Increased glucose transporter-1 expression on intermediate monocytes from HIV-infected women with subclinical cardiovascular disease

Academic Article


  • Objective: People living with HIV (PLWH) have chronic immune activation and increased cardiovascular disease (CVD) risk. Activation of monocytes and T lymphocytes causes upregulation of glucose transporter-1 (GLUT1) for efficient function. PLWH have an increased percentage of GLUT1-expressing monocytes and T lymphocytes, but it is unclear if these cells are associated with CVD. We evaluated the expression of GLUT1 and CD38 on monocyte and T lymphocyte populations from HIVinfected women with subclinical CVD. Methods: Participants with more than 75th percentile (n-15) and less than 25th percentile (n=15) age-Adjusted intima-media thickness (IMT) at the right common carotid artery and bifurcation were identified from the Women's Interagency HIV Study. Groups were matched by age, race/ethnicity, smoking status, and CD4 cell count. All women were receiving suppressive antiretroviral therapy except for one high and one low IMT participant. Monocyte and T lymphocyte populations were evaluated for GLUT1 and CD38 expression using flow cytometry. Results: Intermediate monocytes from high IMT women had significantly increased expression of GLUT1 (310 MFI vs. 210 MFI, P=0.024) (66.4% vs. 48.5%, P=0.031) and CD38 (339MFI vs. 211MFI, P=0.002) (10.5%vs. 3.8%, P=0.0002) compared withwomen with lowIMT. High and lowIMT participants showed no differences inGLUT1 or CD38 expression on classical monocytes, nonclassical monocytes, CD4 and CD8 T lymphocytes. Conclusion: GLUT1-expressing intermediate monocytes are elevated in HIV-infected women with subclinical CVD. These cells may contribute to development of CVD in PLWH and could be a novel target to limit inflammation.
  • Authors

    Published In

  • AIDS  Journal
  • Digital Object Identifier (doi)

    Author List

  • Butterfield TR; Hanna DB; Kaplan RC; Kizer JR; Durkin HG; Young MA; Nowicki MJ; Tien PC; Golub ET; Michelle AFM
  • Start Page

  • 199
  • End Page

  • 205
  • Volume

  • 31
  • Issue

  • 2