Covid-19

Why the Delta variant of Sars-Cov-2 is more virulent

An electron microscopic image  that shows SARS-CoV-2, the virus that causes COVID-19
An electron microscopic image that shows SARS-CoV-2, the virus that causes COVID-19 Handout National Institutes of Health/AFP/File

With the emergence of the Delta variant of Sars-Cov-2, a number of countries are reimposing tighter restrictions to halt its spread. In a televised address on Monday, French President Emmanuel Macron announced mandatory Covid-19 vaccinations for health staff and a ‘Covid pass” for restaurants, bars and other public venues from August.

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What is the Delta variant and why has it become a cause of worry? In an interview with RFI, Mircea T. Sofonea, associate professor in epidemiology and evolution of infectious diseases at the University of Montpellier, explains why this variant is more virulent.

Why is the Delta variant more worrisome?

The reason why the World Health Organization considers it a variant of concern is because it is more contagious. The Delta variant has a transmission advantage compared to the previous major lineages.

In the UK, it was estimated it is 50 percent more contagious than the Alpha variant. While in France, our team based in Montpellier estimated it to be 70 percent more contagious than the Alpha variant.

Why is it more contagious? What biological advantage does it have?

The mutations are linked to the changes in the corresponding protein structure and hence its affinity for other proteins (that is to say their binding strength).

The main mutations highlighted in SARS-CoV-2 evolution affect the receptor binding domain of the spike protein which is responsible for the binding of the viral particle with the ACE2 receptors of the epithelial cells. Better affinity can lead to an increase in the capacity of the viral particles to enter these cells.

What is the efficiency of the vaccines against the Delta variant?

The fact that the current vaccines elicit an immune response that can access several sites exposed by the viral particle, makes them robust to mutations. This means that the vaccines currently deployed are efficient against the Delta variant as well.

The efficiency in terms of prevention of severe cases of Covid-19 is between 80 and 90 percent. The vaccines provide very good protection against the Delta variant and in the vast majority of the cases can prevent complications.

But for those not vaccinated, there is some evidence that the Delta variant has an increased probability to develop Covid-19 symptoms that will result in hospitalisation.

There are results suggesting this variant is more virulent than others. The mRNA vaccines (Pfizer and Moderna) show a greater efficiency compared to adenovirus vaccines (Astrazeneca). What is important to know is that there is a need to have both doses to be protected against the Delta variant. Having one dose offers only a limited protection.

Why are these mutations advantageous to the virus given that they occur at random? 

This is what we call the survival bias. We only see the variants that are particular mutants with advantages at the epidemiological level. The Sars-Cov-2 pathogen can produce billions of copies in a human host. But each of these copies can differ from one another (of the order of 1 mutation every ten replication cycles).

That’s because genome replication isn’t always perfect. It can include some errors that are not always proofread or corrected. But this great diversity is then filtered by the constraints of the population. These are in the form of preventive measures including vaccination.

We only see those mutants which have acquired some specificities that pass these filters. These are the ones that spread while some other mutations disappear. In an unintentional way, we are the ones as a population that impose selective pressure on the pathogens.

Given the Delta variant's rapid spread, is there a need for a third vaccine dose to protect against it?

We still don’t really know the whole kinetics of the immune response induced by the vaccines in the long run. That’s because we have to consider both the neutralising antibodies circulating in the blood as well as the cellular immune response.

At some point, it is expected that the level of antibodies must be high enough to induce a quick response. But the bigger the lag between the first injection and exposure to the new variant, the greater the difference between the kind of spike protein the immune response has been exposed to during the previous vaccination and the existing version of the spike protein. In such cases, there is potentially a need for a third injection.

But there isn't enough data to generalise it. It may appear important for those that are more at risk for having complications. If we consider the less-at-risk groups which have been vaccinated more recently, they can still benefit from the current immune memory. We will have more quantitative answers about this issue next month.

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