Did we get Covid-19 disease mechanisms all wrong? Part 2
Why did scientists come up with the ACE2 receptor theory in the first place? The answer’s in the kidneys...
This is the second instalment of a three-part series by my guest author Janine Gallizia. To read Part 1, click here.
If ACE2 is not the SARS-CoV-2 receptor, as posited in Part 1, why is there a cascade of symptoms resembling ACE2 deficiency in Covid-19 patients? Get Well Fast author Janine Gallizia offers a clear and compelling hypothesis in this next instalment. Read on!
Part 2: The Inhibitor
By Janine Gallizia
As we saw in Part 1, in early 2020 the ACE2 receptor was proposed as the main site of viral entry allowing SARS-CoV-2 to infiltrate human cells.
Scientists proposed this primarily for two reasons: firstly, ACE2 was believed to be the compatible cell receptor for the first SARS-CoV (Severe Acute Respiratory Syndrome) viral outbreak that originated in Foshan, Guangdong province in China, in November 2002. The first SARS-CoV epidemic occurred from November 2002 to July 2003, and mostly affected countries in Asia, including China, Hong Kong, Taiwan, and Singapore. When the World Health Organization (WHO) declared a similar viral outbreak on March 11, 2020, sparked by a similar coronavirus in nearby Wuhan, Hubei Province in China, just 650km (400 miles) from Foshan, a series of parallels were logically drawn.
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