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Published on: September 5, 2016
Tirofiban protects mice against severe RSV pneumonia by potentially inhibiting platelet activation via the GPIbα-vWF
Yu-Si Luo1, Huyan Shen2, Ping Ling3
1Emergency ICU, Department of Cardiology, The Affiliated Hospital of Guizhou Medical University, Guiyang, 550004, China; Guizhou Key Laboratory of Microbio and Infectious Disease Prevention & Control, Virology Institute, Department of Parasitology, Department of Pharmacology, School of Basic Medical Sciences, Guizhou Medical University, Guiyang, 561113, China; Department of Emergency, Liupanshui Hospital of the Affiliated Hospital of Guizhou Medical University, Liupanshui, 553000, China.
Abstract:
This study aimed to investigate the role of platelets in mediating lethal respiratory syncytial virus (RSV) infection and to explore the potential of antiplatelet therapy as a novel therapeutic approach for RSV infection. Ex vivo and in vivo experiments were used to study the effects of lethal RSV infection on platelet activation, aggregation, and thrombus formation. The emerging therapeutic effect of tirofiban, a GPIIb/IIIa inhibitor, in mitigating RSV-induced pneumonia was also evaluated. Mice infected with a highly virulent RSV strain (R96-5) developed severe RSV pneumonia and showed significantly increased mortality rates, along with extensive platelet infiltration and thrombus formation in the lungs. In situ hybridization revealed co-localization of RSV nucleocapsid RNA with the platelet GPIbα gene in lung tissue. RSV infection induced marked platelet aggregation through the GPIbα-vWF pathway. Notably, tirofiban significantly protected mice from severe pneumonia caused by R96-5. These findings highlight the critical involvement of platelet activation and aggregation in RSV infection and suggest that targeting platelet through the GPIbα-vWF signaling axis may represent a promising therapeutic strategy for severe RSV infection.
Insights
Platelets play a key role in severe respiratory syncytial virus (RSV) infection, contributing to lung damage and mortality. Antiplatelet therapy, specifically tirofiban, shows promise in treating RSV-induced pneumonia.
Area of Science:
- Virology
- Hematology
- Immunology
Background:
- Respiratory syncytial virus (RSV) is a major cause of respiratory illness.
- Platelets are increasingly recognized for their roles beyond hemostasis, including in inflammatory and infectious diseases.
Purpose of the Study:
- To investigate the role of platelets in mediating lethal RSV infection.
- To evaluate antiplatelet therapy as a potential treatment for RSV infection.
Main Methods:
- Ex vivo and in vivo experiments using a highly virulent RSV strain in mice.
- Assessment of platelet activation, aggregation, and thrombus formation.
- Evaluation of tirofiban, a GPIIb/IIIa inhibitor, for therapeutic effects.
Main Results:
- Lethal RSV infection in mice led to severe pneumonia, increased mortality, and significant platelet infiltration and thrombus formation in the lungs.
- RSV nucleocapsid RNA co-localized with the platelet GPIbα gene in lung tissue.
- RSV infection induced platelet aggregation via the GPIbα-von Willebrand factor (vWF) pathway.
- Tirofiban treatment significantly protected mice from severe RSV-induced pneumonia.
Conclusions:
- Platelet activation and aggregation are critically involved in the pathogenesis of severe RSV infection.
- Targeting the GPIbα-vWF signaling axis with antiplatelet agents like tirofiban represents a promising therapeutic strategy for severe RSV infection.
