What Makes The Delta COVID-19 Variant So Dreadfully Successful?

Colorized scanning electron micrograph of an apoptotic cell (green) heavily infected with SARS-COV-2 virus particles (orange). Image credit: NIAID

The Delta variant has become the most dominant strain of SARS-CoV-2 worldwide in less than a year. After first being identified in India in October 2020, the variant sparked a catastrophic second wave of COVID-19 cases and deaths in India that started around March 2021. It then snuck into other countries around the world, outcompeting all other variants, and quickly established itself as the most prevalent strain, leading to surges of infections, a rise in hospitalizations, and further deaths.

But what made this particular variant so dreadfully effective at infecting humans, even ones that are fully vaccinated? A new study, led by the University of Cambridge and reported in the journal Nature this week, carried out a number of lab experiments to identify why the Delta variant has become responsible for so many cases. They found that it's largely due to its ability to evade neutralizing antibodies and its skills in invading host cells.

First up, it appears the Delta variant is more efficient at breaking into cells compared to other variants because it’s armed with more cleaved spikes on its surface. SARS-CoV-2 viral particles are covered in spike proteins. For the virus to infect one of our cells, the spike protein binds to a protein receptor found on the surface of cells in our body. Both proteins then become cleaved, or split, allowing genetic material from the virus to enter the host cell. More cleaved spikes mean better access. Once inside the cell, it also appears that the Delta variant is able to replicate more efficiently, according to the authors.

Paired with this skill, the Delta variant is also better at avoiding immune responses, whether that’s from vaccination or a previous infection. To find out how, the team extracted serum from blood samples collected from a range of people, some who had been vaccinated with either the Oxford/AstraZeneca or Pfizer vaccines and some who had been infected with COVID-19. The samples included a range of variants, including the original strain first identified in Wuhan. Since these people had been infected with COVID-19 or received the vaccine, their blood serum will contain some neutralizing antibodies against the virus.

They found that the Delta variant virus was 5.7-fold less sensitive to the sera (that’s the singular of serum) from individuals that had been previously infected, and eight-fold less sensitive to the sera of vaccinated people, compared with the Alpha variant. In other words, it takes more antibodies from a vaccinated person than a person who has already had COVID-19 to block the virus. However, it takes significantly more antibodies — whether they're from a vaccine or a natural infection— to block the Delta variant compared to other strains.

Make no mistake, it’s still worth getting vaccinated because even though "breakthrough infections" are possible, vaccines will significantly reduce the risk of you falling severely ill and being hospitalized with COVID. However, the study concludes by saying their findings affirm the view that scientists need to continue working on the vaccines if we are going to control the spread of Delta and other variants that are still transmissible.

“Infection of vaccinated healthcare workers with the Delta variant is a significant problem. Although they themselves may only experience mild COVID, they risk infecting individuals who have suboptimal immune responses to vaccination due to underlying health conditions – and these patients could then be at risk of severe disease,” joint senior author Professor Anurag Agrawal said in a statement.

“We urgently need to consider ways of boosting vaccine responses against variants among healthcare workers. It also suggests infection control measures will need to continue in the post-vaccine era.”

 
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