A comparison of 21 people with long COVID and 24 asymptomatic controls found lower white-cell, monocyte, and platelet counts and longer APTT. Integrated with a separate public transcriptomic dataset, the findings support a proposed inflammation-coagulation model, but the small and non-identical datasets cannot establish mechanism.
Key findings
- Long-COVID participants had lower total white-cell counts (p=0.031), monocytes (p=0.008), and platelets (p=0.040), plus longer APTT (p=0.016). Transcriptomic analysis enriched inflammation, cellular-stress, and coagulation pathways and identified IL6, MYC, CDKN1A, SERPINE1, CD44, and PLAUR as network hubs.
Why this matters globally
The work supplies hypotheses and candidate markers for prospective studies of long-COVID subgroups and immune-coagulation crosstalk. It does not yet provide a clinically usable biomarker panel or therapeutic target.
Thai researcher contribution
University of Phayao researchers integrated hematology with bioinformatics, combining medical technology, occupational public health, and immunodiagnostic expertise.
Limitations to consider
The clinical sample comprised only 45 people, and the comparative design cannot establish temporality. Matching, comorbidities, medication, time since infection, and multiple-testing control are not reported in the abstract. Transcriptomics came from a separate public dataset, so CD44, SERPINE1, and PLAUR expression does not directly prove endothelial adhesion or hypofibrinolysis.