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本文引用的文献

1
Early Gag immunodominance of the HIV-specific T-cell response during acute/early infection is associated with higher CD8+ T-cell antiviral activity and correlates with preservation of the CD4+ T-cell compartment.急性/早期感染期间,HIV 特异性 T 细胞反应的早期 Gag 免疫优势与更高的 CD8+ T 细胞抗病毒活性相关,并与 CD4+ T 细胞的保存相关。
J Virol. 2013 Jul;87(13):7445-62. doi: 10.1128/JVI.00865-13. Epub 2013 Apr 24.
2
Persistent LCMV infection is controlled by blockade of type I interferon signaling.持续的 LCMV 感染受 I 型干扰素信号阻断的控制。
Science. 2013 Apr 12;340(6129):207-11. doi: 10.1126/science.1235214.
3
Blockade of chronic type I interferon signaling to control persistent LCMV infection.阻断慢性 I 型干扰素信号转导以控制持续性 LCMV 感染。
Science. 2013 Apr 12;340(6129):202-7. doi: 10.1126/science.1235208.
4
Natural variation in Fc glycosylation of HIV-specific antibodies impacts antiviral activity.HIV 特异性抗体 Fc 糖基化的自然变异影响抗病毒活性。
J Clin Invest. 2013 May;123(5):2183-92. doi: 10.1172/JCI65708. Epub 2013 Apr 8.
5
Somatic mutations of the immunoglobulin framework are generally required for broad and potent HIV-1 neutralization.抗体框架区的体细胞突变通常是广谱和强效 HIV-1 中和作用所必需的。
Cell. 2013 Mar 28;153(1):126-38. doi: 10.1016/j.cell.2013.03.018.
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A molecular basis for the control of preimmune escape variants by HIV-specific CD8+ T cells.HIV 特异性 CD8+ T 细胞控制预免疫逃逸变异的分子基础。
Immunity. 2013 Mar 21;38(3):425-36. doi: 10.1016/j.immuni.2012.11.021.
7
Inadequate T follicular cell help impairs B cell immunity during HIV infection.在 HIV 感染期间,辅助性 T 滤泡细胞不足会损害 B 细胞免疫。
Nat Med. 2013 Apr;19(4):494-9. doi: 10.1038/nm.3109. Epub 2013 Mar 10.
8
Cytotoxic capacity of SIV-specific CD8(+) T cells against primary autologous targets correlates with immune control in SIV-infected rhesus macaques.SIV 特异性 CD8(+) T 细胞对原发性自体靶标的细胞毒性与 SIV 感染恒河猴的免疫控制相关。
PLoS Pathog. 2013 Feb;9(2):e1003195. doi: 10.1371/journal.ppat.1003195. Epub 2013 Feb 28.
9
Enhanced phagocytic activity of HIV-specific antibodies correlates with natural production of immunoglobulins with skewed affinity for FcγR2a and FcγR2b.HIV 特异性抗体的增强吞噬活性与偏向于 FcγR2a 和 FcγR2b 的免疫球蛋白的自然产生相关。
J Virol. 2013 May;87(10):5468-76. doi: 10.1128/JVI.03403-12. Epub 2013 Mar 6.
10
Interferon-α is the primary plasma type-I IFN in HIV-1 infection and correlates with immune activation and disease markers.干扰素-α是 HIV-1 感染中主要的 I 型 IFN,与免疫激活和疾病标志物相关。
PLoS One. 2013;8(2):e56527. doi: 10.1371/journal.pone.0056527. Epub 2013 Feb 20.

宿主免疫层面的网络:持续性病毒感染期间免疫细胞的相互作用。

Networking at the level of host immunity: immune cell interactions during persistent viral infections.

机构信息

Department of Immunology and Microbial Science, The Scripps Research Institute, La Jolla, CA 92037, USA.

出版信息

Cell Host Microbe. 2013 Jun 12;13(6):652-64. doi: 10.1016/j.chom.2013.05.014.

DOI:10.1016/j.chom.2013.05.014
PMID:23768490
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3713852/
Abstract

Persistent viral infections are the result of a series of connected events that culminate in diminished immunity and the inability to eliminate infection. By building our understanding of how distinct components of the immune system function both individually and collectively in productive versus abortive responses, new potential therapeutic targets can be developed to overcome immune dysfunction and thus fight persistent infections. Using lymphocytic choriomeningitis virus (LCMV) as a model of a persistent virus infection and drawing parallels to persistent human viral infections such as human immunodeficiency virus (HIV) and hepatitis C virus (HCV), we describe the cellular relationships and interactions that determine the outcome of initial infection and highlight immune targets for therapeutic intervention to prevent or treat persistent infections. Ultimately, these findings will further our understanding of the immunologic basis of persistent viral infection and likely lead to strategies to treat human viral infections.

摘要

持续性病毒感染是一系列连续事件的结果,最终导致免疫功能下降和无法消除感染。通过深入了解免疫系统的不同组成部分在产生性和中止性反应中的个体和集体作用,我们可以开发新的潜在治疗靶点,以克服免疫功能障碍,从而对抗持续性感染。我们使用淋巴细胞性脉络丛脑膜炎病毒(LCMV)作为持续性病毒感染的模型,并与持续性人类病毒感染(如人类免疫缺陷病毒(HIV)和丙型肝炎病毒(HCV))进行类比,描述了决定初始感染结果的细胞关系和相互作用,并强调了免疫治疗靶点,以预防或治疗持续性感染。最终,这些发现将加深我们对持续性病毒感染的免疫学基础的理解,并可能为治疗人类病毒感染提供策略。