New research from India suggests that a deficiency of the protein Alpha-anti-trypsin (AAT) in populations across Europe and North America has contributed to the relatively rapid spread of Covid-19 compared to Asia.
The new study, published in the journal Infection, Genetics and Evolution, examines the role that a lung-protective protein plays in the spread of the pandemic in the West compared to Asia.
Specifically, researchers from the National Institute of Biomedical Genomics (NIBMG) in Kalyani, West Bengal, investigated the way in which the D614G mutation, predominant in the first waves in Europe and North America, spread so rapidly.
Between February and March 2020, about 64.11 percent of people with Covid-19 were infected with the D614G variant, compared to only 1.95 percent in January.
It took 2.15 months to reach the relative frequency of 50% in the population in Europe and 2.83 months in North America, but 5.5 months to reach the same prevalence in East Asia.
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The researchers warn that their analysis focuses more on the transmission and spread of the pathogen through the body, but not necessarily on the severity of the disease in each region.
“For the coronavirus to enter cells, it binds vein protein with the ACE2 receptor in human cells, and the human enzyme TMPRSS2 cleaves at the intersection of two subunits S1 and S2 of the protein, enabling the virus to interact with the cell to merge, “ said author Nidhan K. Biswas of NIBMG.
The D614G mutation in the vein protein gives the virus extra access to human cells.
The protein neutrophil elastase cleanses bacterial infections in the lungs, but high levels can do more harm than good.
Therefore, this protein is moderated by AAT, whose primary function is to reduce tissue damage and inflammation in the lungs.
However, the delicate balance between these two is down across large sections of the European and North American population due to a shortage of AAT, particularly in Italy and Spain, the one-time center of Covid-19 in Europe.
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“The problem is that individuals with AAT deficiencies have high neutrophil levels and if they are infected with the SARS-CoV-2 virus with the D614G mutation, their cells can absorb the virus quickly and introduce it into the entire system,” say the researchers.
This deficiency, combined with a variety of other factors, may explain its relatively rapid spread and other mutations of the coronavirus in Europe and the US, including the newer British and South African variants, both of which boast the same “Backbone” as the D614G mutation.
The scientists suggest that AAT supplementation, after more in-depth research and subsequent analysis, could form part of future preventative measures to combat the pandemic.
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