An interesting article by Sarah Reardon in the Scientific American answers this question.
If researchers were predicting which coronavirus variant would take over the world, the Delta variant would not have been their first guess. However, since its first appearance in India in December 2020, the highly contagious variant has become the predominant strain of the virus, accounting for more than 90% of new COVID cases in the U.S. and in the United Kingdom.
Delta’s emergence has caused a number of countries to reinstate travel and mask restrictions that had been loosened as vaccination rates rose. Although the vaccines appear mostly effective against Delta, the sheer number of cases increases the likelihood that there could be breakthrough infections in vaccinated people. It is still unclear whether this results in more severe disease than the previously circulating strains.
What is clear, however, is that Delta has a strong evolutionary advantage over the earlier strains. Vaughn Cooper, an evolutionary biologist at the University of Pittsburgh tells us that its rate of increase is unlike any other in the history of this pandemic. One has to ask a question why has this particular variant, which carries a suite of different mutations, been so successful?
The virus rapid spread may be in part result from a fast replication rate.
A recent study found that people infected with Delta had on average, around 1000 times more virus in their bodies, known as viral load, than those infected with the original strain, allowing them therefore to infect more people quickly.
The variant’s advantage seems to stem from a combination of mutations in the spike protein: The part of the novel coronavirus that binds to the ACE2 receptors on the surface of cells and allows the virus to infect them.
Scientists have also wondered whether Delta, in addition to its increased transmissibility, is able to escape the human immune system.
It appears to lack a mutation called E484K, which helps a number of other variants partially avoid being neutralised by antibodies, but lab studies suggested that a Delta mutation called L452R was even better at performing the same function.
In a recent preprint study, which has not as yet been published in a journal, epidemiologist Nathan Grubaugh of Yale School of Public Health in New Haven, Connecticut tested 18 different variants reacted to serum taken from the plasma from 40 fully vaccinated healthcare workers.
He found that the participants’ antibodies were able to neutralise the Alpha variants well, and the Delta fairly well, but they were less effective against variants that carry the E484K mutations such as Beta or Gamma, variants that were first identified in South Africa and Brazil, respectively.
These findings were surprising, given that Delta has been much more effective at spreading than Beta or Gamma. Even though the L452R mutation alone improved immune evasion, the actual Delta virus was not actually that good at it, suggesting that the specific combination of mutations on Delta gave the virus a unique function.
Grubaugh goes go on to say that the Delta’s success suggests immune evasion might not give the virus as strong an evolutionary advantage as transmissibility, at least amongst those who are unvaccinated.
That might not be true in every population. The Gamma variant, for example, spread rapidly in Brazil but very little throughout the rest of the world.
Researchers suspect that COVID infection rates may have been higher in Brazil than in most countries, meaning that by the time the Gamma appeared, the majority of people were already able to mount a strong immune reaction. In that population, evading the immune system would have been helpful for the virus.
Mehul Suthar, a virologist at Emory University in Atlanta believes that there may be a limit to how many mutations a virus can acquire on the spike protein before it is no longer able to bind to the ACE2 receptor. He feels that there is always going to be a tug-of-war between the virus being able to gain ability to transmit and spread and replicate and its ability to escape an antibody response.
Suthar points out that the Kappa variant, which arose in India around the same time as Delta, shares most of Delta’s mutations as well as a mutation similar to the E484K, but Kappa as yet has not spread worldwide, suggesting that these mutations may interact in some way that makes the virus less evolutionarily fit.
Grubaugh thinks it is unlikely that significant new spike protein mutations are going to appear. He feels that the fittest virus will have a combination of the best mutations that will let it spread widely amongst the population. Cooper agrees with this and feels that combination of high transmissibility and the ability to evade antibodies will evolve if it can, provided infection numbers stay high.
The more people who remain unvaccinated, the greater the chance that something more lethal than the Delta will arise.
Such a potential nightmare virus actually appeared last year: A variant called B.1.620 that was first noted in Africa. It carried the E484K mutation, along with a number of other spike protein mutations that might increase transmissibility.
However, the number of B.1.260 cases soon declined, so it is considered not quite as simple as having all these mutations for things to be worse.
The good news, however, is that it is relatively simple to tweak the mRNA vaccines made by Pfizer and Moderna to make them more effective against such a variant.
In the meantime, however, the current vaccines remain the best way to prevent new variants from arising.
Suthar says it is clear that with these viruses it is not that if we defeat Delta that we will beat the pandemic, there is just another one that keeps emerging.
If too few people get vaccinated and the virus spreads unchecked, he says there will just be this endless cycle of infections, mutations and transmission.
The London General Practice, the leading London doctors’ clinic in Harley Street commends the Government on its vaccination programme and encourages all those eligible to be vaccinated.
Dr Paul Ettlinger
BM, DRCOG, FRCGP, FRIPH, DOccMed