Guo Liping, Gu Yuchen, Zhang Ying, Zhang Haimei, Weng Weizhen, Wu Shuai, Yuan Jing
Department of Microbiology, School of Basic Medicine, Guangxi Medical University, Nanning, China.
Shenzhen Key Laboratory of Pathogen and Immunity, National Clinical Research Center for Infectious Disease, State Key Discipline of Infectious Disease, Shenzhen Third People's Hospital, Second Hospital Affiliated to Southern University of Science and Technology, Shenzhen, China.
New Microbes New Infect. 2025 Aug 23;67:101624. doi: 10.1016/j.nmni.2025.101624. eCollection 2025 Oct.
Dengue fever, the most prevalent arthropod-borne viral disease, causes ∼400 million infections annually. Although thrombocytopenia is commonly associated with dengue, how it evolves in relation to viral load and immune responses remains poorly understood. This study aimed to elucidate platelet-virus-immune interactions in acute dengue by systematically tracking of viral load, platelet parameters, and leukocyte dynamics.
A prospective cohort study was conducted at Third People's Hospital in 2024, involving 135 confirmed dengue cases, supported by retrospective data from 2014 to 2023. Platelet counts, hematocrit (HCT), and cellular immunity markers (lymphocyte/neutrophil percentages) were longitudinally tracked. Viral load was quantified via NS5 gene Ct values. Statistical analyses involved LOESS regression and Pearson/Spearman correlations.
Platelet counts exhibited a biphasic decline, reaching nadir levels (mean: 97.65 × 10/L) at 6 days post-onset, with recovery by day 9. Thrombocytopenia severity was stratified as intermediate-low (50-99 × 10/L; 50 %, 64/128) and very low (<50 × 10/L; 14.8 %, 19/128). Platelet decline correlated with elevated lymphocyte percentages (40 % vs. 17.8 % pre-decline; p < 0.001) and suppressed neutrophils (46.6 % vs. 68.3 %; p < 0.001). Critically, platelet counts inversely correlated with viral load (Ct values: R = 0.25, p = 0.028), HCT (R = -0.25), and platelet activation markers (MPV: R = -0.55; P-LCR: R = -0.57), while positively associating with platelet hematocrit (PCT: R = 0.97). No cases progressed to severe dengue despite extreme thrombocytopenia.
This study identifies distinct dengue thrombocytopenia kinetics driven by viral load. Predominant moderate thrombocytopenia (50-99 × 10/L) challenges conventional risk stratification, advocating integrated monitoring of platelet indices and viral replication. These data advance both risk prediction and mechanistic knowledge of platelet-virus interactions.
登革热是最常见的节肢动物传播的病毒性疾病，每年造成约4亿人感染。尽管血小板减少症通常与登革热有关，但它与病毒载量和免疫反应的关系如何演变仍知之甚少。本研究旨在通过系统追踪病毒载量、血小板参数和白细胞动态，阐明急性登革热中血小板-病毒-免疫相互作用。
2024年在第三人民医院进行了一项前瞻性队列研究，纳入135例确诊登革热病例，并得到2014年至2023年回顾性数据的支持。纵向追踪血小板计数、血细胞比容（HCT）和细胞免疫标志物（淋巴细胞/中性粒细胞百分比）。通过NS5基因Ct值对病毒载量进行定量。统计分析包括局部加权回归（LOESS回归）和Pearson/Spearman相关性分析。
血小板计数呈双相下降，发病后6天达到最低点（平均：97.65×10⁹/L），第9天恢复。血小板减少症的严重程度分为中低水平（50-99×10⁹/L；50%，64/128）和极低水平（<50×10⁹/L；14.8%，19/128）。血小板下降与淋巴细胞百分比升高（下降前为40%，下降后为17.8%；p<0.001）和中性粒细胞受抑制（46.6%对68.3%；p<0.001）相关。至关重要的是，血小板计数与病毒载量（Ct值：R=0.25，p=0.028）、HCT（R=-0.25）和血小板活化标志物（平均血小板体积：R=-0.55；血小板大细胞比率：R=-0.57）呈负相关，而与血小板血细胞比容（血小板压积：R=0.97）呈正相关。尽管血小板减少极为严重，但无一例进展为重症登革热。
本研究确定了由病毒载量驱动的独特的登革热血小板减少动力学。主要为中度血小板减少（50-99×10⁹/L）对传统风险分层提出了挑战，主张对血小板指标和病毒复制进行综合监测。这些数据推进了血小板-病毒相互作用的风险预测和机制知识。
