细胞免疫功能障碍可能被认为是后covid综合征的征兆吗?

N. Asfandiyarova, M. Rubtsova
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引用次数: 0

摘要

我们的目的是研究COVID后外周血淋巴细胞增殖活性与发生COVID后综合征的关系,并确定细胞免疫功能障碍是否可以作为其标志。这项回顾性队列研究涉及242例感染新型冠状病毒的患者(男性56例,女性186例,年龄在18至85岁之间)。其中,确诊后肺炎综合征180例(病程3个月以上)。根据患者临床病程(即是否存在急性呼吸道疾病和肺炎)的严重程度以及pha诱导的淋巴细胞母细胞转化对患者进行分类。在pha诱导应答的同时,我们用形态学方法研究了产环加氧酶(COG)的细胞。对照组由200名没有任何冠状病毒感染特征的健康人群组成。所有患者均由多学科医疗小组根据其投诉进行询问和检查。我们还记录了与细胞免疫缺陷相关的合并症的发生率。肺炎后综合征患者与对照组相比,pha诱导的淋巴细胞增殖减少(急性呼吸道感染患者p < 0.01,肺炎患者p < 0.05)。在所有组中,cog生成细胞的活性相似,独立于是否存在后covid综合征。通过存在细胞免疫功能障碍(pha诱导的母细胞转化50%)对患者进行分类,可以检测到产生cog的细胞的较高活性。已知这种酶参与炎症促进免疫缺陷的发展,因此,可能在COVID-19后疱疹病毒感染的临床激活中表现出来。cog合成细胞活性在中重度和重度新型冠状病毒感染合并肺炎后出现的后冠状病毒综合征中较高。covid - 19后综合征的慢性炎症与产cog细胞的高活性相关,可能促进细胞免疫功能障碍,从而成为综合征演变的原因,如其生物标志物。在其他covid后特征中,缺乏免疫细胞功能障碍标志物导致covid后患者登记减少,并导致对所获得结果的误解。
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May be dysfunction of cellular immunity considered a sign of post-COVID syndrome?
Our aim was to study association between proliferative activity of peripheral blood lymphocytes after COVID, and developing post-COVID syndrome, and to determine whether the cell immunity dysfunction may be regarded as its marker. The retrospective cohort study involved 242 patients (56 males, 186 females, 18 to 85 years old) who contracted new coronavirus infection. Of them, post-COVID syndrome was diagnosed in 180 cases (duration over 3 months). The patients were classified by severity of clinical course of COVID (i.e., presence of acute respiratory disease and pneumonias), and PHA-induced blast transformation of lymphocytes. Along with PHA-induced response, we studied cyclooxygenase (COG)-producing cells by morphological method. Control group consisted of 200 healthy people without any features of coronavirus infection. All patients were questioned and examined by multidisciplinary medical team, dependent on their complaints. We also registered incidence of comorbidities associated with cellular immune deficiency. The patients with post-COVID syndrome exhibited a decrease of PHA-induced lymphocyte proliferation as compared with control group (significant at p 0.01 in cases of acute respiratory infection, and p 0.05 in patients with pneumonia). Activity of COG-producing cells was similar in all groups, independently on presence of post-COVID syndrome. Classification of patients by presence of cellular immune dysfunction (PHA-induced blast transformation 50%) allowed to detect higher activity of COG-producing cells. This enzyme is known to participate in development of inflammation promoting immune deficiency, thus, probably, manifesting in clinical activation of herpesvirus infection following COVID-19. Activity of COG-synthesizing cells was found to be higher in post-COVID syndrome which evolves after middle-severe and severe forms of new coronavirus infection complicated by pneumonias. Chronic inflammation in post-COVID syndrome associated with high activity of COG-producing cells may promote dysfunction of cell immunity, thus being a cause of evolving syndrome, like as its biomarker. Absence of the immune cell dysfunction markers among other post-COVID features leads to decreased registration of post-COVID patients and misinterpretation of the results obtained.
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