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Virus-associated idiopathic thrombocytopenic purpura
1Division of Haematology/Oncology, Hospital for Sick Children, Toronto, Ontario, Canada.
Insights
Most children with acute idiopathic thrombocytopenic purpura (ITP) experience an infection prior to platelet reduction. Viral infections can trigger ITP through enhanced platelet clearance, possibly via molecular mimicry.
Area of Science:
- Pediatrics
- Immunology
- Infectious Diseases
Background:
- Acute idiopathic thrombocytopenic purpura (ITP) is characterized by a low platelet count.
- A significant proportion of pediatric ITP cases follow a preceding infectious illness.
Purpose of the Study:
- To explore the etiological link between viral infections and the development of thrombocytopenia in children.
- To elucidate the mechanisms underlying virus-associated ITP.
Main Methods:
- Review of clinical histories of children diagnosed with acute ITP.
- Identification of specific viral pathogens in a subset of patients.
- Analysis of proposed mechanisms for thrombocytopenia, including thrombopoiesis inhibition and platelet clearance.
Main Results:
- Two-thirds of children with acute ITP reported a recent infectious illness.
- Specific viruses (e.g., varicella zoster, Epstein-Barr) were identified in some cases.
- Enhanced platelet clearance by the reticuloendothelial system is a primary mechanism, not thrombopoiesis inhibition.
- Molecular mimicry is suggested as a potential factor in virus-associated ITP.
Conclusions:
- Preceding viral infections play a significant role in the etiology of acute ITP in children.
- Enhanced platelet destruction, potentially mediated by molecular mimicry, is the main cause of thrombocytopenia in virus-associated ITP.
- Further research into molecular mimicry mechanisms is warranted.
Abstract:
Two-thirds of children with acute idiopathic thrombocytopenic purpura (ITP) have a history of an infectious illness a few days to a few weeks before the onset of thrombocytopenia. In a subset of affected children, identification of a specific virus can be made, such as varicella zoster virus, rubella, Epstein-Barr virus, influenza, or human immunodeficiency type 1 virus, indicating an etiological role for preceding viral infection in these children with ITP. While inhibition of thrombopoiesis has been established to play a role in thrombocytopenia associated with infection with some viruses, it does not appear to play a major role in the etiology of most typical ITP cases. Rather, enhanced clearance of platelets by the reticuloendothelial system is considered to be, at least in part, responsible for the thrombocytopenia which occurs during the viremic phase of acute virus infection or which develops days to weeks following the virus illness. Molecular mimicry between viral antigens and host proteins has been implicated in a number of autoimmune phenomena, and may be involved in the enhanced platelet clearance in virus-associated ITP.