COVID-19 causes 'hyperactivity' in blood-clotting cells

Date:
June 30, 2020
Source:
University of Utah Health
Summary:
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 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.



FULL STORY ========================================================================== [Illustration of | Credit: (c) SciePro / stock.adobe.com] Illustration
of platelets and red blood cells (stock image).

Credit: (c) SciePro / stock.adobe.com [Illustration of | Credit: (c)
SciePro / stock.adobe.com] Illustration of platelets and red blood cells
(stock image).

Credit: (c) SciePro / stock.adobe.com Close 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." This study titled, "Platelet Gene Expression
and Function in COVID-19 Patients," was funded by the National Institutes
of Health, the University of Utah Health 3i Initiative, and the American
Heart Foundation.


========================================================================== Story Source: Materials provided by University_of_Utah_Health. Note:
Content may be edited for style and length.


========================================================================== Journal Reference:
1. Robert A. Campbell, Matthew T. Rondina, Christian Con Yost,
Andrew S.

Weyrich, Mark J. Cody, Li Guo, Neal D. Tolley, Aaron C. Petrey,
Chris J.

Stubben, Jesse W Rowley, Irina Portier, Elizabeth A Middleton,
Frederik Denorme, Bhanu Kanth Manne. Platelet Gene Expression
and Function in COVID-19 Patients. Blood, 2020; DOI:
10.1182/blood.2020007214 ==========================================================================

Link to news story: https://www.sciencedaily.com/releases/2020/06/200630125129.htm

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