Journal
PLOS ONE
Volume 7, Issue 8, Pages -Publisher
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0041021
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Funding
- Consejo Nacional de Ciencia y Tecnologia, Mexico [SALUD-2009-01-115265]
- University of California San Francisco-Gladstone Institute of Virology & Immunology Center for AIDS Research (CFAR)
- National Institutes of Health (NIH) [P30 AI027763]
- University of California San Francisco (UCSF) Clinical and Translational Science Institute [UL1 RR024131]
- National Institute of Allergy and Infectious Diseases (NIAID) [AI087145, AI76059, AI84113, K24AI069994]
- American Foundation for AIDS Research [106710-40-RGRL]
- NIH/NIAID CFAR Network of Integrated Clinical Systems (CNICS) [1 R24 AI067039-1]
- Peter and Shelagh Godsoe Family Foundation
- UCSF AIDS Research Institute (ARI)
- UC Mexus grant
- Ragon Institute
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Human endogenous retroviruses (HERV) are remnants of ancestral retroviral infections integrated into the germ line, and constitute approximately 8% of the genome. Several autoimmune disorders, malignancies, and infectious diseases such as HIV-1 are associated with higher HERV expression. The degree to which HERV expression in vivo results in persistent inflammation is not known. We studied the association of immune activation and HERV-K expression in 20 subjects with chronic, untreated progressive HIV-1 infection and 10 HIV-1 negative controls. The mean HERV-K gag and env RNA expression level in the HIV-1 infected cohort was higher than in the control group (p = 0.0003), and was negatively correlated with the frequency of activated CD38+HLA-DR+CD4+ T cells (Rho = -0.61; p = 0.01) and activated CD38+HLA-DR+CD8+ T cells (Rho = -0.51; p = 0.03). Although HIV-infected persons had higher levels of HERV-K RNA expression (as expected), the level of RNA expression was negatively associated with level of T cell activation. The mechanism for this unexpected association remains to be defined.
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