Imaging the interaction between dengue 2 virus and human blood platelets using atomic force and electron microscopy

Area of Science:

• Virology
• Hematology
• Immunology

Background:

• Thrombocytopenia is a common complication of dengue virus infection.
• The precise mechanisms by which dengue virus causes thrombocytopenia are not fully understood.
• The direct role of dengue virus in platelet interaction and function alteration requires further investigation.

Purpose of the Study:

• To investigate the direct effects of dengue virus type 2 (DENV-2) on human platelet morphology and activation.
• To determine if DENV-2 can directly interact with and alter platelet hemostatic properties.

Main Methods:

• Human platelets from healthy donors were exposed to DENV-2 in vitro.
• Platelet activation and morphology were assessed using flow cytometry, atomic force microscopy (AFM), scanning electron microscopy (SEM), and transmission electron microscopy (TEM).
• Japanese encephalitis virus (JEV) was used as a control to assess specificity.

Main Results:

• DENV-2 exposure led to increased P-selectin expression and fibrinogen binding, indicating platelet activation.
• Microscopy revealed activation-related morphological changes in DENV-2-exposed platelets, including altered membrane architecture, degranulation, filopodia formation, and open canalicular system dilatation.
• JEV exposure did not induce platelet activation or morphological changes.

Conclusions:

• Dengue virus type 2 can directly interact with and activate human platelets.
• This direct platelet activation by DENV-2 may play a significant role in the development of dengue-associated thrombocytopenia.
• Further molecular studies are needed to understand this interaction and develop strategies to prevent hemostatic complications.