Here's an article from Nature.

• NEWS
• 18 July 2024

Long COVID lung damage linked to immune system response

https://www.nature.com/articles/d41586-024-02352-2?utm_source=Live+Audience&utm_campaign=0fca53b761-nature-briefing-translational-research-20242407&utm_medium=email&utm_term=0_b27a691814-0fca53b761-49227427

So I searched my RVX-208 DD file for protein IFN-y and this is what is said of Apabetalone's effects (my bolding):

 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7657365/

Macrophages present in the atherosclerotic plaque are largely derived from circulating monocytes infiltrating blood vessels’ walls [7, 75]. In mice, monocytes have been shown to enter into the plaque more readily in the context of diabetes and hypercholesterolemia [76–78]. In non-stimulated conditions, apabetalone suppressed protein secretion of key monocyte chemoattractants MCP-1, MCP-3, GRO-α and IL-8 (87%, 79%, 55% and 32% reduction in DM2 + CVD monocytes, respectively). Apabetalone treatment also potently downregulated the transcription of genes differentially induced by IFNγ in DM2 + CVD monocytes, including the pro-inflammatory cytokine TNF gene (33% reduction), and monocyte chemokine genes CCL7 and CCL8 (90% and 85% reduction, respectively). Additional chemokines that promote chemotaxis and tissue extravasation, CCL2 [62, 64], CXCL9 [79] and CXCL10 [79], were induced by IFNγ in both monocyte populations and were strongly suppressed by apabetalone (91%, 80% and 61% reduction, respectively) (Table (Table3).3). BETi treatment is thus predicted to reduce the migratory phenotype of DM2 + CVD monocytes, potentially preventing atherosclerotic plaque infiltration by activated monocytes.

Seems like apabetalone would be a great solution.

I just can't stop thinking about the annual billions in value being lit on fire and the literally millions of people needlessly suffering....all for the sake of a sole person's ego and self-interest. 

Atrocious, Don!

JMHO