The examine famous that the protein expression was constantly excessive within the intestines, kidney, gallbladder, coronary heart, male reproductive organs, placenta, eye and vascular tissues, whereas it was restricted within the respiratory system.
- Last Updated: August 6, 2020, 12:02 PM IST
Scientists have analysed the presence all through the human physique of a protein which the novel coronavirus makes use of to enter host cells, and have discovered that it’s produced solely at “very low levels, if at all,” within the respiratory system, an advance which highlights the necessity for additional research to reassess the organic mechanisms accountable for COVID-19.
The examine, printed within the journal Molecular Systems Biology, offered a scientific analysis of the manufacturing of ACE2 — the ‘coronavirus entry gate’ protein — in additional than 150 cell varieties within the human physique.
It famous that the protein expression was constantly excessive within the intestines, kidney, gallbladder, coronary heart, male reproductive organs, placenta, eye and vascular tissues, whereas it was restricted within the respiratory system.
“Previous studies have indicated that ACE2 protein is highly expressed in the human lung. But these expression profiles have not been reliably presented along with tissues and organs from the entire human body, or based on several different datasets,” mentioned examine senior creator Cecilia Lindskog from Uppsala University in Sweden.
“Here, in contrast to previous studies, we were able to confidently show that no ACE2 protein is present, or that it occurs at only very low levels, in the normal respiratory system,” Lindskog mentioned.
Earlier research had prompt that the novel coronavirus SARS-CoV-2 employs ACE2 for host cell entry, and that penetration of the virus by way of this receptor would clarify the extreme scientific manifestations noticed in varied tissues and organs, together with the respiratory system.
“Considering the clinical manifestations of COVID-19, with acute respiratory distress syndrome and extensive damage to the lung parenchyma, the results highlight the need for further study of the biological mechanisms responsible for COVID-19 infection and disease progression,” Lindskog mentioned.
“Further studies addressing the dynamic regulation of ACE2, and to confirm whether the low ACE2 expression in the human respiratory system is sufficient for SARS-CoV-2 infection, or whether other factors are needed for host cell entry, are urgently needed,” she added.
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