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SIV/SHIV-Zika 合并感染不会改变成年非妊娠恒河猴模型中的疾病发病机制。

SIV/SHIV-Zika co-infection does not alter disease pathogenesis in adult non-pregnant rhesus macaque model.

机构信息

Department of Pharmacology and Experimental Neuroscience, University of Nebraska Medical Center, Omaha, NE, United States of America.

Department of Genetics, Cell Biology and Anatomy, University of Nebraska Medical Center, Omaha, NE, United States of America.

出版信息

PLoS Negl Trop Dis. 2018 Oct 25;12(10):e0006811. doi: 10.1371/journal.pntd.0006811. eCollection 2018 Oct.

DOI:10.1371/journal.pntd.0006811
PMID:30359380
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6201872/
Abstract

Due to the large geographical overlap of populations exposed to Zika virus (ZIKV) and human immunodeficiency virus (HIV), understanding the disease pathogenesis of co-infection is urgently needed. This warrants the development of an animal model for HIV-ZIKV co-infection. In this study, we used adult non-pregnant macaques that were chronically infected with simian immunodeficiency virus/chimeric simian human immunodeficiency virus (SIV/SHIV) and then inoculated with ZIKV. Plasma viral loads of both SIV/SHIV and ZIKV co-infected animals revealed no significant changes as compared to animals that were infected with ZIKV alone or as compared to SIV/SHIV infected animals prior to ZIKV inoculation. ZIKV tissue clearance of co-infected animals was similar to animals that were infected with ZIKV alone. Furthermore, in co-infected macaques, there was no statistically significant difference in plasma cytokines/chemokines levels as compared to prior to ZIKV inoculation. Collectively, these findings suggest that co-infection may not alter disease pathogenesis, thus warranting larger HIV-ZIKV epidemiological studies in order to validate these findings.

摘要

由于暴露于寨卡病毒(ZIKV)和人类免疫缺陷病毒(HIV)的人群在地理上有很大的重叠,因此迫切需要了解合并感染的发病机制。这就需要开发一种 HIV-ZIKV 合并感染的动物模型。在这项研究中,我们使用慢性感染猴免疫缺陷病毒/嵌合猴免疫缺陷病毒(SIV/SHIV)的成年非妊娠猕猴,然后接种 ZIKV。与单独感染 ZIKV 的动物或与接种 ZIKV 之前感染 SIV/SHIV 的动物相比,同时感染 SIV/SHIV 和 ZIKV 的动物的血浆病毒载量没有明显变化。同时感染动物的 ZIKV 组织清除率与单独感染 ZIKV 的动物相似。此外,与接种 ZIKV 之前相比,合并感染的猕猴血浆细胞因子/趋化因子水平没有统计学上的显著差异。总的来说,这些发现表明合并感染可能不会改变疾病的发病机制,因此需要进行更大规模的 HIV-ZIKV 流行病学研究来验证这些发现。

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