Unique molecular profiling of monocyte responses to a high dose of DENV-NS1 reflected the effect of NS1 on hemostasis
1
Issued Date
2026-12-01
Resource Type
ISSN
03008584
eISSN
14321831
Scopus ID
2-s2.0-105039927673
Journal Title
Medical Microbiology and Immunology
Volume
215
Issue
1
Rights Holder(s)
SCOPUS
Bibliographic Citation
Medical Microbiology and Immunology Vol.215 No.1 (2026)
Suggested Citation
Saisingha K., Kaofai C., Modhiran N., Watterson D., Paiboonpol S., Pawaputanun A., Leaungwutiwong P., Hanboonkunupakarn B., Mansanguan C., Limthongkul J., Ponpuak M., Jearanaiwitayakul T., Ubol S. Unique molecular profiling of monocyte responses to a high dose of DENV-NS1 reflected the effect of NS1 on hemostasis. Medical Microbiology and Immunology Vol.215 No.1 (2026). doi:10.1007/s00430-026-00876-0 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/117037
Title
Unique molecular profiling of monocyte responses to a high dose of DENV-NS1 reflected the effect of NS1 on hemostasis
Corresponding Author(s)
Other Contributor(s)
Abstract
The pathogenesis of dengue is complex and requires further study. Infection with the dengue virus can lead to severe dengue, in which patients experience severe plasma leakage and excessive bleeding. The dengue virus non-structural protein 1 (DENV NS1) is among several factors that affect the outcome. The secreted form of this protein induces severe cases through direct and indirect immunopathogenesis mechanisms. Previously, we discovered that the stimulation of blood monocytes by NS1 upregulates transcripts involved in inflammation, and suppresses transcripts involved in antiviral processes. In this study, we examined the specific responses unique to high-dose NS1 exposure of cultured human monocytes. We found that genes involved in hemostasis were altered following NS1 exposure and were associated with platelet activation, fibrinolysis, and hemostatic regulation. Some of these expression changes were also observed in patients with dengue fever (DF) or dengue hemorrhagic fever (DHF). The altered expression of these genes suggests that fibrinolysis is more likely balanced during DF, whereas coagulation may be impaired in DHF.