Abstract
The COVID-19 pandemic caused by the coronavirus SARS-COV-2 has cost many lives worldwide. In dealing with affected patients, the physician is faced with a very unusual pattern of organ damage that is not easily explained on the basis of prior knowledge of viral-induced pathogenesis. It is established that the main receptor for viral entry into tissues is the protein angiotensin-converting enzyme-2 [“ACE-2”, (1)]. In a recent publication (2), a theory of autoimmunity against ACE-2, and/or against the ACE-2/SARS-COV-2 spike protein complex or degradation products thereof, was proposed as a possible explanation for the unusual pattern of organ damage seen in COVID-19. In the light of more recent information, this manuscript expands on the earlier proposed theory and offers additional, testable hypotheses that could explain both the pattern and timeline of organ dysfunction most often observed in COVID-19.
Highlights
OF COVID-19The first epidemic involving Severe Acute Respiratory Syndrome (“SARS”) was identified in 2003 as a novel clinical entity [3]
This is likely to be an early type of immune response in SARS-COV-2, with IgM produced against ACE and ACE-2, primarily targeting the endothelial blood vessels in the lung and small intestines
The following timeline and associated symptoms are based on the hypothesis of autoimmunity as the primary cause of disease: Approximately 70% of people with COVID-19 are asymptomatic [69]
Summary
The first epidemic involving Severe Acute Respiratory Syndrome (“SARS”) was identified in 2003 as a novel clinical entity [3]. The current COVID-19 pandemic was triggered by the spread of a novel coronavirus SARSCOV-2 [10], with the earliest reports coming out of Wuhan, China, in late 2019 It has an 80% similarity to SARS-COV, there are specific differences within the receptor-binding domain of the spike protein which impact on infectivity [1, 11]. The purpose of shedding is unclear [26], but it seems to occur more frequently in hypertension and heart disease [27] Relevant stimuli, such as supplemental oxygen at levels routinely used in neonatal medicine (FiO2 0.95), have been shown to result in ACE2 shedding from human lung cells in culture [28]. Exploring differences in ACE-2 binding with the virus has not been straightforward, with some research suggesting
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