New insight on dengue virus-induced thrombocytopenia

Goldthorpe, Stacy C.; Conway, Michael J.

doi:10.1080/21505594.2017.1368943

Cited by 6 publications

(5 citation statements)

References 13 publications

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“…However, the exact reasons and viral factors that lead to thrombocytopenia remain elusive. DENV EIII has shown to have cytotoxic effect on megakaryocytes ( 15 , 58 ). At the same time, DENV NS1 was demonstrated to enhance endothelial permeability and vascular leaks through a toll-like receptor 4 ( 52 , 53 ).…”

Section: Discussionmentioning

confidence: 99%

Exposure of Platelets to Dengue Virus and Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent Platelet Cell Death and Thrombocytopenia in Mice

et al. 2021

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In tropical and subtropical regions, mosquito-borne dengue virus (DENV) infections can lead to severe dengue, also known as dengue hemorrhage fever, which causes bleeding, thrombocytopenia, and blood plasma leakage and increases mortality. Although DENV-induced platelet cell death was linked to disease severity, the role of responsible viral factors and the elicitation mechanism of abnormal platelet activation and cell death remain unclear. DENV and virion-surface envelope protein domain III (EIII), a cellular binding moiety of the virus particle, highly increase during the viremia stage. Our previous report suggested that exposure to such viremia EIII levels can lead to cell death of endothelial cells, neutrophils, and megakaryocytes. Here we found that both DENV and EIII could induce abnormal platelet activation and predominantly necrotic cell death pyroptosis. Blockages of EIII-induced platelet signaling using the competitive inhibitor chondroitin sulfate B or selective Nlrp3 inflammasome inhibitors OLT1177 and Z-WHED-FMK markedly ameliorated DENV- and EIII-induced thrombocytopenia, platelet activation, and cell death. These results suggest that EIII could be considered as a virulence factor of DENV, and that Nlrp3 inflammasome is a feasible target for developing therapeutic approaches against dengue-induced platelet defects.

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Section: Discussionmentioning

confidence: 99%

Exposure of Platelets to Dengue Virus and Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent Platelet Cell Death and Thrombocytopenia in Mice

et al. 2021

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“…Analyses were extended to human parvovirus B19 because B19 infection, although predominantly affects erythrocytes, shows clinically nonsignificant lymphopenia, neutropenia, and thrombocytopenia [36] and to dengue virus because thrombocytopenia and clotting abnormalities are at the heart of dengue pathology [37]. Tobacco mosaic virus was utilized as a negative TTP-unrelated viral control.…”

Section: Resultsmentioning

confidence: 99%

From influenza infection to anti-ADAMTS13 autoantibodies via cross-reactivity

Kanduc

2018

Infection International

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Autoantibodies (AAbs) against von Willebrand factor (vWF)-cleaving protease ADAMTS13 causally relate to thrombotic thrombocytopenic purpura (TTP). How anti-ADAMTS13 AAbs are generated is unknown. Starting from reports according to which influenza infection can trigger TTP by the production of ADAMTS13 AAbs, this study explores influenza viruses and ADAMTS13 protein for common peptide sequences that might underlie anti-influenza immune responses able to cross-react with ADAMTS13. Results document that numerous peptides are shared between influenza A and B viruses and ADAMTS13, thus supporting the hypothesis of cross-reactivity as a mechanism driving the generation of anti-ADAMTS13 AAbs.

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“…Various viral infections can cause occult viremia without subjective symptoms [8]. CMV infection, which is a viral infection [9], is prevalent among older asymptomatic patients, and most patients do not require treatment with antiviral drugs [10]. In contrast, thrombocytopenia may be an initial manifestation of active CMV infection [11].…”

Section: Discussionmentioning

confidence: 99%

Thrombocytopenia in Anti-neutrophil Cytoplasmic Antibody-Associated Vasculitis Indicating the Presence of Cytomegalovirus Infection: A Case Report

Ohta¹,

Naito²,

Nishikura³

et al. 2023

Cureus

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Although cytomegalovirus (CMV) usually colonizes the human body without causing symptoms, CMV infections often develop in immunocompromised hosts. Immunosuppression can trigger CMV infection, and its prediction is essential; however, this is challenging without specific criteria.We present the case of an 87-year-old male patient who visited a rural community hospital with the chief complaint of persistent cough, productive of bloody sputum. Initially, the patient developed thrombocytopenia without any abnormalities of liver function; however, a positive myeloperoxidase antineutrophil cytoplasmic antibody (ANCA) test and the presence of alveolar hemorrhage and glomerulonephritis confirmed ANCA-associated vasculitis. The patient's symptoms and thrombocytopenia resolved transiently after treatment with prednisolone and rituximab. However, the recurrence of thrombocytopenia and the appearance of urinary intracytoplasmic inclusion bodies during the treatment course were investigated using an antigenemia test, which ultimately confirmed CMV viremia. Valganciclovir treatment resolved all the symptoms. This case report showed that thrombocytopenia might indicate the presence of CMV infection in ANCA-associated vasculitis and that intracytoplasmic inclusion bodies in immunosuppressed patients require investigation of CMV infection for effective treatment.

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New insight on dengue virus-induced thrombocytopenia

Cited by 6 publications

References 13 publications

Exposure of Platelets to Dengue Virus and Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent Platelet Cell Death and Thrombocytopenia in Mice

Exposure of Platelets to Dengue Virus and Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent Platelet Cell Death and Thrombocytopenia in Mice

From influenza infection to anti-ADAMTS13 autoantibodies via cross-reactivity

Thrombocytopenia in Anti-neutrophil Cytoplasmic Antibody-Associated Vasculitis Indicating the Presence of Cytomegalovirus Infection: A Case Report

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