A team of scientists from the National Institute of Biomedical Genomics in Kalyani, West Bengal, have found a biological reason for the slower spread of a mutant of coronavirus in Asia compared to the West. They explained how higher levels of a human protein — neutrophil elastase — helps the virus to enter the human cell, multiply and also spread faster from infected individuals.
However, this protein is kept in check by the biological system, which produces another protein called alpha-1 antitrypsin (AAT). AAT deficiency leads to higher levels of neutrophil elastase in the cells, which in turn helps in faster spread of the virus. This deficiency is known to be much higher in Europe and America than among Asians. The study has been published in the journal Infection, Genetics and Evolution.
The team of scientists led by Nidhan Biswas and Partha Majumder observed that the rate of the spread of the mutant virus — D614G — has been non-uniform across geographical regions. The researchers say that, “…in order to reach 50% relative frequency, the 614G subtype took significantly longer time in East Asia (5.5 months) compared to Europe (2.15 months) as well as North America (2.83 months).”
The researchers linked the differential spread to an additional cleavage site created by the D614G mutant virus, for entry into the human cell.
“However, some naturally-occurring mutations in the AAT-producing gene results in deficiency of the AAT protein,” said Majumder. “This deficiency is known to be much higher in the Caucasians of Europe and America than among Asians. While we used AAT deficiency data from East Asia, along with North America and Europe, for the study, considering the pace at which the coronavirus is spreading, the numbers are representative of other Asian regions too, including India.”
Per their data, AAT deficiency is the least in East Asian countries — 8 per 1,000 individuals in Malaysia, 5.4 per 1,000 in South Korea, 2.5 in Singapore. On the other hand, 67.3 in per 1,000 individuals in Spain are AAT deficient, 34.6 in the UK and 51.9 in France and in the US it is prevalent in 29 individuals among 1,000.