ACE2 Isn’t Solely Responsible for Covid-19, Which Explains A Lot

The discovery of two new receptors — neuropilin-1 and CD147 — explains why Covid-19 is a mix of respiratory, vascular, nervous, olfactory, and immunological diseases.

Shin Jie Yong, MSc (Res)
Microbial Instincts

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Abstract vector created by macrovector — www.freepik.com

It has been odd right from the start. If SARS-CoV-2 (the novel coronavirus that causes Covid-19) uses the angiotensin-converting enzyme 2 (ACE2) as a receptor to infect cells, then why is it a lung disease when the lungs have low levels of ACE2?

This was determined back in May 2020 in a study finding that alveolar cell type 2 (the primary target of SARS-CoV-2) in the lungs has ACE2 expression that is “4.7-fold lower than the average expression level of all ACE2 expressing cell types,” such as the liver, stomach, ileum, kidney, and colon.

Later, a systematic review published over a month ago further points out that SARS-CoV-2 tend to end up in places not consistent with ACE2 expression levels. Looking at the figure below, organs SARS-CoV-2 tend to localize (e.g., lungs and brain) do not always have high expression of ACE2, and vice-versa.

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Shin Jie Yong, MSc (Res)
Microbial Instincts

Independent science writer and researcher | Named Standford's world top 1% scientists | Medium's boost nominator | Elite Powerlifter | Ghostwriter | Malaysian