We should also look for risk factors that pile on top of age and comorbidity, risk facts like immune system genetics, that might raise the odds of a cytokine storm caused by COVID.
- Jocelyn Kaiser at SCIENCE provides an article, dateline March 27, on this theme, here.
The journalist includes quotes from CEO Kari Stefansson of Icelandic "DeCode Genetics," from the Finnish FinnGen initiative, the UK Biobank effort, and others. Targets include scanning the whole genome for currently unguessable risk factors, balanced by looking at obvious genomic candidates, like variations in the ACE2 receptor (angiotensin converting enzyme receptor) that COVID must bind to before entering a cell.
Searching for co-pathogens that spike the risk of a patient's deterioration could also be fruitful and could be undertaken by NGS pathogen metagenomics, given that end stage patients are often on high dose antibiotics that can interfere with culture (e.g. Karius and others). There's some preliminary journal publications that a patient's early procalcitonin bioresponse to infection (more commonly tested in US and Asia than USA) may flag early cases that are likely to deteriorate (Pubmed here). The point is that answers could come from many different directions and help us better than "aging or comorbidity."
Adaptive Biotechnologies in Seattle, partnering with Microsoft's massive data systems, has started an open call for samples in an initiative to seek immune system variations that develop during, or predispose to, the COVID response (entry point here).
I had an early blog on this theme March 1 - here.
