Clonal Hematopoiesis Might Explain Extra Risk of COVID-19 Wi
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People with cardiovascular disease and clonal hematopoiesis of indeterminate potential (CHIP) appeared to be primed for the excessive inflammatory response typical of COVID-19, a small study found.

People with the most common acquired mutations in CHIP -- DNMT3A or TET2 sequence variations - had mutated white blood cells with significantly increased expression of inflammatory genes, including:

- Interleukin 1 Beta
- The interleukin 6 (IL-6) receptor
- The NLRP3 inflammasome complex
- CD163, a cellular receptor capable of mediating infection, macrophage activation syndrome, and other genes involved in cytokine response syndrome (CRS).

CHIP, an age-associated condition of expanded somatic blood cell clones (due to acquired leukemic sequence variations) without other hematological abnormalities, has been associated with excess cardiovascular risk, including coronary artery disease, chronic heart failure, and severe calcified aortic valve stenosis.

The implications from the new study are that people with DNMT3A or TET2 CHIP-driver sequence variations may be identified as high-risk for adverse outcomes of COVID-19, and that patients infected with SARS-CoV-2 could be tested for these variations to personalize IL-6-targeted treatment strategies to mitigate CRS, the investigators suggested.

However, this hypothesis linking CHIP and COVID-19 is based on the controversial idea that exuberant inflammation is a major contributing factor to poor outcomes in COVID-19, researchers suggested.

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