The COVID spread in Asia is slower than the other countries and the reason here is a specific protein. Deficiency of a lung-protecting protein in the Caucasian population may have made Europe and North America more susceptible to the COVID spread (mutant) as compared to Asia, suggest a study by Indian scientists which also reveals how mutant forms of the virus may find new ways to infect people.
The study, published in the journal Infection, Genetics, and Evolution, assessed the global spread of the corona virus variant with the D614G mutation, which is the predominant lineage infecting North America and the European population.
This variant spread so rapidly that in just 10 weeks between February and March 2020 over 64.11% of globally infected individuals were identified to carry the mutant virus starting from only 1.95% in January.
However, the researchers, including those from the National Institute of Biomedical Genomics (NIBG) in Kalyani, West Bengal, said this subtype took a significantly longer time to reach a 50% relative frequency in East Asia 5.5 months compared to the 2.15 months it took in Europe and the 2.83 months it took in North America.
According to the scientists, a deficiency of the protein Alpha-anti-trypsin (AAT) across the populations of Europe and North America is one of the main factors that explain the rapid spread of this variant in the two continents compared to its transmission in Asia.
In lineages of the COVID carrying the D614G mutation, the 614th molecule of the virus spike protein aspartic acid denoted by D is replaced by the molecule glycine noted as G.
Based on the current study, he said this site in the virus is cleaved by the host protein neutrophil elastase which is normally involved in clearing up bacterial infections in the lungs.
The levels of the elastase molecules in the body are naturally kept in check by AAT whose main function is to protect the lungs from inflammation and tissue damage, the study noted.
According to the study, AAT deficiency is highly prevalent in European and North American populations, but much less in East Asia.
Specifically, the study corresponding author Nidhan K Biswas from NIBMG said AAT deficiency in the general populations is very high in Italy and Spain.
He explained that the lack of this protein makes it much easier for the neutrophil elastase molecule to act on the virus spike subunits, resulting in a significantly faster COVID spread of this mutant.
The researchers believe this finding, along with other social factors may explain the differential geographical/ethnic spread of 614G. While the findings offer clues about the transmission of the virus variant, Biswas cautioned against any interpretations of the study on disease severity and mortality caused by the strain.