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

COVID-19会导致凝血细胞‘过度活跃’

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.

犹他大学医疗专家介绍，由COVID-19所引起的血小板变化可能导致某些存在疾病的患者出现心脏病、中风以及其他严重的并发症。研究人员发现，感染期间所产生的炎症蛋白会极大改变血小板的功能，使其过度活跃并更容易形成危险并具有潜在致命性的血凝块。

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.

研究人员表示，对这些变化进行更加深入的了解可能会帮助COVID-19患者出现上述病症。研究报告发表于《血液》，美国血液学会的期刊上。

"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."

“我们的发现对于我们发现C0VID-19这一谜团具有重要意义。我们发现，由于感染所引发的炎症和系统变化都会对血小板的功能产生影响并导致他们在更短的时间内聚集，而这也解释了为什么COVID患者中血块的数量在不断增加”，Robert A.Campbell，博士、研究资深作者及内科助教表示。

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.

已经有证据表明，C0VID-19和血液凝结风险增加有关，而这会导致某些患者，尤其是已经存在健康问题，比如糖尿病、肥胖症或高血压的患者出现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.

为了了解清楚原因，研究者们对在盐湖城犹他大学医院住院的41位COVID-19患者进行研究。在这41位患者中，有17在ICU，其中包括9位需要靠呼吸机呼吸的患者。研究人员将这些患者的血液同年龄和性别与之相匹配的健康个人所抽取的血样进行对比。

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.

通过利用差异基因分析，研究人员发现SARS-CoV-2,即引起C0VID-19的病毒似乎会导致血小板内的基因发生变化。在实验室研究中，研究人员研究了血小板凝聚，这是血块形成的一个重要部分并观察到COVID-19患者的血小板更加容易聚集。研究人员还注意到，这些变化会极大改变血小板和免疫系统相互作用的方式，并可能导致呼吸道发炎并反过来造成更加严重的肺部伤害。

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.

让人感到惊讶的是，Campbell和他的同事并没有发现病毒在绝大多数血小板中存在的证据，这也就说明，它可能会在这些细胞内部间接引起基因变化。

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.

据Bhanu Kanth Manne，博士，研究领先作者之一兼犹他大学分子药物项目研究助理介绍，一个可能的机理就是炎症。在理论上，由COVID-19引起的炎症可能会影响巨核细胞，一种可以产生血小板的细胞。因此，重大的基因变化由巨核细胞传递给了血小板，并反过来导致血小板过度活跃。

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.

在试管研究中，研究人员发现，提前用阿司匹林对感染SARS-CoV-2患者的血小板进行提前治疗可以防止其过度活跃。这些研究结果表明，阿司匹林可能会改善治疗结果；然而，这还需要在临床试验中进行进一步研究。目前，Campbell不建议使用阿司匹林治疗COVID-19,除非有医生建议。

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

同时，研究人员也开始在寻找其他可能的治疗方案。

"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."

我们所针对的基因过程可能会防止血小板发生变化，Campbell表示。如果我们能够发现COVID-19如何与巨核细胞或血小板发生作用，我们也许可以避免这一反应并降低患者血液出现血凝块的风险。

来源：科学日报    编辑：质控部Susan