Brief Report: No Evidence for an Association between Statin Use and Lower Biomarkers of HIV Persistence or Immune Activation/Inflammation during Effective ART

Roger J. Bedimo, Hanna Mar, Ronald J. Bosch, Henning Drechsler, Joshua C. Cyktor, Barnard J.C. MacAtangay, Christina Lalama, Charles Rinaldo, Ann Collier, Catherine Godfrey, Evelyn Hogg, Christopher Hensel, Joseph J. Eron, Deborah K. McMahon, John W. Mellors, Pablo Tebas, Rajesh T. Gandhi

Research output: Contribution to journalArticlepeer-review

5 Scopus citations

Abstract

Background: Statins exert pleiotropic anti-inflammatory and immune-modulatory effects, which might translate into antiviral activity. We evaluated whether reported current statin exposure is associated with lower levels of markers of HIV persistence and immune activation/inflammation. Methods: We compared levels of markers of HIV viral persistence [cell-associated HIV RNA (CA-RNA), CA-DNA, and single copy assay plasma HIV RNA] and immune activation/inflammation (IL-6, IP-10, neopterin, sCD14, sCD163, and TNF-alpha) between statin users and nonusers among participants of ACTG A5321 who initiated antiretroviral therapy (ART) during chronic infection and maintained virologic suppression (HIV-1 RNA levels ≤50 copies/mL) for ≥3 years. Results: A total of 303 participants were analyzed. Median time on the current statin was 2.9 years (1.2-5.1). There were no differences between statin users and nonusers in levels of CA-DNA (median 650 vs. 540 copies/106 CD4+ T cells; P = 0.58), CA-RNA (53 vs. 37 copies/106 CD4+ T cells; P = 0.12), or single copy assay (0.4 vs. 0.4 copies/mL; P = 0.45). Similarly, there were no significant differences between statin users and nonusers in markers of inflammation/activation, except for IP-10 (137 vs. 118 pg/mL; P = 0.028). Findings were unchanged after adjustment for factors including pre-ART CD4 and HIV RNA, and years on ART. Conclusions: In this cohort of persons on long-term suppressive ART, current statin use was not associated with lower levels of HIV persistence or immune activation/inflammation. These results do not support a major role for statins in reducing HIV persistence, although an early transient effect cannot be excluded. Prospective, randomized studies are needed to confirm these findings.

Original languageEnglish (US)
Pages (from-to)E27-E31
JournalJournal of Acquired Immune Deficiency Syndromes
Volume82
Issue number2
DOIs
StatePublished - Oct 1 2019

Keywords

  • immune activation
  • inflammation
  • statin
  • viral persistence

ASJC Scopus subject areas

  • Infectious Diseases
  • Pharmacology (medical)

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