A Supercomputer crunched data for a week in order to better understand Covid-19. The computer revealed a new theory about how Covid-19 impacts the body called: ‘The Bradykinin Hypothesis. Excess of the inflammatory molecule bradykinin may explain the fluid build-up in the lungs of patients with coronavirus infections. They believe that a dysregulated bradykinin system was leading to leaky blood vessels in the lungs, and other parts of the body. This is likely the reason that COVID-19 can cause heart disease in people with no prior history. About one in five hospitalized Covid-19 patients have damage to their hearts.
“The bradykinin hypothesis also accounts for Covid-19’s neurological effects, which are some of the most surprising and concerning elements of the disease. These symptoms (which include dizziness, seizures, delirium, and stroke) are present in as many as HALF of hospitalized Covid-19 patients.” According to the author of ‘A Supercomputer Analyzed Covid-19 — and an Interesting New Theory Has Emerged (A closer look at the Bradykinin hypothesis)‘
Of Note: The ACE2 Receptor
The Novel Coronavirus SAR-Cov2 attaches itself to human ACE2 receptors. Those receptors are found in abundance in the nasal cavity (NOSE) – and thus the reason it is so important to wear a mask that COVERS THE NOSE. (DIY Face Mask For Coronavirus Protection instructions here.)
For More Information on the ‘Bradykinin Hypothesis’:
For a more scientific view and information on this, I’d encourage you to read:
‘Is a Bradykinin Storm Brewing in COVID-19?’ (Excess of the inflammatory molecule bradykinin may explain the fluid build-up in the lungs of patients with coronavirus infections. Clinical trials of inhibitors are putting this hypothesis to the test.)
Neither the disease mechanism nor treatments for COVID-19 are currently known. Here, we present a novel molecular mechanism for COVID-19 that provides therapeutic intervention points that can be addressed with existing FDA-approved pharmaceuticals. The entry point for the virus is ACE2, which is a component of the counteracting hypotensive axis of RAS. Bradykinin is a potent part of the vasopressor system that induces hypotension and vasodilation and is degraded by ACE and enhanced by the angiotensin1-9 produced by ACE2. Here, we perform a new analysis on gene expression data from cells in bronchoalveolar lavage fluid (BALF) from COVID-19 patients that were used to sequence the virus. Comparison with BALF from controls identifies a critical imbalance in RAS represented by decreased expression of ACE in combination with increases in ACE2, renin, angiotensin, key RAS receptors, kinogen and many kallikrein enzymes that activate it, and both bradykinin receptors. This very atypical pattern of the RAS is predicted to elevate bradykinin levels in multiple tissues and systems that will likely cause increases in vascular dilation, vascular permeability and hypotension. These bradykinin-driven outcomes explain many of the symptoms being observed in COVID-19.
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JT
