> A large study based on samples from patients with long COVID revealed systemic inflammation and immune dysregulation. Several other studies have found elevated levels of various plasma inflammatory markers in long COVID

🔗 https://www.nature.com/articles/s44324-024-00038-x

> Here, we have reviewed the observations of mitochondrial dysfunction in the pathology of COVID-19. During the acute phase, mitochondrial dysfunction has been demonstrated to be directly correlated with viral entry into the mitochondria of the host cells. Both in the acute and post-acute phases, the impairment of mitochondrial function is linked to the immune response of the infection. Observations have associated cGas-Sting activation via mtDNA release to COVID-19, a pathway known to be activated in various diseases, including kidney, heart, and lung diseases. This constitutes a credible correlation between the acute, and the post-acute phase of COVID-19 and decreased organ function. Furthermore, inflammatory signaling via the RIG-I pathway is dependent on mitochondrial health and plays a key role in the inflammatory response to SARS-CoV-2 infection. The importance of these innate immune pathways is highlighted by the multitude of evasion strategies SARS-CoV-2 has evolved to evade their activation. Blocking the acute innate immune response during infection, allowing continued viral replication and ongoing attraction of immune cells to damage the microenvironment, may create the necessary conditions for sustained and excessive inflammation in the post-acute phase, via release of DAMPs, including mtDNA and mtRNA, from the damaged tissues.

This indicates that we should NOT expect LC rates to decrease over time as SARS2 mutates, because its fitness is contingent on immune interference that probably contribues to LC.

In other words it would be a LESS FIT virus if it did NOT cause LC. Water runs downhill; viruses do not evolve to become less fit.

#LongCOVID #COVID #COVID19 #CovidIsNotOver

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