A new study published on bioRxiv in September 2020 reported on the effects of the mutated virus. It’s thought the mutation took place early in the course of the pandemic, and superseded most local strains.
The research group wanted to understand how the spike protein mutation affected the virus-host interactions.
Scientists reviewed its viral replication on human lung epithelial cells and primary human airway tissues.
In addition, they looked at the viral fitness by going ahead with animal testing.
In the UK alone, the Government has stated there have been a total of 41,527 coronavirus-related deaths.
A severe infection with COVID-19 has been linked to an unregulated immune response, with excessive and systemic inflammation.
Focusing on the spike protein, researchers have discovered the mutation – believed to have taken place in March – encodes amino acids of a different sort.
The spike protein is “key for viral entry into the host cells via the angiotensin-converting enzyme 2 (ACE2)”.
“Such mutations may cause alterations in the host range, pathogenesis and tissue tropism,” the researchers noted.
Three accompanying mutations were identified too, but the D6146 mutation has become the most dominant.
This suggests it may have developed a “fitness advantage”, including “infectious potential”.
Such a notion was supported, as the mutant is “associated with higher viral loads in COVID-19 patients”.
The researchers concluded: “The spike substitution D614G enhances viral replication in the upper respiratory tract.”
It was also confirmed that the mutation “increases neutralisation susceptibility”.
Importantly, this preliminary scientific report hasn’t yet been peer-reviewed.
Thus, these findings shouldn’t be regarded as conclusive or to guide clinical practice.