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

COVID-19會導(dǎo)致凝血細(xì)胞‘過度活躍’

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.

猶他大學(xué)醫(yī)療專家介紹，由COVID-19所引起的血小板變化可能導(dǎo)致某些存在疾病的患者出現(xiàn)心臟病、中風(fēng)以及其他嚴(yán)重的并發(fā)癥。研究人員發(fā)現(xiàn)，感染期間所產(chǎn)生的炎癥蛋白會極大改變血小板的功能，使其過度活躍并更容易形成危險并具有潛在致命性的血凝塊。

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.

研究人員表示，對這些變化進(jìn)行更加深入的了解可能會幫助COVID-19患者出現(xiàn)上述病癥。研究報(bào)告發(fā)表于《血液》，美國血液學(xué)會的期刊上。

"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."

“我們的發(fā)現(xiàn)對于我們發(fā)現(xiàn)C0VID-19這一謎團(tuán)具有重要意義。我們發(fā)現(xiàn)，由于感染所引發(fā)的炎癥和系統(tǒng)變化都會對血小板的功能產(chǎn)生影響并導(dǎo)致他們在更短的時間內(nèi)聚集，而這也解釋了為什么COVID患者中血塊的數(shù)量在不斷增加”，Robert A.Campbell，博士、研究資深作者及內(nèi)科助教表示。

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.

已經(jīng)有證據(jù)表明，C0VID-19和血液凝結(jié)風(fēng)險增加有關(guān)，而這會導(dǎo)致某些患者，尤其是已經(jīng)存在健康問題，比如糖尿病、肥胖癥或高血壓的患者出現(xiàn)心血管疾病和器官衰竭。

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.

為了了解清楚原因，研究者們對在鹽湖城猶他大學(xué)醫(yī)院住院的41位COVID-19患者進(jìn)行研究。在這41位患者中，有17在ICU，其中包括9位需要靠呼吸機(jī)呼吸的患者。研究人員將這些患者的血液同年齡和性別與之相匹配的健康個人所抽取的血樣進(jìn)行對比。

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.

通過利用差異基因分析，研究人員發(fā)現(xiàn)SARS-CoV-2,即引起C0VID-19的病毒似乎會導(dǎo)致血小板內(nèi)的基因發(fā)生變化。在實(shí)驗(yàn)室研究中，研究人員研究了血小板凝聚，這是血塊形成的一個重要部分并觀察到COVID-19患者的血小板更加容易聚集。研究人員還注意到，這些變化會極大改變血小板和免疫系統(tǒng)相互作用的方式，并可能導(dǎo)致呼吸道發(fā)炎并反過來造成更加嚴(yán)重的肺部傷害。

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.

讓人感到驚訝的是，Campbell和他的同事并沒有發(fā)現(xiàn)病毒在絕大多數(shù)血小板中存在的證據(jù)，這也就說明，它可能會在這些細(xì)胞內(nèi)部間接引起基因變化。

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.

據(jù)Bhanu Kanth Manne，博士，研究領(lǐng)先作者之一兼猶他大學(xué)分子藥物項(xiàng)目研究助理介紹，一個可能的機(jī)理就是炎癥。在理論上，由COVID-19引起的炎癥可能會影響巨核細(xì)胞，一種可以產(chǎn)生血小板的細(xì)胞。因此，重大的基因變化由巨核細(xì)胞傳遞給了血小板，并反過來導(dǎo)致血小板過度活躍。

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.

在試管研究中，研究人員發(fā)現(xiàn)，提前用阿司匹林對感染SARS-CoV-2患者的血小板進(jìn)行提前治療可以防止其過度活躍。這些研究結(jié)果表明，阿司匹林可能會改善治療結(jié)果；然而，這還需要在臨床試驗(yàn)中進(jìn)行進(jìn)一步研究。目前，Campbell不建議使用阿司匹林治療COVID-19,除非有醫(yī)生建議。

In the meantime, the researchers are beginning to look for other possible treatments.

同時，研究人員也開始在尋找其他可能的治療方案。

"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."

我們所針對的基因過程可能會防止血小板發(fā)生變化，Campbell表示。如果我們能夠發(fā)現(xiàn)COVID-19如何與巨核細(xì)胞或血小板發(fā)生作用，我們也許可以避免這一反應(yīng)并降低患者血液出現(xiàn)血凝塊的風(fēng)險。

來源：科學(xué)日報(bào)    編輯：質(zhì)控部Susan