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Updated: Aug 20, 2026

Amplification of Near Full-length HIV-1 Proviruses for Next-Generation Sequencing
Published on: October 16, 2018
Circulating proviral HIV DNA and HIV-associated dementia
Bruce Shiramizu1, Suzanne Gartner, Andrew Williams
1Hawaii AIDS Clinical Research Program, University of Hawaii, Honolulu, Hawaii, USA. bshirami@hawaii.edu
Objective:
Individuals continue to develop HIV-1-associated dementia (HAD) despite treatment with highly active antiretroviral therapy (HAART). Monocytes/macrophages (M/MPhi) can harbor proviral DNA that is not eradicated by HAART. To determine if HAD is associated with the level of HIV-1 infection within circulating leukocytes, we quantified HIV-1 DNA copy number in peripheral blood mononuclear cells (PBMC), and in PBMC subsets.
Design:
Cross-sectional analysis within the Hawaii Aging with HIV Cohort comparing participants with HAD to those with normal cognition (NC).
Methods:
Real-time PCR assays assessing HIV DNA copy number/1 x 10 cells were performed on PBMC and subsets.
Results:
Individuals with HAD (n = 27) had a median (interquartile range) of 9.11 (37.20) HIV DNA per 1 x 10 PBMC compared to 0.49 (0.89) HIV DNA per 1 x 10 PBMC in individuals with NC (n = 22). Using a univariate analysis in the subset of individuals with undetectable viral load (HAD, n = 11; NC, n = 13), the odds of HAD attributable to HIV DNA copy number was 2.76 (1.28-5.94), P < 0.01. Preliminary analysis of a small subset of patients (n = 5) suggested that the primary source of HIV DNA may be the activated M/MPhi (CD14/CD16) subset.
Conclusions:
These findings suggest a potentially important association between circulating provirus and HAD.
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