PRAVASISAMWAD.COM
Inadequacy of a lung-protecting protein in the Western population may have made Europe and North America vulnerable to the spread of a Coronavirus variant as compared to Asian countries, suggests a research study by Indian scientists which also finds how mutant forms of the virus may find new ways to infect people.
While the second wave of COVID-19 cases has compelled various European and western countries to curb social gatherings, closing down pubs and shopping malls, open field hospitals, such preventive measures have become remote memories in Asian countries, especially India. For months now, life across the Asian continent, where the virus first emerged, has largely returned to normal.
What was being speculated as the explanation for variation in spread stands nowhere as there is no relation with temperature in Covid-19 mutant’s spread.
A team of expert scientists, from the National Institutes of Biomedical Genomics in Kalyani, West Bengal have come up with the biological cause for the slower spread of the new mutant strain of the Coronavirus in Asia, as compared to the Caucasian population.
The team has explained how increased levels of a protein found in the human body named Neutrophil Elastase, enables the virus to enter and multiply in the human cell easily and spread faster from infected individuals. However, this Neutrophil Elastase protein is restricted by the biological system, which stimulates another protein called alpha-1 antitrypsin (AAT). Decreased levels of AAT lead to increased levels of Neutrophil Elastase in the body, which in turn helps in the rapid spread of the virus. This deficiency is learned to be higher in European countries and America than in Asian countries. The research has been published in the journal, Infection, Genetics and Evolution.
Nidhan Biswas and Partha Majumdar led the team of scientists who studied the cause of the uneven spread of the new mutant virus across geographical regions. The study says that the mutant virus known as D614G took a considerably longer time to spread in East Asia as compared to the European region and the Americas.
The researchers asserted that “ the 614G subtype took 5.5 months in East Asia as compared to 2.15 months in Europe as well as 2.83 months in North-America.”
Partha Majumder said: “Many were speculating why coronavirus spreads differently across the globe. The most popular assumption was that 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”
The scientists linked the differential spread to an extra cleavage area developed by the D614G mutant virus strain, for threshold in the human cell.
According to Partha Majumder and Nidhan Biswas, AAT deficiency is as low as 8 persons per thousand individuals in Malaysia, 5.4 per 1,000 individuals in South Korea, and 2.5 per 1,000 in Singapore. However, in Spain 67.3 per 1,000 individuals have AAT deficiency. France and the US, have 51.9 per 1,000 and 29 individuals among 1,000 AAT deficient respectively. The researchers further said that their findings along with other common factors might explain the differential geographical or racial spread of the SARS-CoV2 virus.