<story><title>Supercomputer analysis of Covid-19 leads to new theory</title><url>https://elemental.medium.com/a-supercomputer-analyzed-covid-19-and-an-interesting-new-theory-has-emerged-31cb8eba9d63</url></story><parent_chain></parent_chain><comment><author>woeirua</author><text>Seems like it should be really straightforward to determine if this hypothesis is right by measuring bradykinin levels in Covid patients versus non-Covid patients.&lt;p&gt;One thing that I think strongly suggests that this hypothesis is wrong is that there is no strong relation between ACE-inhibitors and Covid mortality. Indeed, most of the studies that I&amp;#x27;ve seen suggest that ACE-inhibitors have a somewhat protective effect whereas ARBs actually seem to have a minor detrimental effect [1]. So for the article to claim that covid behaves pharmacologically like ACE-inhibitors seems wrong at face value.&lt;p&gt;[1] &lt;a href=&quot;https:&amp;#x2F;&amp;#x2F;www.nejm.org&amp;#x2F;doi&amp;#x2F;full&amp;#x2F;10.1056&amp;#x2F;NEJMoa2007621&quot; rel=&quot;nofollow&quot;&gt;https:&amp;#x2F;&amp;#x2F;www.nejm.org&amp;#x2F;doi&amp;#x2F;full&amp;#x2F;10.1056&amp;#x2F;NEJMoa2007621&lt;/a&gt;</text></comment>
<story><title>Supercomputer analysis of Covid-19 leads to new theory</title><url>https://elemental.medium.com/a-supercomputer-analyzed-covid-19-and-an-interesting-new-theory-has-emerged-31cb8eba9d63</url></story><parent_chain></parent_chain><comment><author>zby</author><text>They found out that some genes related to ACE in comparison to genes related to ACE2 are more &amp;#x27;expressed&amp;#x27; in Covid patients than normally and they conclude that that must have resulted in too much bradykinine. Hmm - that strikes me as kind of roundabout - why they couldn&amp;#x27;t just measure bradykinine levels directly? Is that too hard?&lt;p&gt;&amp;quot;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.&amp;quot;</text></comment>