Journal
PLOS ONE
Volume 7, Issue 11, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0050486
Keywords
-
Categories
Funding
- National Institutes of Health (NIH) [K08 AI081754, R01 AI087145, K24AI069994]
- University of California San Francisco (UCSF) Centers for AIDS Research (CFAR) [P0 AI27763]
- UCSF Clinical & Translational Science Institute (CTSI) [UL1 RR024131]
- NIH/National Institute of Allergy and Infectious Diseases (NIAID) CFAR Network of Integrated Clinical Systems (CNICS) [1 R24 AI067039-1]
- Ragon Institute
- [106710-40-RGRL]
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Many human immunodeficiency virus (HIV) infected individuals suffer from persistent immune activation. Chronic inflammation and immune dysregulation have been associated with an increased risk of age-related diseases even among patients on highly active antiretroviral therapy. The factors leading to immune activation are complex, but have been hypothesized to include persistent viral replication with cellular death as well as microbial translocation across the gastrointestinal tract. Both processes may trigger innate immune responses since many native molecules released from dying cells are similar in structure to pathogen associated molecular patterns. These damage associated molecular patterns include mitochondrial DNA and formylated peptides. We hypothesized that circulating mitochondrial nucleic acid could serve as a biomarker for HIV-associated cell death and drive innate immune activation in infected individuals. We developed a quantitative polymerase chain reaction assay for plasma mitochondrial DNA and validated it on normal blood donors. We then measured mitochondrial DNA levels in acute and chronic HIV infection. While the assay proved to be accurate with a robust dynamic range, we did not find a significant association between HIV disease status and circulating mitochondrial DNA. We did, however, observe a negative correlation between age and plasma mitochondrial DNA levels in individuals with well-controlled HIV. Citation: Lauring AS, Lee T-H, Martin JN, Hunt PW, Deeks SG, et al. (2012) Lack of Evidence for mtDNA as a Biomarker of Innate Immune Activation in HIV Infection. PLoS ONE 7(11): e50486. doi:10.1371/journal.pone.0050486
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