Antiplatelet autoantibodies elicited by dengue virus non‐structural protein 1 cause thrombocytopenia and mortality in mice

Sun, Der-Shan; King, Chwan-Chuen; Huang, Hsuan-Shun; Shih, Yung‐Luen; Lee, C.‐C.; Tsai, Wei‐Jern; Yu, Changhui; Chang, Hsin-Hou

doi:10.1111/j.1538-7836.2007.02754.x

Cited by 127 publications

(149 citation statements)

References 31 publications

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“…58,59 After 72 h post-LT treatment (4.4 mg/kg), the mice were euthanized and the tissues were removed and minced before being incubated with formamide-water (1:1) for 48 h at 37 C. The concentration of dye was determined according to a standard curve of Evans blue in formamide using a spectrophotometer (Hitachi, Japan).…”

Section: Plasma Leakage Analysismentioning

confidence: 99%

Acquired coagulant factor VIII deficiency induced byBacillus anthracislethal toxin in mice

Sun¹,

Lee

Kau

et al. 2015

Virulence

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(2015) Acquired coagulant factor VIII deficiency induced by Bacillus anthracis lethal toxin in mice, Virulence, 6:5, 466-475, DOI: 10.1080/21505594.2015 Keywords: Anthrax, coagulation factor VIII, hemorrhage, lethal toxinMice treated with anthrax lethal toxin (LT) exhibit hemorrhage caused by unknown mechanisms. Moreover, LT treatment in mice induced liver damage. In this study, we hypothesized that a suppressed coagulation function may be associated with liver damage, because the liver is the major producing source of coagulation factors. The hepatic expression of coagulant factors and the survival rates were analyzed after cultured cells or mice were exposed to LT. In agreement with our hypothesis, LT induces cytotoxicity against hepatic cells in vitro. In addition, suppressed expression of coagulation factor VIII (FVIII) in the liver is associated with a prolonged plasma clotting time in LT-treated mice, suggesting a suppressive role of LT in coagulation. Accordingly, we further hypothesized that a loss-of-function approach involving treatments of an anticoagulant should exacerbate LT-induced abnormalities, whereas a gain-offunction approach involving injections of recombinant FVIII to complement the coagulation deficiency should ameliorate the pathogenesis. As expected, a sublethal dose of LT caused mortality in the mice that were non-lethally pretreated with an anticoagulant (warfarin). By contrast, treatments of recombinant FVIII reduced the mortality from a lethal dose of LT in mice. Our results indicated that LT-induced deficiency of FVIII is involved in LT-mediated pathogenesis. Using recombinant FVIII to correct the coagulant defect may enable developing a new strategy to treat anthrax.

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Section: Plasma Leakage Analysismentioning

confidence: 99%

Acquired coagulant factor VIII deficiency induced byBacillus anthracislethal toxin in mice

Sun¹,

Lee

Kau

et al. 2015

Virulence

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“…Pacientes com dengue hemorrágica apresentam níveis maiores de anticorpos anti-plaquetas da classe IgM quando comparados com indivíduos com dengue clássica. Ensaios clínicos, demonstram altos níveis de anticorpos antiplaquetas da classe IgG e IgM além de uma maior atividade dos macrófagos que levam os indivíduos infectados a trombocitopenia durante a infecção primária ou secundária pelo vírus (SUN et al, 2007). MITRAKUL et al, (1977) demonstrou que durante a fase aguda do estado hemorrágico, a sobrevida das plaquetas diminuiu principalmente por destruição hepática.…”

Section: Seu Uso Portanto é Desaconselhado(martins; Setúbal; Castiñeunclassified

Platelet Count on Dengue

Santin¹,

Silva

Henneberg

2013

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RESUMO:A dengue clássica e sua forma grave (hemorrágica) são causadas por um dos quatro tipos de sorotipos do vírus da dengue. Os principais marcadores que diferenciam as duas formas da doença são o aumento da permeabilidade vascular, seguida de hipovolemia e choque nos casos severos. As mudanças hematológicas que constantemente ocorrem na forma hemorrágica incluem a supressão da medula óssea, com consequente leucopenia e trombocitopenia. As causas da trombocitopenia são geralmente relacionadas a atuação direta do vírus sobre a medula óssea e pela ativação de mecanismos imunológicos que aumentam a destruição das plaquetas na circulação. Pela alta incidência das endemias de dengue que ocorrem no Brasil, o entendimento do comportamento de alguns parâmetros laboratoriais é essencial para a melhora das formas de diagnóstico além de auxiliar nas medidas terapêuticas na cura da doença.Palavras-chave: Dengue, Febre Hemorrágica da Dengue, trombocitopenia. ABSTRACT:The classic dengue and its severe form (hemorrhagic) are caused by one of four types of dengue virus serotypes. The main markers that differentiate the two forms of the disease are increased vascular permeability, followed by hypovolemia and shock in severe cases. Hematologic changes constantly occur as hemorrhagic include bone marrow suppression, with consequent thrombocytopenia and leukopenia. The causes of thrombocytopenia are usually related to direct action of the virus on the bone marrow and activation of immune mechanisms that increase the destruction of platelets in the circulation. The high incidence of endemic dengue occurring in Brazil, understanding the behavior of some laboratory parameters is essential for the improvement of the forms of diagnostic besides assisting in therapeutic measures to cure the disease.

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“…La presencia de anticuerpos antiplaquetarios en casos de infección por dengue ha sido evaluada en varios estudios (54-62), los cuales han informado la presencia de autoanticuerpos tanto de tipo IgM (58) como de tipo IgG (61,62), sin diferenciar entre infección primaria y secundaria. Sin embargo, se ha logrado evidenciar mayores niveles de anticuerpos antiplaquetarios en los pacientes con dengue hemorrágico y síndrome de choque por dengue, que en pacientes con dengue clásico (58).…”

Section: Virus Del Dengueunclassified

“…Existen algunas teorías que intentan explicar su aparición. La primera es que algunos epítopos antigénicos del virus del dengue, como la proteína NS1, inducen la formación de anticuerpos con reactividad cruzada contra las plaquetas (62)(63)(64); otra es que la activación policlonal de los linfocitos B conduce a la producción de anticuerpos heterotípicos capaces de reaccionar contra las plaquetas (57,61). Consideramos que estas dos posibilidades no son mutuamente excluyentes y podrían participar de forma sinérgica en la generación de la trombocitopenia.…”

Section: Virus Del Dengueunclassified

Papel de los anticuerpos antiplaquetarios en la infección viral: una revisión sistemática de la literatura

et al. 2011

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Introducción. La trombocitopenia es un fenómeno frecuente en las infecciones virales. Uno de los mecanismos propuesto como posible explicación de su desarrollo es la destrucción plaquetaria periférica mediada por anticuerpos antiplaquetarios. Objetivo. Revisar los resultados de los trabajos originales que existen en la literatura sobre infección viral y anticuerpos antiplaquetarios en humanos, y su efecto sobre el recuento total de plaquetas. Materiales y métodos. Se hizo una búsqueda en PubMed empleando la combinación de términos: "viral infection (OR Virus diseases) AND antibody antiplatelet (OR thrombocytopenia); y antibody antiplatelet AND HIV (OR Measles, OR Dengue, OR Chickenpox OR varicella, OR Epstein Barr, OR Mumps, OR Rubella". Se obtuvieron 218 referencias, de las cuales, 65 correspondían al objetivo de la revisión. Resultados. En la búsqueda se encontró que la trombocitopenia mediada por anticuerpos antiplaquetarios se ha documentado en infecciones virales por VIH, sarampión, dengue, varicelazóster, Epstein-Barr, parotiditis y rubéola. La presencia de anticuerpos antiplaquetarios en infecciones virales por VIH, virus de Epstein-Barr y dengue, se ha asociado con la presencia de la trombocitopenia y con la gravedad de la enfermedad. Conclusiones. Aunque la aparición de anticuerpos antiplaquetarios no se considera el único mecanismo que explica la trombocitopenia desarrollada en las infecciones virales mencionadas, de acuerdo con la literatura científica disponible, su presencia se asocia con la gravedad de la trombocitopenia y con potenciales implicaciones clínicas en los pacientes.Palabras clave: virosis, anticuerpos, plaquetas, trombocitopenia, humanos. Roll of antibodies antiplatelets in viral infection: a systematic review of literatureIntroduction. Thrombocytopenia is a frequent phenomenon in viral infections. Peripheral platelet destruction mediated by anti-platelet antibodies has been one of the proposed causal mechanisms. Objective. Results were collected and analyzed from published studies on associations of human viral infections on anti-platelet antibodies and total platelet counts. Materials and methods. A PubMed search was conducted using the following terms: Viral infection (OR Virus diseases) AND antiplatelet antibody (OR thrombocytopenia) AND HIV (OR measles OR dengue OR chickenpox OR varicella OR Epistein Barr OR mumps OR rubella). Two hundred eighteen reference hits were obtained, 65 of which were relevant to this review. Results. Antiplatelet antibody-mediated thrombocytopenia has been documented in cases of HIV, measles, dengue, chickenpox, Epstein-Barr, mumps and rubella. Moreover, the presence of these antibodies has been associated with severity the disease and thrombocytopenia in viral infections. Conclusions. Although the presence of antiplatelet antibodies was not the only mechanism for explaining the thrombocytopenia developed in these viral infections, their presence was associated with severity of thrombocytopenia and with the clinical presentation of these patients.

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Antiplatelet autoantibodies elicited by dengue virus non‐structural protein 1 cause thrombocytopenia and mortality in mice

Cited by 127 publications

References 31 publications

Acquired coagulant factor VIII deficiency induced byBacillus anthracislethal toxin in mice

Acquired coagulant factor VIII deficiency induced byBacillus anthracislethal toxin in mice

Platelet Count on Dengue

Papel de los anticuerpos antiplaquetarios en la infección viral: una revisión sistemática de la literatura

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