Abu Dhabi researchers have developed a way of modelling hundreds of coronavirus mutations in just a few days. The method means they can quickly see whether particular changes help the virus become more infectious or evade antibodies.
The scientists say their computer-based technique could be used to help develop vaccines in response to new variants.
“Our method can be used as a real-time surveillance tool to screen for emerging infectious Covid-19 variants,” Prof Kristin Gunsalus, faculty director of bioinformatics at NYU Abu Dhabi.
“It allows for a more timely response to emerging outbreaks and could be used to guide the development of new vaccines.”
The coronavirus enters human cells by binding its spike protein to a human cell's ACE2 receptor. The easier a virus can bind to this receptor the more infectious it is.
Most current coronavirus vaccines cause the body to produce harmless versions of these spike proteins. Then, when the real things comes along, the immune response is to attack it like any other known invader.
Coronavirus particles with mutations in the spike protein may be able to evade the body’s defences – including those from vaccination – because the immune system does not yet defend itself against the new kind of spike protein.
The researchers say as many as 5,000 variants could be created by changes to the spike protein alone, which makes assessing them a daunting task.
“Screening such a large set of variants poses a tremendous challenge for conventional experimental methods,” said Hin Hark Gan, a senior research scientist NYU’s Centre for Genomics and Systems Biology in New York and the study’s first author.
“An advantage of computer-based modelling is that a hundred mutations can be readily assessed in a few days.”
The researchers looked at 1,003 combinations of mutations affecting the region where the spike protein binds to the ACE2 receptor.
Results suggest that spike protein mutations are more likely to occur in two particular “hotspots” because these regions are flexible and can change shape.
Modelling single, double and triple mutations has shown that the variants first detected in Brazil, South Africa, the UK and the US could bind more easily to ACE2. This means these variants are more contagious than the original strain.
However, this is not the case with the variant first detected in India. Contrary to popular belief it is not thought to bind more strongly to ACE2, meaning it is not more contagious. But two of its mutations do help it to evade antibodies.
This would make vaccines, and antibodies from a previous infection, less effective in fighting that particular strain.
“Due to viral mutations, the efficacy of existing antibodies and vaccines may diminish,” said Mr Gan. “This scenario is a likely cause for the rapid spread of the variant in India.”
The other authors of the study were Benoit Marchand, of NYU Abu Dhabi’s high performance computing group, and Alan Twaddle, of NYU in New York.