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在猕猴HIV感染模型中,庚型肝炎病毒可逃避免疫识别,但不会减轻急性期疾病。

Pegivirus avoids immune recognition but does not attenuate acute-phase disease in a macaque model of HIV infection.

作者信息

Bailey Adam L, Buechler Connor R, Matson Daniel R, Peterson Eric J, Brunner Kevin G, Mohns Mariel S, Breitbach Meghan, Stewart Laurel M, Ericsen Adam J, Newman Christina M, Koenig Michelle R, Mohr Emma, Tan John, Capuano Saverio, Simmons Heather A, Yang David T, O'Connor David H

机构信息

Wisconsin National Primate Research Center, Madison, Wisconsin, United States of America.

Department of Pathology and Laboratory Medicine, University of Wisconsin-Madison, Madison, Wisconsin, United States of America.

出版信息

PLoS Pathog. 2017 Oct 26;13(10):e1006692. doi: 10.1371/journal.ppat.1006692. eCollection 2017 Oct.

DOI:10.1371/journal.ppat.1006692
PMID:29073258
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5675458/
Abstract

Human pegivirus (HPgV) protects HIV+ people from HIV-associated disease, but the mechanism of this protective effect remains poorly understood. We sequentially infected cynomolgus macaques with simian pegivirus (SPgV) and simian immunodeficiency virus (SIV) to model HIV+HPgV co-infection. SPgV had no effect on acute-phase SIV pathogenesis-as measured by SIV viral load, CD4+ T cell destruction, immune activation, or adaptive immune responses-suggesting that HPgV's protective effect is exerted primarily during the chronic phase of HIV infection. We also examined the immune response to SPgV in unprecedented detail, and found that this virus elicits virtually no activation of the immune system despite persistently high titers in the blood over long periods of time. Overall, this study expands our understanding of the pegiviruses-an understudied group of viruses with a high prevalence in the global human population-and suggests that the protective effect observed in HIV+HPgV co-infected people occurs primarily during the chronic phase of HIV infection.

摘要

人pegivirus病毒(HPgV)可保护HIV感染者免受与HIV相关疾病的侵害,但其保护作用机制仍知之甚少。我们用猿猴pegivirus病毒(SPgV)和猿猴免疫缺陷病毒(SIV)先后感染食蟹猴,以模拟HIV+HPgV合并感染。SPgV对急性期SIV发病机制无影响,通过SIV病毒载量、CD4+T细胞破坏、免疫激活或适应性免疫反应来衡量,这表明HPgV的保护作用主要在HIV感染的慢性期发挥。我们还以前所未有的细节研究了对SPgV的免疫反应,发现尽管该病毒在血液中长时间持续保持高滴度,但几乎不会引发免疫系统的激活。总体而言,这项研究扩展了我们对pegivirus病毒的理解,这是一类在全球人群中普遍存在但研究不足的病毒,并表明在HIV+HPgV合并感染人群中观察到的保护作用主要发生在HIV感染的慢性期。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/e27c3cdc2b4a/ppat.1006692.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/0977ca94ca0d/ppat.1006692.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/fb7bb9beab47/ppat.1006692.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/a4c8eea67d29/ppat.1006692.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/c34b29098bc3/ppat.1006692.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/26b19ff36759/ppat.1006692.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/0fa95bada325/ppat.1006692.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/e27c3cdc2b4a/ppat.1006692.g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/0977ca94ca0d/ppat.1006692.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/fb7bb9beab47/ppat.1006692.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/a4c8eea67d29/ppat.1006692.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/c34b29098bc3/ppat.1006692.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/26b19ff36759/ppat.1006692.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/0fa95bada325/ppat.1006692.g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/820f/5675458/e27c3cdc2b4a/ppat.1006692.g007.jpg

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