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University of Nebraska Medical Center

Long COVID: Mitochondria, the Big Miss, and Hope

Medscape

This week there was news on Long COVID in two very different directions: emergence of strong data to support mitochondrial dysfunction as the basis for the condition in some people, and learning how the $1.15 billion allocation to the NIH RECOVER initiative has largely been wasted. In this edition of Ground Truths, I’ll review this news and offer a plan to get clinical trials testing treatments into high gear.

Sick Mitochondria as a Root Cause

When we published our review of Long COVID earlier this year, we highlighted the key established underpinnings as shown in the figure below. As you’ll note, mitochondria was not one of them. There was a body of data emerging to support the role of mitochondria, as we asserted: “Long COVID research has found mitochondrial dysfunction including loss of mitochondrial membrane potential and possible dysfunctional mitochondrial metabolism, altered fatty acid metabolism…” and that this had also been seen in myalgic encephalomyelitis (ME/CFS).

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