Cause of lower corona infection in Asia:
SARS-CoV-2 was first reported from China. Within three months, it evolved to 10 additional subtypes. Two evolved subtypes (A2 and A2a) carry a non-synonymous Spike protein mutation (D614G).
A new study:
A phylodynamic analysis of over 70,000 SARS-CoV-2 coronaviruses worldwide, sequenced until July2020, and found that the mutant sub-type (614G) out competed the pre-existing type (614D), significantly faster in Europe and North-America than in East Asia. A study has concluded that:
Bioinformatically and computationally, scientists identified a novel neutrophil elastase (ELANE) cleavage site introduced in the G-mutant, near the S1-S2 junction of the Spike protein. We hypothesised that elevation of neutrophil elastase level at the site of infection will enhance the activation of Spike protein thus facilitating host cell entry for 614G, but not the 614D, subtype. The level of neutrophil elastase in the lung is modulated by its inhibitor α1-antitrypsin (AAT). AAT prevents lung tissue damage by elastase. However, many individuals exhibit genotype-dependent deficiency of AAT. AAT deficiency eases host-cell entry of the 614G virus, by retarding inhibition of neutrophil elastase and consequently enhancing activation of the Spike protein.[https://www.sciencedirect.com/science/article/pii/S1567134821000575?]
In plain English it means that 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 is highly prevalent in European and North-American populations, but much less so in East Asia. Therefore, the 614G subtype is able to infect and spread more easily in populations of the former regions than in the latter region.
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.