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New research from India suggests that alpha-anti-trypsin (AAT) protein deficiency in populations in Europe and North America may have contributed to the relatively rapid spread of Covid-19 compared to Asia.
Published in the journal Infection, Genetics and Evolution, the new study examines the role played by a protective protein in the lungs in the spread of the pandemic in the West compared to Asia.
Specifically, researchers at the National Institute of Biomedical Genomics (NIBMG) in Kalyani, West Bengal, examined the means by which the D614G mutation, predominant in early waves in Europe and North America, spread. so fast.
Between February and March 2020, around 64.11% of people with Covid-19 were infected with the D614G variant, up from just 1.95% in January.
It took 2.15 months to reach a relative frequency of 50 percent 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 transmissibility and spread of the pathogen through the body, but not necessarily on the severity of the disease in each region.
“In order for the coronavirus to enter cells, its spike protein binds to the ACE2 receptor in human cells, and the human enzyme TMPRSS2 cleaves at the junction of two S1 and S2 subunits of the protein, allowing the virus to merge with cell, “ said study correspondent Nidhan K. Bis was from NIBMG.
The D614G mutation in the spike protein provides the virus with an additional entry point into human cells.
Neutrophil protein elastase cleanses bacterial infections in the lungs, but high levels can do more harm than good.
Therefore, this protein is moderated by AAT, the main function of which is to reduce tissue damage and inflammation of the lungs.
However, the delicate balance between these two elements is out of balance in large swathes of the European and North American population due to AAT deficiency, especially in Italy and Spain, the epicenters of Covid-19 in Europe.
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“The problem is that people with AAT deficits have high levels of neutrophils and if they are infected with the SARS-CoV-2 virus with the D614G mutation, their cells can quickly take up the virus and enter the whole system.” . say the researchers.
This deficiency, in combination with a variety of other factors, could explain the relatively rapid spread of this disease and other coronavirus mutations across Europe and the United States, including new variants from the United Kingdom and from South Africa, who both boast the same thing. “spine” like the D614G mutation.
Scientists suggest that with further research and further analysis, supplementation with AAT may be part of future preventive measures to fight the pandemic.
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