A protein deficiency found commonly in large swathes of the populations in Europe and North America could explain why these regions have been worse hit by Covid-19 than people in Asia, researchers at a Calcutta-based national institute have established.
The protein, Alpha-1-antitrypsin (AAT), prevents lung tissue damage and its deficiency reduces the body’s ability to fight off the D614G mutant of the Coronavirus (Sars-CoV-2) which is now the dominant strain globally.
This finding which could have major implications for understanding Covid-19 and how it has spread globally has emerged in a study conducted by the National Institute of Biomedical Genomics (NIBG) in Calcutta.
Protein deficiency, not age or weather, drives Covid-19 pandemic: Report
February 10, 2021
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The study revealed that it was not the age factor or weather condition that should be blamed for the unchecked spread of the coronavirus
According to a new study carried out by researchers from the National Institute of Biomedical Genomics-Kalyani, protein deficiency led to the rapid spread of Covid-19 in Europe and the United States.
The study revealed that it was not the age factor or weather condition that should be blamed for the unchecked spread of the coronavirus,
Hindustan Times reported.
The SAS-CoV-2 virus uses two approaches to enter the host body. The first method involves binding its spike protein with ACE2 receptors present in the lungs, intestine, and other organs. The second is through another human protein TMPRSS2 that breaks the S1-S2 junction in the spike protein to allow the genetic material of the virus to enter the human cell.
Follow RT on New research from India suggests that a deficiency of the protein Alpha-anti-trypsin (AAT) in populations across Europe and North America may have contributed to the comparatively rapid spread of Covid-19 when compared with Asia.
Published in the journal Infection, Genetics and Evolution, the new study examines the role played by a lung-protecting protein in the spread of the pandemic in the West compared with 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 the first waves in Europe and North America, spread so fast.
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