it to harm different organs and tissues. Mutations in this region are also associated with higher viral loads, Cooper said.
Delta also contains mutations in a part of the spike protein called the N-terminal domain, which provides a “supersite” for antibodies to attach to the virus and prevent it from entering cells, said Dr Hana Akselrod, infectious disease specialist in the George Washington University School of Medicine and Health Sciences.
Mutations in this region make monoclonal antibodies less effective in treating covid and increase the ability of the delta variant to escape the antibodies generated by the vaccine, Akselrod said. This may explain why vaccinated people are slightly more likely to be infected with the delta, mainly causing mild illness but allowing them to transmit the virus.
Delta’s future journey
Scientists say it’s impossible to predict exactly how the delta will behave in the future, although Topol said: “It will get worse.”
Topol noted that delta outbreaks tend to last 10 to 12 weeks, as the virus “burns” susceptible populations.
If the United States continues to follow a pattern seen in the United Kingdom and the Netherlands, infections could drop from the current seven-day moving average of 42,000 cases to 250,000 per day. Still, Topol said the United States is unlikely to experience the high death rates seen in India, Tunisia and Indonesia, as nearly half of the population here is fully vaccinated.
While some studies have concluded that the Johnson & Johnson vaccine stimulates strong and persistent antibodies against delta, a new report has found that antibodies elicited by a single injection may not be enough to neutralize delta. The authors of this study, from New York University Grossman School of Medicine, suggested that a second dose might be needed.
According to a new study published in the New England Journal of Medicine, two doses of Pfizer-BioNTech vaccine protect 94% of people against any symptomatic infection with the alpha variant, compared to 88% against the delta variant. Two doses of the AstraZeneca vaccine protect 75% of people against alpha and 67% against delta.
Cooper said covid vaccines offer remarkably good protection. “I will always celebrate these vaccines as the scientific achievement of my life,” he said.
The best way to slow the progression of variants is to share vaccines with the world, vaccinating as many people as possible, Bedford said. Because viruses undergo genetic changes only when they spread from one host to another, stopping transmission prevents them from mutating.
Whether the coronavirus evolves into more deadly variants “is totally in our hands,” Cooper said. “If the number of infections remains high, it will continue to evolve. “
By failing to contain the virus through vaccination, wearing masks and avoiding crowds, people are allowing the coronavirus to develop into increasingly dangerous forms, said Dr William Haseltine, a former professor at the Harvard Medical School which has helped design treatments for HIV / AIDS.
“It’s getting better, and we’re improving it,” he said. “Having half the population vaccinated and half unvaccinated and unprotected – that’s the exact experience I would have if I were a devil and trying to design an anti-vaccine virus.”
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