Every day, a little flotilla of refrigerated vans arrives at the Wellcome Sanger Institute in rural Cambridgeshire to deliver waste material from the many thousands of PCR tests conducted across the country, to a small team of dedicated and highly trained scientists.

This is the beating heart of the UK’s Covid-19 surveillance system, which uses the PCR swab samples to conduct genome sequencing. Its aim? To monitor the rise and spread of new variants. This information can then be used to identify how the virus is evolving as it moves through the population and gathers mutations which enable it to adapt to human cells.

Over the past month, the rapid spread of the so-called Delta variant – otherwise known as the B.1.617.2 strain of SARS-CoV-2 – the most virulent and transmissible form of the virus to emerge thus far, has meant the monitoring work has never been more vital. “Right now we’re sequencing around 4,000 genomes a day,” says Jeffrey Barrett, director of the Covid-19 Genomics Initiative at the Wellcome Sanger Institute, who is leading the operation. “Because the case numbers in the UK are going up.”

The Delta variant has now established itself as the UK’s dominant strain. It currently accounts for 90 per cent of new Covid-19 cases in the UK, with studies suggesting it to be 60 per cent more transmissible than Alpha, which in itself was 50 per cent more transmissible than the original Wuhan strain. This infectivity has already precipitated the onset of a third wave, with the number of daily Covid-19 cases in the UK topping 9,000 last Wednesday for the first time since February.

While Delta is believed to have first appeared in India sometime last autumn, before reaching the UK in late March, its rate of spread and potency in recent months has caught the scientific community off guard. Barrett admits that most genomic scientists, including those at the Wellcome Sanger Institute, were anticipating the next ‘super-spreader’ variant to be a new evolution of the Alpha, or Kent, variant which emerged in South-East England in September 2020. “But in fact, the next worrying thing wasn't Alpha at all,” says Barrett. “It was this ancestor of Delta, which was circulating for quite a while in India, a place which didn't have very good genomic surveillance, and we didn't see it coming.”

In fact, when scientists first identified that there were three novel strains of SARS-CoV-2 in India – known as B.1.617.1, B.1.617.2, and B.1.617.3 – starting to cause concern, B.1.617.2 or Delta was not initially the main focus of attention. “In March and April, Delta was the dominant strain in India, but it took time to really take off and grow in the UK,” Barrett says. “Everyone was initially focused on B.1.617.1, as the mutations in that one looked a bit more worrying, but that has fizzled away now.”

So why did the Delta variant take over so quickly? Yatish Turakhia, a genomic scientist at the University of California, Santa Cruz, explains that Delta contains 20 different mutations, compared to the original strain of SARS-CoV-2. However there are seven particularly key adaptations in the virus’ mushroom-shaped spike proteins, which latch onto human cells, and are driving its increased transmissibility. These spike protein mutations are thought to increase how tightly the virus binds to the ACE2 receptor protein – the keyhole it uses to invade cells – as well as enabling more of its genetic material to penetrate inside.

“You can think of the way the virus enters cells as like a lock and key mechanism,” says Turakhia. “So when some of these mutations happen, it means the key fits the lock better, meaning it can make a more effective entry into the cell.”

Two of the spike protein mutations have already been seen in other variants. One, on locations 681 of the spike protein, is also present on the Alpha variant, while the mutation on locations 452 has been seen in viral strains found in California. But the other five are completely new, and scientists are racing to try and figure out what their biological function is. “Delta is playing the same trick as other variants, grabbing onto human cells a bit more tightly, but using mutations we haven’t seen before,” says Barrett. His team at the Wellcome Sanger Institute are still figuring out the precise function of all of these new mutations, but they believe that some of them alter the shape of the spike protein, in a way which benefits the virus.

Scientists are in a rush to understand the mutations. As well as being more transmissible, there seems to be evidence that Delta is more virulent than previous strains. While the original strain of SARS-CoV-2 predominantly impacted the elderly and those with underlying health conditions, Delta appears to threaten even the young and fit.

Public Health England’s latest report – which covers surveillance of Delta up until June 3 – revealed that the majority of the new Covid-19 cases are in the younger, unvaccinated segments of the population. In Scotland, analysis published in the Lancet journal on hospital admissions between April 1 and June 6 suggests that Delta has caused twice as many hospitalisations as Alpha. This has led to questions about the UK’s border policy, which some – including Labour leader Keir Starmer – blame for facilitating the spread of Delta from India to the UK. According to the Civil Aviation Authority, some 42,406 people travelled between India and the UK in April.

Barrett says that there are multiple ongoing hypotheses for exactly how Delta’s mutations have made it more infectious. One is that every cough or breath contains more virus, because the variant has been more successful at reproducing within human cells. The other is that infected people might be shedding live virus for a longer period of time. “All of this would make it more transmissible, and mean that there’s more virus getting into people, resulting in more severe disease,” he says.

There are also some suggestions that Delta may have changed the widely accepted symptoms of Covid-19, meaning that people go longer before they realise they have the virus. While people have learnt to associate symptoms of a fever, and loss of smell and taste with Covid-19, early analysis conducted by the ZOE COVID Symptom Study suggest that headache, runny nose and sore throat tend to be more common early symptoms of Delta.

“That could be the critical thing,” says Barrett. “If people have a headache or a runny nose, they probably initially think it’s a cold or allergies, rather than Covid-19. And if on average, they’re spending one or two more days in circulation with the rest of the population before isolating, that will be driving the spread.”

The rise of Delta has prompted Boris Johnson’s government to take two steps, one being the postponement of ‘Freedom Day’ – marking the end of public health restrictions in the UK – and accelerating the vaccine rollout. The NHS has announced that all over 18s will be able to book a vaccine appointment by the end of the week.

Vaccines still represent highly effective forms of protection against Delta, although its mutations have made a slight dent in their efficacy. The Pfizer-BioNTech vaccine has been found to be 88 per cent effective in preventing symptomatic disease from Delta in fully vaccinated people, a slight reduction from its 93 per cent efficacy against Alpha. But after just a single dose, the vaccine is only 33 per cent efficient against Delta, compared to 51 per cent against Alpha.

One of the reasons for this is that while the vaccines still generate effective T cell immunity against the Delta, they appear to induce lower concentrations of protective antibodies. “Some of those mutations might mean the antibodies that are made by the vaccine just aren't quite the right shape anymore,” says Barrett. “So basically they don't stick to the virus as well, and the virus is better able to get past them and get into cells.”

But while the UK population is shielded from the worst effects of Delta by the efficiency of the national vaccination program, there are growing fears that Delta could trigger major spikes in the Covid-19 death rate elsewhere in the world over the coming months. As well as being the dominant variant in India and Singapore, it has already reached more than 70 countries. It accounts for six per cent of cases across the US, but that figure is up to 18 per cent in some states, and while Delta is well monitored in the UK – which has one of the world’s most efficient systems for spotting variants – few countries are capable of tracking it to the same extent, meaning it may already be gaining traction, unnoticed, in other parts of the globe.

In the meantime, as scientists are still attempting to understand the intricacies of Delta, they are also on the lookout for the next major variant. The worry is a variant that severely impacts the efficacy of vaccines. “It's hard to make predictions,” says Nathaniel Landau, a microbiology professor at NYU School of Medicine, who is studying the new variants. “The question is whether the virus will continue to come up with these novel mutations, or whether we're kind of reaching the saturation points, where the virus has developed all the mutations it can.”

However, there are signs that SARS-CoV-2 may still have some evolutionary tricks up its sleeve. Barrett points out that a new form of Delta already exists, adding a mutation called K417N initially found on the Beta or South Africa variant that further reduces antibody binding. While there are very few cases of this variant so far it is being closely monitored.

“We’re continuing to do all this genome sequencing to hopefully catch these things as early as possible,” he says. “We're running analysis on all 100,000 genomes we've generated over the last couple of months, to see which mutations are arising, and updating this every day to look for patterns that might predict a variant growing and becoming really problematic. But making these predictions is easier said than done, because the virus keeps on surprising us.”

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This article was originally published by WIRED UK