A key amino-acid mutation in the SARS-CoV-2 spike proteinmight explain why the Delta variant of Covid-19 has spread so swiftly acrossthe world, say researchers.
SARS-CoV-2 Delta variant has rapidly replaced the Alpha variantaround the world. According to epidemiological studies, the Delta variant,first identified in India in late 2020, is at least 40 per cent moretransmissible than the Alpha variant, first identified in the UK, last year.
However, the mechanism that drives this globalreplacement has not been defined yet.
The study, yet to be peer-reviewed and posted onpre-print server bioRxiv, showed how P681R mutation in the Delta spike plays akey role in the replacement of Alpha-to-Delta variant.
"Delta SARS-CoV-2 efficiently outcompeted the Alphavariant in human lung epithelial cells and primary human airway tissues,"wrote researchers from the University of Texas and others in the abstract.
The P681R mutation falls within an intensely studiedregion of the spike protein called the furin cleavage site, Nature reported.
The short string of amino acids P681R is associated withheightened infectivity in other viruses such as influenza. However, it has notpreviously been found in sarbecoviruses -- the family of coronaviruses to whichSARS-CoV-2 belongs.
"The key hallmark of Delta is that transmissibilityseems to be ramping up to the next notch," Pei-Yong Shi, a virologist atthe University of Texas's Medical Branch in Galveston was quoted as saying.
"We thought Alpha was pretty bad, very good atspreading. This one seems to be even more," Shi added.
Further, the presence of P681R mutation enabled the Deltavariant to rapidly outcompete the Alpha variant, in cultured human-airwayepithelial cells infected with equal numbers of Delta and Alpha viralparticles. However, when the team eliminated the P681R mutation, Delta'sadvantage waned.
The study also suggested that the mutation also speeds upthe spread of SARS-CoV-2 from cell to cell, Nature report said.
Researchers at the University of Tokyo found that spikeproteins bearing the P681R mutation fuses with the plasma membranes ofuninfected cells -- a key step in infection -- almost three times faster thanthe spike proteins that lack the change.
The team suggests that the P681R mutation may not bealone, and further studies are needed to examine other mutations in the spikeprotein of Delta to understand its swift transmission.