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Protein Behind Covid-19 ’s Slow Asia Spread: Indian Researchers

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. The team has 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.

MUMBAI: Deficiency in a particular human protein, which is more common in Europe and the United States than in Asia, could explain why coronavirus is not spreading as fast in Asian countries.
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. The team has 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).”
“Many were speculating why coronavirus spreads differentially across geographies. The most popular speculation was the higher temperature in Asia was not congenial to the spread of the coronavirus. We believed the cause had to be biological, rather than physical or social,” said Majumder.
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. This deficiency is known to be much higher in the Caucasians of Europe and America than among Asians,” said Majumder. “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.”
As 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.
The researchers emphasized that this finding along with other social factors may explain the differential geographical/ethnic spread of the mutant virus.


Source: ToI