Subneutralizing antibodies to enterovirus 71 induce antibody-dependent enhancement of infection in newborn mice

研究成果: Article

21 引文 (Scopus)

摘要

Antibody-dependent enhancement (ADE) of virus infections can be induced by subneutralizing concentrations of specific antibodies. We recently demonstrated ADE in human monocytes infected with enterovirus 71 (EV71). The current study was designed to extend these observations by determining the effect of ADE on the pathogenesis of EV71 infection in newborn mice. We compared the clinical manifestations, mortality, virus titer, histopathology, and serum levels of cytokines and chemokines in newborn mice pretreated with subneutralizing antibodies to EV71 or normal mouse IgG with and without virus. Seven-day-old ICR mice were pretreated with a wide range of mouse anti-EV71 IgG 24 h prior to intraperitoneal injection of EV71. Mice were protected from infection by neutralizing doses of anti-EV71 IgG ranging from 6.43 × 10-1 to 329.6 μg/ml. Subneutralizing doses ranging from 2.01 × 10-2 to 3.21 × 10-1 μg/ml were found to significantly increase 14-day mortality compared to virus alone. The ADE effect was not evident at lower doses. Histopathological examination of mice given a subneutralizing dose of 8.04 × 10-2 μg/ml revealed extensive neuronal and muscular damage compared to untreated infected controls. Higher serum levels of interferon (IFN)-γ and monocyte chemoattractant protein (MCP)-1 were noted in mice pretreated with subneutralizing doses than untreated infected controls. These findings support the concept that subneutralizing antibodies directed enhance EV71 induce ADE in newborn mice.

原文English
頁(從 - 到)259-265
頁數7
期刊Medical Microbiology and Immunology
202
發行號4
DOIs
出版狀態Published - 2013 八月 1

指紋

Antibody-Dependent Enhancement
Enterovirus
Antibodies
Infection
Immunoglobulin G
Enterovirus Infections
Viruses
Inbred ICR Mouse
Mortality
Chemokine CCL2
Virus Diseases
Intraperitoneal Injections
Viral Load
Serum
Chemokines
Interferons
Monocytes
Cytokines

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Microbiology (medical)

引用此文

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abstract = "Antibody-dependent enhancement (ADE) of virus infections can be induced by subneutralizing concentrations of specific antibodies. We recently demonstrated ADE in human monocytes infected with enterovirus 71 (EV71). The current study was designed to extend these observations by determining the effect of ADE on the pathogenesis of EV71 infection in newborn mice. We compared the clinical manifestations, mortality, virus titer, histopathology, and serum levels of cytokines and chemokines in newborn mice pretreated with subneutralizing antibodies to EV71 or normal mouse IgG with and without virus. Seven-day-old ICR mice were pretreated with a wide range of mouse anti-EV71 IgG 24 h prior to intraperitoneal injection of EV71. Mice were protected from infection by neutralizing doses of anti-EV71 IgG ranging from 6.43 × 10-1 to 329.6 μg/ml. Subneutralizing doses ranging from 2.01 × 10-2 to 3.21 × 10-1 μg/ml were found to significantly increase 14-day mortality compared to virus alone. The ADE effect was not evident at lower doses. Histopathological examination of mice given a subneutralizing dose of 8.04 × 10-2 μg/ml revealed extensive neuronal and muscular damage compared to untreated infected controls. Higher serum levels of interferon (IFN)-γ and monocyte chemoattractant protein (MCP)-1 were noted in mice pretreated with subneutralizing doses than untreated infected controls. These findings support the concept that subneutralizing antibodies directed enhance EV71 induce ADE in newborn mice.",
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