A A variant of the coronavirus that appeared in the United Kingdom forced London to close, caused some countries to ban travel to and from the United Kingdom and launched a worldwide hunt to find out where this version has reached.
So what’s next?
Whenever a potentially significant viral variant occurs, experts want to study its effects on three key factors: how well it spreads, the disease it causes, and whether it can evade human protection against the pathogen, or for that they have already been infected or are vaccinated against it.
advertisement
Scientists have begun to discover the answer to the first: many increasingly believe that this variant is more transmissible. So far, however, it does not seem to change how ill it makes people.
With regard to immunity, experts are working to answer this question and ensure that vaccines that are just reaching people remain effective.
advertisement
“It’s obviously associated with a lot of uncertainty right now,” said Kristian Andersen, an infectious disease expert at the Scripps Research Institute.
Is immunity intact?
So far, there is no evidence that the virus has changed enough to avoid existing immune protection. But experts say it is crucial to confirm this, as the variant has a number and a number of mutations, unlike other versions of the virus that have appeared during the pandemic.
“We shouldn’t just rely on our priorities, which would be like, ‘No, the virus wouldn’t evolve this immune evasion,'” Andersen told STAT on Monday. The constellation of changes that this variant has “is really unusual,” he said.
Andersen added that he did not predict that there would necessarily be some impact on the effectiveness of vaccines, but stressed that studies, which are already underway in the UK, could address this. The studies involve extracting antibodies from the blood of people who have either recovered from Covid-19 or been immunized and, in laboratory experiments, testing whether it neutralizes the variant.
Coronaviruses evolve more slowly than viruses such as the flu, but they receive mutations as they spread. SARS-CoV-2 has added one or two changes a month to its RNA genome since it first appeared in China last year, and various versions of the virus have been circulating continuously throughout the pandemic.
But this variant, called B.1.1.7 or VUI-202012/01, appeared with at least 17 mutations, according to a genetic analysis. Some are located in the genome with instructions for the virus’s spike protein, which binds to human cells and allows the virus to infect them. Peak vaccines have been designed to teach the immune system to produce antibodies that can recognize and block peptide proteins, so pivotal changes may alter how well vaccines work.
The same could happen with antibodies generated by an initial case of Covid-19, said Monday Wendy Barclay, head of infectious diseases at Imperial College London.
“There is a chance that the antibodies that were produced in the first infection will not work as well against the new variant,” she said.
But Barclay pointed out that the immune system has other components that contribute to protection, including fighters called T cells that can also recognize the virus. She also mentioned that vaccines get antibodies that can get into different parts of the spike protein and take different approaches to fighting the virus, so even if some have lost their ability to target the spike, vaccines have other ways to block the virus.
In addition, if the virus were to evolve to get rid of vaccines – now or at some point in the future – it would most likely not make immunizations completely ineffective; it would just make them less protective and should be updated. It is possible, Barclay said, that the vaccines will be “compromised to some extent and we need to check that.”
As the vast majority of the world remains susceptible to the virus, there has not been much evolutionary pressure on the virus to adapt, although this will change as larger proportions of the population are vaccinated. But in this case, experts believe that B.1.1.7 did not evolve through the normal pattern of incorporating mutations into its genome as it copied as it spread.
Instead, they say it’s possible that an immunocompromised person who had a rare, chronic case of Covid-19 – whose long-term infection would have allowed the virus to replicate for weeks or more, building up mutations quickly – could be the source of the new variant that has since spread to others.
Does it make people sick?
Researchers are also investigating whether B.1.1.7 has any impact – for better or worse – on the disease that affects humans, although so far mutations appear to have affected only transmissibility, not pathogenicity (how the virus causes disease). ). Experts in the UK analyze the rates at which people with the variant are hospitalized and how long they stay, as well as deaths.
“It’s the first few days, so as people know, both hospitalizations and mortality are delayed indicators, it usually takes two to four weeks to see,” said Susan Hopkins, an epidemiologist at Public Health England. “I think we will be very careful until we have enough time to make accurate assessments.”
Is it easier to spread?
All viruses are mutating, and researchers have been searching for potential variants of SARS-2 for several months. Already, a variant, known as D614G, has helped increase the efficiency with which the virus spreads, most researchers agree. But other mutations that triggered alarms sometimes turned out to be puzzling. Mutations occur all the time and can help spread or make the virus sick or reduce it; many have no effect at all. Some forms of the virus appear and then disappear.
British researchers and public officials said B.1.1.7 is more transmissible than other versions of the coronavirus – with estimates ranging from 50% to 70% more infectious.
But some scientists want even more evidence. It is possible, for example, for a variant to look more contagious if it happens to first gain a starting point in an area, so that it has the most running space or benefits from a few over-spread pivot events. .
But several research teams have come to the same finding that B.1.1.7 spreads more efficiently than other strains, based on epidemiological and genetic analyzes.
“We now have high confidence that this variant has a transmission advantage over other virus variants currently in the UK,” Peter Horby, an infectious disease expert at Oxford University, said on Monday, improving his assessment. from last week’s “moderate” confidence. The variant continues to surpass other forms of SARS-2 in the country, scientists said.
There are various estimates of what it means to increase transmission, but researchers say the new variant could have increased the number of reproductions – a figure known as R-zero, which is the average number of people a person will infect – from 1 , 1 to 1.5. This is a big difference: with the former, on average, 10 infected people would lead to 11 new infections, but with the latter, those 10 people would cause 15 new infections – a difference that would increase from that date, because these secondary cases they caused new infections themselves. (Outbreaks will increase if the number is above 1 and decreases if it is brought below 1.)
Experts are still not sure what about B.1.1.7 seems to help it spread more easily. They noticed that people with this version tend to have higher levels of the virus in the upper respiratory tract than other people with Covid-19, so more virus may be “thrown away.” Maybe people get infected sooner after they get infected themselves. One of the mutations, called N501Y, has been shown to help the virus get better at the receptor it uses to infect cells, called ACE2. Another mutation affects what is known as the furin cleavage site, which helps the virus enter cells as it attaches to them. These differences offer what Barclay called “biological plausibility” to make the variant a better distributor.
Indeed, researchers reported on Monday that a separate variant observed in South Africa that shares at least one mutation with the British strain – N501Y – also has higher transmission rates.
British researchers on Monday raised another concern about the new variant: it may be able to infect children at higher rates than other versions.
One of the saving grace of the pandemic is that SARS-2 did not infect children at the adult rate (and generally did not make them nearly sick). One hypothesis for this is that children do not have as many ACE2 receptors on their cells compared to adults.
But in the UK, epidemiologists find that more infections among children are caused by the new variant compared to other versions. It tries to determine the significance of the pattern, but it is possible that if the variant catches better on ACE2 than other strains, it does not take so many receptors to establish an infection.
“If the virus has an easier binding time and entry into cells, then this would put children on a fairer ground,” Barclay said. “In a way, it overcomes one of those barriers that the virus faced before.”
Already, at least one case of B.1.1.7 has been confirmed each in the Netherlands, Denmark, Italy, Iceland and Australia. But experts have found that sites that sequence the most viral samples from infected people report the variant. In other words, if countries look for it, they can find it.
“It’s very likely to appear here,” Hopkins said, referring to Britain. However, it is very likely to be in other countries as well, as there have been shipments back and forth between many European countries in the last three months. “(British researchers first noticed the apparent advantage of B.1.1.7 transmission this month, but after that, they looked back by sequencing the data and found that the variant first appeared in September).
One country that does not have a coordinated sequencing system is the United States. Some research institutions have studied the genetic data and submitted it to a national database, but there is no federal effort to ensure that viral samples are collected and sequenced from patient groups in a way that is representative of geography and demography. . For example, this summer, for example, there was no sequencing information from any Pennsylvania patient in the database, an expert told STAT.
“There was a fairly random assortment of sequences,” said Diane Griffin, a virologist at the Johns Hopkins Bloomberg School of Public Health, who chaired a committee for the National Academy of Sciences on genomic epidemiology for SARS-2.
Despite concerns about the new variant, experts reiterated on Monday that the same public health measures preached since the early days of the pandemic could combat its spread. Mike Ryan, head of the World Health Organization’s emergency program, said that R-zero in some places far exceeded 1.5 at various times and that the virus was still under control. “In a way, it means we have to work harder,” Ryan said.
WHO officials also noted that reducing transmission reduces the possibility of dangerous variants.
“The conclusion is that we must stop the transmission of all SARS-CoV-2 viruses as soon as possible,” said WHO Director-General Tedros Adhanom Ghebreyesus. “The more we allow it to spread, the more opportunities it has to change.”