Breakthrough hypothesis on autoimmunity in COVID-19
Through detailed research on COVID-19, a theory of autoimmunity to angiotensin-converting enzyme II (ACE-2) was formulated in April 2020. At that time, the hypothesis that COVID-19 is a viral-mediated autoimmune disease was not regarded by many as plausible. However, as the disease continued to baffle scientists and the medical community, the hypothesis gradually gained credence.
Discussions took place with international immunology experts (China, Canada, US and UK). Collaboration with Professor Bruce Uhal (Michigan State University), the top pulmonary ACE-2 researcher in the world, led to a scientific paper published in May 2020, explaining the concept of autoimmunity in COVID-19. A follow up paper, proposing a more detailed and comprehensive explanation of the symptoms associated with COVID-19, was published in March 2021.
Access the May 2020 paper here…
Access the March 2021 paper here…
The principle of autoimmunity in COVID-19 can be summarised as follows:
The viral spike protein binds to serum ACE-2 to trigger an autoantibody response. This may lead to severe disease in people who have elevated levels of serum ACE-2 – the elderly and those with obesity, hypertension, heart disease and/or diabetes.
Sex and ancestry are also determinants of elevated serum ACE-2.
This theory of autoimmunity could explain the symptoms, timeline and associated comorbidities in people with severe disease in COVID-19.
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McMillan Research does not currently have real world evidence data regarding all aspects of autoimmunity in COVID-19. The theory of autoimmunity in COVID-19 could form the basis for clinical investigation and medical monitoring. There are many challenges associated with clinical trials, especially clinical human trials. A clinical trial study requires a comprehensive development plan, and may use clinical biostatistics. A centre for clinical research focused on long COVID, could potentially provide much needed solutions.