The biological mechanism linking shingles or shingles (triggered by the varicella virus) to increased risk of stroke has been identified.
Chicken pox virus. Credit: wikipedia
Almost all of us get chickenpox in childhood, a rash disease caused by the varicella zoster virus (VZV), a DNA, not RNA, pathogen such as the SARS-CoV-2 coronavirus (causes of COVID-19) or influenza viruses . Although the characteristic rash usually heals within a few weeks, the chickenpox virus is actually much more subtle than generally imagined. Indeed, it does not completely disappear from our body once the disease has been overcome, but remains at rest in the body, above all confined to the nervous system, where at a certain point in our life it can be reactivated – especially in frail subjects – and trigger the herpes zoster, known as “shingles”. About 30% of those who have had chickenpox have it. This herpes usually occurs after the age of 50, and anyone infected with chickenpox in childhood – 90% of the world’s population – is at risk. While shingles can already be very painful and can reduce quality of life, patients with shingles also have an 80% higher risk of stroke than the general population, as explained in an article in The Conversation by Professor Andrew Bubak, professor of neurology at the Anschutz Medical Campus of the University of Colorado.
In very simple terms, the varicella virus can expose us to a significant risk of life, given the potential consequences of ischemic stroke. How the varicella zoster virus (VZV) catalyzes the development of stroke — or stroke — hasn’t been clear for many years, but now researchers may have unraveled the biological mechanism behind the link. It was identified by an American research team led by scientists from the University of Colorado, who collaborated with colleagues from the University of Texas Health Science Center. Researchers led by Professor Bubak found that reactivation of the varicella zoster virus “triggers the formation of cellular sacs or exosomes that carry proteins that contribute to blood clotting and inflammation,” as explained in The Conversation. These vesicles are like cargo shuttles that transfer proteins and nucleic acids from cells to tissues. Among these “goods” there are also proteins that promote blood clotting, which in turn can lead to clinical cases. Ischemic stroke can be caused by narrowing of the arteries or a blood clot blocking blood flow.
The researchers found that patients with shingles had nine times higher levels of exosomes carrying clotting-related proteins than healthy patients. To understand whether these exosomes could trigger potentially dangerous clots, Professor Bubak and his colleagues exposed platelets from healthy people to exosomes from shingles patients and healthy subjects. They observed that platelets exposed to the exosomes of patients with shingles are induced to clump with other blood cells, forming clots. Simply put, reactivation of the chickenpox virus in someone with shingles can promote clot formation, which in turn can catalyze the risk of stroke. It is not known how long the risk of developing potentially dangerous clots lasts after the herpes is gone. Further studies will be conducted to better understand the correlation. Researchers recommend chickenpox vaccination to reduce potential health risks. Details of the research “Prothrombotic plasma exosomes associated with shingles and increased risk of stroke” in the authoritative scientific journal Journal of Infectious Disease.
