A fatal case report of antibody-dependent enhancement of dengue virus type 1 following remote Zika virus infection.

A fatal case report of antibody-dependent enhancement of dengue virus type 1 following remote Zika virus infection.
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DOI:
10.1186/s12879-021-06482-0
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发表时间:
2021-08-04
影响因子:
3.7
通讯作者:
Wong SJ
Wong SJ
中科院分区:
医学3区
文献类型:
--
作者:
Bonheur AN;Thomas S;Soshnick SH;McGibbon E;Dupuis AP 2nd;Hull R;Slavinski S;Del Rosso PE;Weiss D;Hunt DT;McCabe ME;Dean AB;Folkerth R;Laib AM;Wong SJ

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登革病毒(DENV)是世界上许多地区的地方病。当具有初级免疫力的人感染第二种不同的DENV毒株时,DENV感染中就会发生抗体依赖性增强(ADE)。2015年在西半球出现的寨卡病毒(ZIKV)抗体与DENV交叉反应,理论上可能会在DENV初治个体中引发ADE。 一名最近从多米尼加共和国逗留一个月返回的儿童疑似感染登革病毒。患儿出现发热、呕吐、腹痛和低血容量性休克。容量和加压复苏均不成功,患儿在住院后不到24小时死亡。实验室结果表明,早期急性首次登革病毒感染,因为血清,血浆,和脊髓液有登革病毒1检测聚合酶链反应(PCR),但血清缺乏IgG抗体登革病毒非结构蛋白1(NS1)的所有四个血清型。这种急性DENV感染发生在远程ZIKV感染的存在下,如通过多重微球免疫测定法通过针对ZIKV NS 1包膜的抗体和针对ZIKV的异常高的空斑减少中和滴度所确定的。ZIKV IgG亲合力指数高,证实了既往感染。PCR检测10种器官和组织中均检测到DENV1 RNA。这里报道的严重和致命的并发症表明,当主要被DENV 1感染时,远程ZIKV感染可能引起过度的免疫应答,导致低血容量性休克。 我们报告了美国首例已知的旅行相关DENV快速进展和致命病例,其中既往接触ZIKV可能在引发ADE现象方面发挥了作用。先前的ZIKV免疫和随后的新登革热感染的这种关联是令人担忧的现象,并且是对黄病毒免疫的知识体系的重要贡献。
Dengue virus (DENV) is endemic in many parts of the world. Antibody dependent enhancement (ADE) in DENV infections occurs when a person with primary immunity is infected by a second, different DENV strain. Antibodies to Zika virus (ZIKV), which emerged in the Western Hemisphere in 2015, are cross reactive with DENV and theoretically could provoke ADE in a DENV naïve individual. DENV infection was suspected in a child who had recently returned from a one-month stay in the Dominican Republic. The child presented with fever, vomiting, abdominal pain, and in hypovolemic shock. Volume and pressor resuscitation were unsuccessful, and the child died less than 24 h after hospitalization. Laboratory results suggested an early acute first DENV infection since serum, plasma, and spinal fluid had DENV1 detected by polymerase chain reaction (PCR), yet the serum lacked IgG antibodies to DENV nonstructural protein 1 (NS1) of all four DENV serotypes. This acute DENV infection occurred in the presence of a remote ZIKV infection as determined by antibodies to ZIKV NS1 envelope by multiplex microsphere immunoassay and an exceptionally high plaque reduction neutralization titer to ZIKV. ZIKV IgG avidity index was high, confirming a past infection. DENV1 RNA was detected in all ten organs and tissues examined by PCR. The severe and fatal complications reported here suggest that a remote ZIKV infection may provoke an exaggerated immune response leading to hypovolemic shock when primarily infected by DENV1. We report the first known patient in the United States with a rapidly progressive and fatal case of travel-associated DENV in which prior exposure to ZIKV likely played a role in triggering an ADE phenomenon. This association of prior ZIKV immunity and subsequent new dengue infection is a worrisome phenomenon and an important contribution to the body of knowledge on immunity to flaviviruses.
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