Platelet Dynamics and Thrombocytopenia in Dengue Fever: A Prospective Cohort Study from Shenzhen, China

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 × 109/L) at 6 days post-onset, with recovery by day 9. Thrombocytopenia severity was stratified as intermediate-low (50-99 × 109/L; 50 %, 64/128) and very low (<50 × 109/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 × 109/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.