Changes in blood
platelets triggered by COVID-19 could contribute to the onset of heart attacks,
strokes, and other serious complications in some patients who have the disease,
according to University of Utah Health scientists. The researchers found that
inflammatory proteins produced during infection significantly alter the
function of platelets, making them “hyperactive” and more prone to form
dangerous and potentially deadly blood clots.
They say better understanding
the underlying causes of these changes could possibly lead to treatments that
prevent them from happening in COVID-19 patients. Their report appears in Blood,
an American Society of Hematology journal.
“Our finding adds an important piece to the jigsaw
puzzle that we call COVID-19,” says Robert A. Campbell, Ph.D., senior author of
the study and an assistant professor in the Department of Internal Medicine.
“We found that inflammation and systemic changes, due to the infection, are
influencing how platelets function, leading them to aggregate faster, which
could explain why we are seeing increased numbers of blood clots in COVID
patients.”
Emerging evidence suggests COVID-19 is associated with
an increased risk of blood clotting, which can lead to cardiovascular problems
and organ failure in some patients, particularly among those with underlying
medical problems such as diabetes, obesity, or high blood pressure.
To find out what might be going on, the researchers
studied 41 COVID-19 patients hospitalized at University of Utah Hospital in
Salt Lake City. Seventeen of these patients were in the ICU, including nine who
were on ventilators. They compared blood from these patients with samples taken
from healthy individuals who were matched for age and sex.
Using differential gene analysis, the researchers
found that SARS-CoV-2, the virus that causes COVID-19, appears to trigger
genetic changes in platelets. In laboratory studies, they studied platelet
aggregation, an important component of blood clot formation, and observed
COVID-19 platelets aggregated more readily. They also noted that these changes
significantly altered how platelets interacted with the immune system, likely
contributing to inflammation of the respiratory tract that may, in turn, result
in more severe lung injury.
Surprisingly, Campbell and his colleagues didn’t
detect evidence of the virus in the vast majority of platelets, suggesting that
it could be promoting the genetic changes within these cells indirectly.
One possible mechanism is inflammation, according to
Bhanu Kanth Manne, Ph.D., one of the study’s lead authors and a research
associate with the University of Utah Molecular Medicine Program (U2M2). In
theory, inflammation caused by COVID-19 could affect megakaryocytes, the cells
that produce platelets. As a result, critical genetic alterations are passed down
from megakaryocytes to the platelets, which, in turn, make them hyperactive.
In test tube studies, the researchers found that
pre-treating platelets from SARS-CoV-2 infected patients with aspirin did
prevent this hyperactivity. These findings suggest aspirin may improve
outcomes; however, this will need further study in clinical trials. For now,
Campbell warns against using aspirin to treat COVID-19 unless recommended by
your physician.
In the meantime, the researchers are beginning to look
for other possible treatments.
“There are genetic processes that we can target that
would prevent platelets from being changed,” Campbell says. “If we can figure
out how COVID-19 is interacting with megakaryocytes or platelets, then we might
be able to block that interaction and reduce someone’s risk of developing a
blood clot.”
Journal article: https://ashpublications.org/blood/article/doi/10.1182/blood.2020007214/461106/Platelet-Gene-Expression-and-Function-in-COVID-19
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