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Brief Report

Higher Levels of Angiopoietin-1 Are Associated With Early and Sustained Viral Suppression in Children Living With Vertically Acquired HIV

Gulhati, Vishrut, BSca; Soo, Jeremy, MSca; Ransy, Doris G., PhDb; Brophy, Jason, MD, MScc; Kakkar, Fatima, MD, MScd; Bitnun, Ari, MD, MSce; Samson, Lindy, MD, MScc; Read, Stanley, MD, PhDe; Soudeyns, Hugo, PhDf; Hawkes, Michael T., MD, PhDg for EPIC4 Study Group

JAIDS Journal of Acquired Immune Deficiency Syndromes: April 15, 2019 - Volume 80 - Issue 5 - p 590–595
doi: 10.1097/QAI.0000000000001955
Translational Research
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Background: Systemic inflammation, platelet dysfunction, and endothelial activation persist in people living with HIV despite sustained virologic suppression (SVS) with combined antiretroviral therapy (cART) and may lead to complications such as atherosclerosis and cardiovascular disease. Angiopoietin-1 (Ang-1) is a key regulator of angiogenesis and endothelial activation and has been studied as an objective biomarker in disease states such as atherosclerosis, sepsis, and severe malaria.

Setting: Eight pediatric HIV care centers across Canada.

Methods: Cross-sectional study of 61 children living with vertically acquired HIV on cART with undetectable RNA viral load. Plasma levels of Ang-1 were measured by ELISA and analyzed in relation to clinical characteristics abstracted from medical records.

Results: Ang-1 levels were directly correlated with clinical indices of virologic control: cumulative proportion of life on effective cART (ρ = +0.35, P = 0.0078) and cumulative proportion of life with SVS (ρ = +0.36, P = 0.0049). Furthermore, higher Ang-1 levels were associated with younger age at SVS (ρ = −0.56, P < 0.0001). These associations remained statistically significant in multivariable linear regression models adjusting for potential confounders (P < 0.05 for all associations).

Conclusions: Early effective cART and SVS were associated with higher Ang-1 levels in children living with vertically acquired HIV-1.

aUniversity of Alberta, Edmonton, Alberta, Canada;

bUnité d'immunopathologie virale, Centre de recherche du CHU Sainte-Justine, Montréal, Québec, Canada;

cChildren's Hospital of Eastern Ontario, Ottawa, Ontario, Canada;

dFaculté de médecine, Université de Montréal;, Montréal, Québec, Canada

eDepartment of Pediatrics, Hospital for Sick Children, University of Toronto;, Toronto, Ontario, Canada

fUnité d'immunopathologie virale, Department of Microbiology, Infectiology and Immunology, Centre de recherche du CHU Sainte-Justine, Université de Montréal;, Montréal, Québec, Canada and

gDepartment of Pediatrics, University of Alberta, Edmonton, Alberta, Canada.

Correspondence to: Michael T. Hawkes, MD, PhD, Department of Pediatrics, University of Alberta, 3-588D Edmonton Clinic Health Academy, 11405 87 Avenue NW, Edmonton, Alberta T6G 1C9, Canada (e-mail: mthawkes@ualberta.ca).

Supported by Canadian Institutes of Health Research (CIHR), International AIDS Society (IAS), Canadian Foundation for AIDS Research (CANFAR), Women and Children's Health Research Institute (University of Alberta).

Presented at the 26th Annual Canadian Conference on HIV/AIDS Research; April 6–9, 2017; Montréal, QC, Canada. Réseau SIDA et maladies infectieuses, Fonds de recherche du Québec-santé (FRQS). FK is a FRQS Junior 1 Scholar.

The authors have no funding or conflicts of interest to disclose.

The members of EPIC4 Study Group are listed in Appendix 1.

Received August 19, 2018

Accepted November 19, 2018

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