Saturday, December 31, 2022

How a dormant viral infection can reactivate and trigger a stroke especially in younger healthy people

Good news! Are we finally learning why healthy young people sometimes suffer heretofore inexplainable strokes

I know someone who was infected with Shingles. And many years later, in his prime and very healthy, he suffered an acute ischemic stroke out of nowhere. The doctor was telling him it was a cryptogenic stroke.

"... In around 30% of people, at some point in their life, the VZV (varicella-zoster) virus reawakens and again causes disease. This time round the illness is called shingles. For most people shingles is characterized by a rash but a number of other health complications can accompany a case of the disease.
“Most people know about the painful rash associated with shingles, but they may not know that the risk of stroke is elevated for a year after infection,” ...
The researchers suspected it had something to do with tiny, sac-like molecules called exosomes. These molecules are formed within cells and carry cargo to tissue in other parts of the body.
The hypothesis was that the reactivated virus triggered the production of exosomes carrying blood clotting proteins. ...
The findings revealed exosomes from shingles patients contained significantly higher volumes of clotting proteins than exosomes from healthy subjects. And even more strikingly, those levels were still elevated when samples were taken from the shingles patients three months after their acute illness had subsided. ..."

"Herpes zoster (HZ; shingles) caused by varicella zoster virus reactivation increases stroke risk for up to 1 year after HZ. The underlying mechanisms are unclear, however, the development of stroke distant from the site of zoster (eg, thoracic, lumbar, sacral) that can occur months after resolution of rash points to a long-lasting, virus-induced soluble factor (or factors) that can trigger thrombosis and/or vasculitis. Herein, we investigated the content and contributions of circulating plasma exosomes from HZ and non-HZ patient samples. Compared with non-HZ exosomes, HZ exosomes (1) contained proteins conferring a prothrombotic state to recipient cells and (2) activated platelets leading to the formation of platelet-leukocyte aggregates. Exosomes 3 months after HZ yielded similar results and also triggered cerebrovascular cells to secrete the proinflammatory cytokines, interleukin 6 and 8. These results can potentially change clinical practice through addition of antiplatelet agents for HZ and initiatives to increase HZ vaccine uptake to decrease stroke risk."

How a dormant viral infection can reactivate and trigger a stroke

Scientists Find Probable Cause of Shingles/Stroke Link Finding could help lower elevated stroke risk with preventive therapies

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