New research from India suggests that a deficiency of alpha-antitrypsin protein (AAT) in populations in Europe and North America may have contributed to the comparatively rapid spread of Covid-19 when compared to Asia.
Published in the journal Infection, Genetics and Evolution, the new study examines the role played by a protective lung protein 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, prevalent in the first waves in Europe and North America, spread so quickly.
Between February and March 2020, about 64.11 percent of people with Covid-19 were infected with the D614G variant, compared to just 1.95 percent in January.
It took 2.15 months to reach 50 percent relative frequency 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 dissemination of the pathogen throughout the body, but not necessarily on the severity of the disease in each region.
“For the coronavirus to enter cells, its spike protein binds to the ACE2 receptor on human cells, and the human enzyme TMPRSS2 cleaves at the junction of two protein S1 and S2 subunits, allowing the virus to merge with the cell,” said the study’s corresponding author, Nidhan K. Biswas, of NIBMG.
The D614G mutation in the spike protein provides the virus with an additional entry point into human cells.
Neutrophil elastase protein clears bacterial infections in the lungs, but high levels can do more harm than good.
Therefore, this protein is moderated by AAT, whose main function is to reduce tissue damage and inflammation in the lungs.
However, the delicate balance between these two is impaired in large sections of the populations of Europe and North America due to an AAT deficiency, most notably in Italy and Spain, the former epicenters of Covid-19 in Europe.
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“The problem is that individuals with AAT deficiencies have high levels of neutrophils and, if they are infected with the SARS-CoV-2 virus with the D614G mutation, their cells can quickly carry the virus throughout the system,” say the researchers.
This deficiency, in combination with a variety of other factors, may explain the comparatively rapid spread of this and other coronavirus mutations in Europe and the United States, including the most recent variants from the United Kingdom and South Africa, which have the same “backbone” such as the D614G mutation.
Scientists suggest that, after further research and subsequent analysis, AAT supplementation may be part of future preventive measures to combat the pandemic.
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