HIV-1 Infection Accelerates Age According to the Epigenetic Clock

被引:376
|
作者
Horvath, Steve [1 ,3 ]
Levine, Andrew J. [2 ]
机构
[1] Univ Calif Los Angeles, Dept Human Genet, Los Angeles, CA 90024 USA
[2] Univ Calif Los Angeles, David Geffen Sch Med, Dept Neurol, Los Angeles, CA 90095 USA
[3] Univ Calif Los Angeles, Sch Publ Hlth, Dept Biostat, Los Angeles, CA 90024 USA
基金
美国国家卫生研究院;
关键词
HIV-1; DNA methylation; epigenetics; aging; biomarker; DNA METHYLATION AGE; RISK; IMMUNODEFICIENCY; DISEASE; BRAIN; CELLS; AIDS;
D O I
10.1093/infdis/jiv277
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Background. Infection with human immunodeficiency virus type 1 (HIV) is associated with clinical symptoms of accelerated aging, as evidenced by the increased incidence and diversity of age-related illnesses at relatively young ages and supporting findings of organ and cellular pathologic analyses. But it has been difficult to detect an accelerated aging effect at a molecular level. Methods. Here, we used an epigenetic biomarker of aging based on host DNA methylation levels to study accelerated aging effects due to HIV infection. DNA from brain and blood tissue was assayed via the Illumina Infinium Methylation 450 K platform. Results. Using 6 novel DNA methylation data sets, we show that HIV infection leads to an increase in epigenetic age both in brain tissue (7.4 years) and blood (5.2 years). While the observed accelerated aging effects in blood may reflect changes in blood cell composition (notably exhausted cytotoxic T cells), it is less clear what explains the observed accelerated aging effects in brain tissue. Conclusions. Overall, our results demonstrate that the epigenetic clock is a useful biomarker for detecting accelerated aging effects due to HIV infection. This tool can be used to accurately determine the extent of age acceleration in individual tissues and cells.
引用
收藏
页码:1563 / 1573
页数:11
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