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通过母体获得的异型登革热抗体增强登革热疾病严重程度的首个体内实验模型。

First experimental in vivo model of enhanced dengue disease severity through maternally acquired heterotypic dengue antibodies.

作者信息

Ng Jowin Kai Wei, Zhang Summer Lixin, Tan Hwee Cheng, Yan Benedict, Martinez Julia Maria, Tan Wei Yu, Lam Jian Hang, Tan Grace Kai Xin, Ooi Eng Eong, Alonso Sylvie

机构信息

Department of Microbiology, Yong Loo Lin School of Medicine, Life Sciences Institute, National University of Singapore, Singapore; Immunology Programme, Yong Loo Lin School of Medicine, Life Sciences Institute, National University of Singapore, Singapore.

Defence Science Organization National Laboratories, Singapore.

出版信息

PLoS Pathog. 2014 Apr 3;10(4):e1004031. doi: 10.1371/journal.ppat.1004031. eCollection 2014 Apr.

Abstract

Dengue (DEN) represents the most serious arthropod-borne viral disease. DEN clinical manifestations range from mild febrile illness to life-threatening hemorrhage and vascular leakage. Early epidemiological observations reported that infants born to DEN-immune mothers were at greater risk to develop the severe forms of the disease upon infection with any serotype of dengue virus (DENV). From these observations emerged the hypothesis of antibody-dependent enhancement (ADE) of disease severity, whereby maternally acquired anti-DENV antibodies cross-react but fail to neutralize DENV particles, resulting in higher viremia that correlates with increased disease severity. Although in vitro and in vivo experimental set ups have indirectly supported the ADE hypothesis, direct experimental evidence has been missing. Furthermore, a recent epidemiological study has challenged the influence of maternal antibodies in disease outcome. Here we have developed a mouse model of ADE where DENV2 infection of young mice born to DENV1-immune mothers led to earlier death which correlated with higher viremia and increased vascular leakage compared to DENV2-infected mice born to dengue naïve mothers. In this ADE model we demonstrated the role of TNF-α in DEN-induced vascular leakage. Furthermore, upon infection with an attenuated DENV2 mutant strain, mice born to DENV1-immune mothers developed lethal disease accompanied by vascular leakage whereas infected mice born to dengue naïve mothers did no display any clinical manifestation. In vitro ELISA and ADE assays confirmed the cross-reactive and enhancing properties towards DENV2 of the serum from mice born to DENV1-immune mothers. Lastly, age-dependent susceptibility to disease enhancement was observed in mice born to DENV1-immune mothers, thus reproducing epidemiological observations. Overall, this work provides direct in vivo demonstration of the role of maternally acquired heterotypic dengue antibodies in the enhancement of dengue disease severity and offers a unique opportunity to further decipher the mechanisms involved.

摘要

登革热(DEN)是最严重的节肢动物传播病毒性疾病。登革热的临床表现从轻度发热疾病到危及生命的出血和血管渗漏不等。早期流行病学观察报告称,登革热免疫母亲所生的婴儿在感染任何血清型登革热病毒(DENV)后,患严重疾病的风险更高。基于这些观察结果,出现了疾病严重程度抗体依赖性增强(ADE)的假说,即母体获得的抗DENV抗体发生交叉反应但无法中和DENV颗粒,导致更高的病毒血症,这与疾病严重程度增加相关。尽管体外和体内实验设置间接支持了ADE假说,但一直缺乏直接的实验证据。此外,最近的一项流行病学研究对母体抗体在疾病结局中的影响提出了质疑。在此,我们建立了一种ADE小鼠模型,与登革热未感染母亲所生的感染DENV2的小鼠相比,DENV1免疫母亲所生的幼鼠感染DENV2后导致更早死亡,这与更高的病毒血症和增加的血管渗漏相关。在这个ADE模型中,我们证明了TNF-α在登革热诱导的血管渗漏中的作用。此外,感染减毒DENV2突变株后,DENV1免疫母亲所生的小鼠出现致命疾病并伴有血管渗漏,而登革热未感染母亲所生的感染小鼠未表现出任何临床表现。体外ELISA和ADE试验证实了DENV1免疫母亲所生小鼠血清对DENV2具有交叉反应性和增强特性。最后,在DENV1免疫母亲所生的小鼠中观察到了年龄依赖性疾病增强易感性,从而重现了流行病学观察结果。总体而言,这项工作提供了母体获得的异型登革热抗体在增强登革热疾病严重程度中作用的直接体内证据,并为进一步解读其中涉及的机制提供了独特的机会。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ed42/3974839/8a4ac66a4dfc/ppat.1004031.g001.jpg

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