Examining Immune Senescence in PLWH and HCV, utilizing the ACTG BIRTH Cohort samples

NIH RePORTER · NIH · UM1 · $370,632 · view on reporter.nih.gov ↗

Abstract

Abstract Infection with human immunodeficiency virus (HIV) is a chronic viral disease process. Early in infection, gut permeability is increased due to translocation of bacterial products. This leads to systemic immune activation, which is reduced but not eliminated with effective antiretroviral therapy. The presence of concomitant chronic viral hepatitis infection with hepatitis C (HCV) may exacerbate systemic immune activation, via activation of hepatic macrophages with proinflammatory downstream effects. It has been suggested that immune senescence or premature aging of immune function accompanies these events and is itself a precursor to clinical outcomes such as accelerated cardiovascular disease and neurocognitive impairment. Immune senescence may be assessed using a variety of measures including DNA methylation, telomere shortening, and changes in T-cell subsets. Cross-sectional analyses have reported varying results depending upon the cohort studied and the method utilized. In this application, we seek to compare and contrast different methods of assessing immune senescence in the setting of HCV/HIV coinfection. Using longitudinal samples from a well established, diverse, and well clinically characterized cohort, the BIRTH Study (ACTG 5294), we propose to evaluate biomarkers of immune senescence and relate them to degree of hepatic fibrosis. We will examine the relationship of HCV cure to determine how senescence biomarkers change, and we will attempt to link immune senescence to alterations in Treg subpopulations.

Key facts

NIH application ID
10846035
Project number
3UM1AI068636-18S3
Recipient
UNIVERSITY OF CALIFORNIA LOS ANGELES
Principal Investigator
Judith S. Currier
Activity code
UM1
Funding institute
NIH
Fiscal year
2024
Award amount
$370,632
Award type
3
Project period
2006-06-29 → 2027-11-30