Breaking the Rules of Respiratory Diseases: Reviewing the Current Perspectives Regarding Thrombotic Conditions Associated with SARS-CoV-2 Infection

Authors: Ben King* and Ian Alrahwan

DOI: 10.23880/nnoaj-16000151

Volume 5, Issue 2

Abstract

Many epidemiologic parameters of the viral infection are still being determined with precision, as the disease continues to spread - from the transmissibility, to the latent and infectious period, to the symptomatic case rate, to the case fatality proportion. Meanwhile, this virus has already broken many of the rules thought to apply to coronavirus-associated respiratory infection. The thrombotic pathology of COVID-19 and associated ischemic stroke risk is one of the most curious examples of this rule-breaking. In this editorial, we summarize the early findings of the COVID-19 pandemic with regard to thrombotic conditions and ischemic stroke in particular, and how these may be explained by the interwoven inflammatory mechanisms and coagulopathic cascade of viral infection. Questions have surfaced about the potential mechanisms and the degree to which thrombotic events like ischemic stroke have resulted from the COVID-19 disease. Unique features of the interaction between SARS-CoV-2 and its cellular receptor protein Angiotensin-Converting Enzyme 2 may illustrate why COVID-19 patients with mild symptoms experience large vessel occlusions. In lieu of a debate, there is a possible middle path that ties these mechanisms all together. Coagulation and inflammation reactions of the immune system are complementary and interrelated, but may also operate independently. Hypothetically, these two systems (inflammatory and coagulopathic) are not just overlapping, but synergistic in their biochemical pathways and therefore in their influence on clinical outcomes of patients infected with SARS-CoV-2.

Keywords: SARS-CoV-2 Infection; Coagulopathic Cascade; Thrombotic Conditions

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