How will Delta develop next? Scientist predicts what the future might look like



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The COVID-19 pandemic is a spectacular display of evolution in action. The theory of evolution explains much of what has already happened, predicts what will happen in the future, and suggests which management strategies are likely to be most effective.

For example, evolution explains why the Delta variant spreads faster than the original Wuhan strain. It explains what we might see with future variants. And that suggests how we might scale up public health measures to address it.

But Delta is not the end of the story of SARS-CoV-2, the virus that causes COVID-19. Here’s what the theory of evolution tells us will happen next.

Remind me again, how do viruses evolve?

Evolution is the result of random mutations (or mistakes) in the viral genome as it replicates. A few of these random mutations will be good for the virus, conferring some benefit. Copies of these beneficial genes are more likely to survive into the next generation, via the process of natural selection.

New viral strains can also develop by recombination, when viruses acquire genes from other viruses or even from their hosts.

Overall, evolution can be expected to favor viral strains that result in a steeper epidemic curve, producing more cases faster, leading to two predictions.

First, the virus should become more transmissible. An infected person will be likely to infect more people; future versions of the virus will have a higher reproductive number or R.

Second, we can also expect evolution to reduce the time it takes between infecting one person and infecting others (a shorter “series interval”).

These two planned changes are clearly good news for the virus, but not for its host.

Aha, so that explains Delta

This theory explains why Delta is now sweeping the world and replacing the original Wuhan strain.

The original Wuhan strain had an R-value of 2-3 but Delta’s R-value is around 5-6 (some researchers say this figure is even higher). So, a person infected with Delta is likely to infect at least twice as many people as the original Wuhan strain.

There is also some evidence that Delta has a much shorter serial interval compared to the original Wuhan strain.

This may be linked to a higher viral load (more copies of the virus) in a person infected with Delta compared to earlier strains. This can allow Delta to pass on sooner after infection.

A higher viral load may also make Delta more easily transmissible in the open and after “fleeting contact“.

Do vaccines affect the course of the virus?

We know that COVID-19 vaccines designed to protect against the original Wuhan strain work against Delta but are less effective. Evolutionary theory predicts it; viral variants that can elude vaccines have an evolutionary advantage.

We can therefore expect an arms race between vaccine developers and the virus, with vaccines trying to catch up with the viral evolution. This is why we are likely to see ourselves having regular booster shots, designed to overcome these newer variations, just as we see with the flu booster shots.

COVID-19 vaccines reduce your chances of passing the virus on to others, but they do not completely block transmission. And the theory of evolution gives us a caveat.

There is a trade-off between transmissibility and a person’s degree of illness (virulence) with most pathogenic microorganisms. This is because you need a certain viral load to be able to transmit.

If vaccines are not 100% effective in blocking transmission, we can expect a trade-off shift to higher virulence. In other words, a side effect of the virus that can be transmitted by vaccinated people is, over time, the theory predicts that it will become more harmful to unvaccinated people.

And the future variants?

In the short term, it is highly likely that evolution will continue to “refine” the virus:

  • its R-value will continue to increase (more people will be infected in a generation)

  • the serial interval will decrease (people will become contagious sooner)

  • the variants will make the vaccines less effective (vaccine escape).

But we don’t know how far these changes could go and how quickly it could happen.

Some scientists believe the virus may already be nearing “peak physical condition.” Nevertheless, he may still have a few tricks up his sleeve.

The UK government’s Scientific Advisory Group for Emergencies (SAGE) recently explored long-term scenarios for the virus.

He says it’s almost certain that there will be “antigen drift,” a build-up of small mutations causing the effectiveness of current vaccines to decrease, so boosters with modified vaccines will be essential.

He goes on to say that more dramatic changes in the virus (“antigenic change”), which could occur by recombination with other human coronaviruses, are a “realistic possibility”. This would require a more substantial reengineering of the vaccines.

SAGE also believes that there is a realistic possibility of a “reverse zoonosis”, leading to a virus that could be more pathogenic (harmful) to humans or able to escape existing vaccines. This would be a scenario in which SARS-CoV-2 would infect animals, before returning to humans. We have already seen SARS-CoV-2 infect mink, felines and rodents.

Will the virus become more deadly?

Versions of the virus that make their host very sick (are very virulent) are usually selected against. This is because people are more likely to die or be isolated, which would reduce the risk of transmitting the virus to others.

SAGE believes this process is unlikely to make the virus less virulent in the short term, but it is a realistic possibility in the long term. Still, SAGE says there is a realistic possibility that more virulent strains could grow through recombination (which other coronaviruses are known to do).

So the answer to this crucial question is that we really don’t know if the virus will become more deadly over time. But we cannot expect the virus to magically become harmless.

Will humans evolve to catch up?

Unfortunately, the answer is no. ”Humans do not reproduce quickly enough and accumulate enough favorable mutations fast enough that we can stay ahead of the virus.

The virus also does not kill most of the people it infects. And in countries with well-endowed health systems, it doesn’t kill many people of reproductive age. So there is no “selection pressure” for humans to mutate favorably to stay ahead of the virus.

What about future pandemics?

Finally, the theory of evolution warns against future pandemics.

A genetic mutation that allows a virus from an obscure and relatively rare species (such as a bat) to gain access to the most common and widespread large animal species on the planet – humans – will be strongly selected.

We can therefore expect future pandemics when animal viruses spread to humans, as they have done in the past. The conversation

Hamish McCallum, Director, Center for Planetary Health and Food Security, Griffith University, Griffith University.

This article is republished from The Conversation under a Creative Commons license. Read the original article.



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