New insights into “bradykinin storms” suggest potential therapies for Covid-19

Very interesting reading this and comparing to my wife's experience (5 months since she had covid for less than two weeks - not a terrible case of it, and was up and about towards the end of the 2 weeks even heading out for walks. Very quickly after that she went down hill and been terribly ill ever since).

Many of the symptoms they described match her journey. Her latest diagnosis from a cardiologist is PoTS - but it could well be the bradykinin issues causing very similar symptoms. Interestingly many people on her groups who have been as ill or iller than her, have made almost spontaneous recoveries. I hope she recovers soon.

Sometimes with enough data and powerful enough computers you can brute force ideas that otherwise might take forever to examine. If you can identify the reasons why certain symptoms appear, you can begin to format potential solutions faster. In programming terms once you understand why something is broken, it's much easier to fix.

These are two very cool findings about the genetic mechanisms which might be at work provoking specific lethal symptoms that are pretty unique to COVID.

This is such a great use of the world’s second fastest supercomputer and a fascinating discovery achieved through genetic data mining!

It might be the coolest thing you read today and even if it doesn’t immediately lead to a treatment breakthrough, it’s at least heartening to know our world’s best resources are being deployed in this fashion.

Grateful for anyone that studies this but there has been so much false hope in the past six months that I came to ignore all these findings.

The original paper A mechanistic model and therapeutic interventions for COVID-19 involving a RAS-mediated bradykinin storm [1]:

> ...our results indicate that the pathology of COVID-19 is likely the result of Bradykinin Storms rather than cytokine storms (although given the induction of IL2 by BK, the two may be intricately linked).

> Several interventional points (most of them already FDA-approved pharmaceuticals) could be explored with the goal of increasing ACE, decreasing BK, or blocking BK2 receptors (Table 1).

[1] https://elifesciences.org/articles/59177

“We have to get this message out,” Jacobson said. “We have started to be contacted by people. But … clinical partners and funding agencies who will hopefully support this work is the next step that needs to happen.”

Yes! Clinical trials are required to isolate bradykinin dysregulation as a primary cause of COVID-19 morbidity. If that happens, the good news is that drug therapies already exist, which means the death toll from the virus could be cut dramatically in a short time.

It's bizarre that the chief scientist for computational systems biology at a prestigious government research facility such as Oak Ridge National Labs doesn't already have connections to facilitate clinical trials in advance.

This is the true cost of the crony capitalism that has seen sham treatments such as hydroxychloroquine dominate clinical opportunities and administrative bandwidth of the pandemic response.

With ebola was standard the use of blood transfusions from people that developped antibodies against it. This path is not being explored here, and sometimes I wonder why. We have plenty of people that recovered

We're well past the time when good ideas were needed. Our biggest problems at the moment are proving ideas up and logistics.

I have a fairly rosy outlook; we're starting to enter the phase of this where the scientists will have useful observations to make. One of my reasonable worst-case scenarios for the next 12 months is someone develops a $5 5 minute coronavirus test and central health agencies don't notice/delay the rollout/start throwing out arbitrary sensitivity & specificity threshold roadblocks so the pandemic continues for stupid reasons.