Brief Report

No Evidence for an Association Between Statin Use and Lower Biomarkers of HIV Persistence or Immune Activation/Inflammation During Effective ART

A5321 Study Team

Research output: Contribution to journalArticle

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/10 CD4 T cells; P = 0.58), CA-RNA (53 vs. 37 copies/10 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 (1999)
Volume82
Issue number2
DOIs
StatePublished - Oct 1 2019

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Hydroxymethylglutaryl-CoA Reductase Inhibitors
Biomarkers
HIV
Inflammation
RNA
Therapeutics
Neopterin
T-Lymphocytes
DNA
Antiviral Agents
HIV-1
Interleukin-6
Anti-Inflammatory Agents
Tumor Necrosis Factor-alpha
Prospective Studies

ASJC Scopus subject areas

  • Infectious Diseases
  • Pharmacology (medical)

Cite this

@article{3b4aa893009a4ebda21c716fd0a5daf6,
title = "Brief Report: No Evidence for an Association Between Statin Use and Lower Biomarkers of HIV Persistence or Immune Activation/Inflammation During Effective ART",
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/10 CD4 T cells; P = 0.58), CA-RNA (53 vs. 37 copies/10 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.",
author = "{A5321 Study Team} and Bedimo, {Roger J} and Hanna Mar and Bosch, {Ronald J.} and Drechsler, {Henning J} and Cyktor, {Joshua C.} and Macatangay, {Barnard J.C.} and Christina Lalama and Charles Rinaldo and Ann Collier and Catherine Godfrey and Evelyn Hogg and Christopher Hensel and Eron, {Joseph J.} and Mcmahon, {Deborah K.} and Mellors, {John W.} and Pablo Tebas and Gandhi, {Rajesh T.}",
year = "2019",
month = "10",
day = "1",
doi = "10.1097/QAI.0000000000002124",
language = "English (US)",
volume = "82",
pages = "e27--e31",
journal = "Journal of acquired immune deficiency syndromes (1999)",
issn = "1525-4135",
publisher = "Lippincott Williams and Wilkins",
number = "2",

}

TY - JOUR

T1 - Brief Report

T2 - No Evidence for an Association Between Statin Use and Lower Biomarkers of HIV Persistence or Immune Activation/Inflammation During Effective ART

AU - A5321 Study Team

AU - Bedimo, Roger J

AU - Mar, Hanna

AU - Bosch, Ronald J.

AU - Drechsler, Henning J

AU - Cyktor, Joshua C.

AU - Macatangay, Barnard J.C.

AU - Lalama, Christina

AU - Rinaldo, Charles

AU - Collier, Ann

AU - Godfrey, Catherine

AU - Hogg, Evelyn

AU - Hensel, Christopher

AU - Eron, Joseph J.

AU - Mcmahon, Deborah K.

AU - Mellors, John W.

AU - Tebas, Pablo

AU - Gandhi, Rajesh T.

PY - 2019/10/1

Y1 - 2019/10/1

N2 - 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/10 CD4 T cells; P = 0.58), CA-RNA (53 vs. 37 copies/10 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.

AB - 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/10 CD4 T cells; P = 0.58), CA-RNA (53 vs. 37 copies/10 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.

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U2 - 10.1097/QAI.0000000000002124

DO - 10.1097/QAI.0000000000002124

M3 - Article

VL - 82

SP - e27-e31

JO - Journal of acquired immune deficiency syndromes (1999)

JF - Journal of acquired immune deficiency syndromes (1999)

SN - 1525-4135

IS - 2

ER -