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September 2, 2020 01:00 pm

A Supercomputer Analyzed COVID-19, and an Interesting New Hypothesis Has Emerged

Thelasko shares a report from Medium: Earlier this summer, the Summit supercomputer at Oak Ridge National Lab in Tennessee set about crunching data on more than 40,000 genes from 17,000 genetic samples in an effort to better understand Covid-19. Summit is the second-fastest computer in the world, but the process -- which involved analyzing 2.5 billion genetic combinations -- still took more than a week. When Summit was done, researchers analyzed the results. It was, in the words of Dr. Daniel Jacobson, lead researcher and chief scientist for computational systems biology at Oak Ridge, a 'eureka moment.' The computer had revealed a new theory about how Covid-19 impacts the body: the bradykinin hypothesis. The hypothesis provides a model that explains many aspects of Covid-19, including some of its most bizarre symptoms. It also suggests 10-plus potential treatments, many of which are already FDA approved. Jacobson's group published their results in a paper in the journal eLife in early July. According to the team's findings, a Covid-19 infection generally begins when the virus enters the body through ACE2 receptors in the nose, (The receptors, which the virus is known to target, are abundant there.) The virus then proceeds through the body, entering cells in other places where ACE2 is also present: the intestines, kidneys, and heart. This likely accounts for at least some of the disease's cardiac and GI symptoms. But once Covid-19 has established itself in the body, things start to get really interesting. According to Jacobson's group, the data Summit analyzed shows that Covid-19 isn't content to simply infect cells that already express lots of ACE2 receptors. Instead, it actively hijacks the body's own systems, tricking it into upregulating ACE2 receptors in places where they're usually expressed at low or medium levels, including the lungs. The renin-angiotensin system (RAS) controls many aspects of the circulatory system, including the body's levels of a chemical called bradykinin, which normally helps to regulate blood pressure. According to the team's analysis, when the virus tweaks the RAS, it causes the body's mechanisms for regulating bradykinin to go haywire. Bradykinin receptors are resensitized, and the body also stops effectively breaking down bradykinin. (ACE normally degrades bradykinin, but when the virus downregulates it, it can't do this as effectively.) The end result, the researchers say, is to release a bradykinin storm -- a massive, runaway buildup of bradykinin in the body. According to the bradykinin hypothesis, it's this storm that is ultimately responsible for many of Covid-19's deadly effects. Several drugs target aspects of the RAS and are already FDA approved, including danazol, stanozolol, and ecallantide, which reduce bradykinin production and could potentially stop a deadly bradykinin storm. Interestingly, the researchers suggest vitamin D as a potentially useful Covid-19 drug. "The vitamin is involved in the RAS system and could prove helpful by reducing levels of another compound, known as REN," the report says. "Again, this could stop potentially deadly bradykinin storms from forming." Other compounds could treat symptoms associated with bradykinin storms, such as Hymecromone and timbetasin.

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