After your COVID-19 infection have your doctor explain EXACTLY to you how prevention of that large artery stroke is going to happen.
Shared genetic background between SARS-CoV-2 infection and large artery stroke
Abstract
Background and aims:
Increased
risk of stroke, particularly large artery stroke (LAS), has been
observed in patients with COVID-19. The biological processes underlying
the observed higher risk are still unknown. We explored the association
between stroke subtypes and COVID-19 susceptibility to understand
whether biological mechanisms specific to SARS-CoV-2 uptake/infection
could be leading to excess stroke risk in this population.
Patients and methods:
We
constructed a polygenic risk score (PRS) of COVID-19 susceptibility and
tested its association with stroke subtypes using individual- and
summary-level genetic data (SiGN, MEGASTROKE). We generated
co-expression networks of genes involved in SARS-CoV-2 uptake/infection (ACE2, TMPRSS2, BEST3, ISLR2 and ADAM17)
based on existing tissue expression libraries. Gene-based association
testing was performed using S-PrediXcan and VEGAS2. Permutation
independence tests were performed to assess SARS-CoV-2-related gene
enrichment in stroke and its subtypes.
Results:
Our
PRS demonstrated an association between COVID-19 susceptibility and LAS
in SiGN (OR = 1.05 per SD increase, 95% CI: (1.00, 1.10), p = 0.04) and
MEGASTROKE (β = 0.510, 95% CI: (0.242, 0.779), FDR-p = 0.0019). The
SARS-CoV-2 risk-related ISLR2 co-expression gene network was
significantly associated with genetic risk of LAS in aorta, tibial
arteries, and multiple brain regions (P < 0.05).
Conclusion:
Presence
of genetic correlation and significant pathway enrichment suggest that
increases in LAS risk reported in COVID-19 patients may be intrinsic to
the viral infection, rather than a more generalized response to severe
illness.
No comments:
Post a Comment