Department of Medicine, Pharmacogenetics Laboratory, Drug Research and Development Center (NPDM), Federal University of Ceará, Fortaleza, CE, Brazil.
Clementino Fraga Group, Central Unity, Molecular Biology Laboratory, Fortaleza, CE, Brazil.
In Vivo. 2024 Nov-Dec;38(6):2853-2863. doi: 10.21873/invivo.13766.
BACKGROUND/AIM: SARS-CoV-2 infection presents different severity levels that suggest the influence of genetic factors on the clinical outcome of the disease. In cases of severe COVID-19, the presence of elevated coagulation markers, increased platelet activation and aggregation and the risk of thrombotic complications are described. Given the participation of these cells in several serious viral infections and their negative role when associated with a prothrombotic response, it is important to understand the mechanistic role of SARS-CoV-2 in platelet physiology. This study evaluated the hyperexpression of platelet-activating factor receptor (PTAFR) and platelet factor 4 (PF4) in unvaccinated and hospitalized patients with COVID-19.
The study included 43 COVID-19 patients stratified according to WHO guidelines. Subsequently, the expression of the PTAFR and PF4 genes were evaluated using the real-time quantitative PCR and their possible correlation with the severity of the disease and clinical variables including hospitalization, outcome, sex, age and laboratory parameters (platelet count, INR and D-dimer).
The analysis demonstrated a significant (p<0.05) hyperexpression of these genes COVID-19 patients (n=43) compared to healthy controls. Expression of these genes in patients was not statistically significant (p>0.05) different between patients stratified according to clinical variables.
The expression of PTAFR and PF4 suggests an important molecular pathway in the pathophysiology of the disease and may be valuable platelet biomarkers to indicate increased risk in patients with COVID-19 who require hospital care, contributing to personalized intervention strategies and improving their clinical management.
背景/目的：SARS-CoV-2 感染呈现出不同的严重程度，这表明遗传因素对疾病的临床结果有影响。在严重 COVID-19 病例中，存在升高的凝血标志物、血小板活化和聚集增加以及血栓并发症风险。鉴于这些细胞参与了多种严重的病毒感染，并且当与促血栓反应相关时具有负面作用，因此了解 SARS-CoV-2 在血小板生理学中的机制作用非常重要。本研究评估了未接种疫苗和住院 COVID-19 患者中血小板激活因子受体（PTAFR）和血小板因子 4（PF4）的过度表达。
该研究纳入了根据世界卫生组织（WHO）指南分层的 43 例 COVID-19 患者。随后，使用实时定量 PCR 评估了 PTAFR 和 PF4 基因的表达，并评估了其与疾病严重程度和临床变量（包括住院、结局、性别、年龄和实验室参数[血小板计数、INR 和 D-二聚体]）的可能相关性。
分析表明，与健康对照组相比，COVID-19 患者（n=43）这些基因的表达显著（p<0.05）增加。根据临床变量分层的患者中，这些基因的表达在统计学上无显著差异（p>0.05）。
PTAFR 和 PF4 的表达表明在疾病的病理生理学中存在重要的分子途径，并且可能是有价值的血小板生物标志物，可指示需要住院治疗的 COVID-19 患者的风险增加，有助于制定个性化干预策略并改善其临床管理。
