Molecular Mechanisms of HIV Immune Evasion of the Innate Immune Response in Myeloid Cells

被引:18
|
作者
Mashiba, Mike [1 ,2 ]
Collins, Kathleen L. [1 ,2 ,3 ,4 ,5 ]
机构
[1] Univ Michigan, Program Immunol, Ann Arbor, MI 48109 USA
[2] Univ Michigan, Med Scientist Training Program, Ann Arbor, MI 48109 USA
[3] Univ Michigan, Dept Internal Med, Ann Arbor, MI 48109 USA
[4] Univ Michigan, Dept Microbiol & Immunol, Ann Arbor, MI 48109 USA
[5] Univ Michigan, Program Cellular & Mol Biol, Ann Arbor, MI 48109 USA
来源
VIRUSES-BASEL | 2013年 / 5卷 / 01期
基金
美国国家卫生研究院;
关键词
HIV; immune evasion; Vpr; Ung2; myeloid; IMMUNODEFICIENCY-VIRUS TYPE-1; RESTRICTION FACTOR SAMHD1; DENDRITIC CELLS; T-CELLS; PRIMATE LENTIVIRUSES; MUTATIONAL ANALYSIS; ACCESSORY PROTEINS; VPR PROTEIN; URACIL DNA; VIRAL-DNA;
D O I
10.3390/v5010001
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The expression of intrinsic antiviral factors by myeloid cells is a recently recognized mechanism of restricting lentiviral replication. Viruses that enter these cells must develop strategies to evade cellular antiviral factors to establish a productive infection. By studying the cellular targets of virally encoded proteins that are necessary to infect myeloid cells, a better understanding of cellular intrinsic antiviral strategies has now been achieved. Recent findings have provided insight into how the lentiviral accessory proteins, Vpx, Vpr and Vif counteract antiviral factors found in myeloid cells including SAMHD1, APOBEC3G, APOBEC3A, UNG2 and uracil. Here we review our current understanding of the molecular basis of how cellular antiviral factors function and the viral countermeasures that antagonize them to promote viral transmission and spread.
引用
收藏
页码:1 / 14
页数:14
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