Dolutegravir in pregnant mice is associated with increased rates of fetal defects at therapeutic but not at supratherapeutic levels.


Journal

EBioMedicine
ISSN: 2352-3964
Titre abrégé: EBioMedicine
Pays: Netherlands
ID NLM: 101647039

Informations de publication

Date de publication:
Jan 2021
Historique:
received: 08 09 2020
revised: 02 11 2020
accepted: 25 11 2020
pubmed: 21 12 2020
medline: 6 10 2021
entrez: 20 12 2020
Statut: ppublish

Résumé

Dolutegravir (DTG) is a preferred regimen for all people with HIV including pregnant women, but its effects on the fetus are not fully understood. Periconceptional exposure to DTG has been associated with increased rates of neural tube defects (NTDs), although it is unknown whether this is a causal relationship. This has led to uncertainty around the use of DTG in women of reproductive potential. Pregnant C57BL/6J mice were randomly allocated to control (water), 1x-DTG (2.5 mg/kg-peak plasma concentration ~3000 ng/ml - therapeutic level), or 5x-DTG (12.5 mg/kg-peak plasma concentration ~12,000 ng/ml - supratherapeutic level), once daily from gestational day 0.5 until sacrifice. DTG was administered with 50 mg/kg tenofovir+33.3 mg/kg emtricitabine. Fetal phenotypes were determined, and maternal and fetal folate levels were quantified by mass-spectrometry. 352 litters (91 control, 150 1x-DTG, 111 5x-DTG) yielding 2776 fetuses (747 control, 1174 1x-DTG, 855 5x-DTG) were assessed. Litter size and viability rates were similar between groups. Fetal and placenta weights were lower in the 1x-DTG vs. control. Placental weight was higher in the 5x-DTG vs. control. Five NTDs were observed, all in the 1x-DTG group. Fetal defects, including microphthalmia, severe edema, and vascular/bleeding defects were more frequent in the 1x-DTG group. In contrast, defect rates in the 5x-DTG were similar to control. Fetal folate levels were similar between control and 1x-DTG, but were significantly higher in the 5x-DTG group. Our findings support a causal relationship of DTG at therapeutic doses with increased risk for fetal defects, including NTDs at a rate that is similar that reported in the Tsepamo study for women exposed to DTG-based ART from conception. The non-monotonic dose-response relationship between DTG and fetal anomalies could explain the previous lack of fetal toxicity findings from pre-clinical DTG studies. The fetal folate levels suggest that DTG is unlikely to be an inhibitor of folate uptake. This project has been funded with Federal funds from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services, under Contract No. HHSN275201800001I.

Sections du résumé

BACKGROUND BACKGROUND
Dolutegravir (DTG) is a preferred regimen for all people with HIV including pregnant women, but its effects on the fetus are not fully understood. Periconceptional exposure to DTG has been associated with increased rates of neural tube defects (NTDs), although it is unknown whether this is a causal relationship. This has led to uncertainty around the use of DTG in women of reproductive potential.
METHODS METHODS
Pregnant C57BL/6J mice were randomly allocated to control (water), 1x-DTG (2.5 mg/kg-peak plasma concentration ~3000 ng/ml - therapeutic level), or 5x-DTG (12.5 mg/kg-peak plasma concentration ~12,000 ng/ml - supratherapeutic level), once daily from gestational day 0.5 until sacrifice. DTG was administered with 50 mg/kg tenofovir+33.3 mg/kg emtricitabine. Fetal phenotypes were determined, and maternal and fetal folate levels were quantified by mass-spectrometry.
FINDINGS RESULTS
352 litters (91 control, 150 1x-DTG, 111 5x-DTG) yielding 2776 fetuses (747 control, 1174 1x-DTG, 855 5x-DTG) were assessed. Litter size and viability rates were similar between groups. Fetal and placenta weights were lower in the 1x-DTG vs. control. Placental weight was higher in the 5x-DTG vs. control. Five NTDs were observed, all in the 1x-DTG group. Fetal defects, including microphthalmia, severe edema, and vascular/bleeding defects were more frequent in the 1x-DTG group. In contrast, defect rates in the 5x-DTG were similar to control. Fetal folate levels were similar between control and 1x-DTG, but were significantly higher in the 5x-DTG group.
INTERPRETATION CONCLUSIONS
Our findings support a causal relationship of DTG at therapeutic doses with increased risk for fetal defects, including NTDs at a rate that is similar that reported in the Tsepamo study for women exposed to DTG-based ART from conception. The non-monotonic dose-response relationship between DTG and fetal anomalies could explain the previous lack of fetal toxicity findings from pre-clinical DTG studies. The fetal folate levels suggest that DTG is unlikely to be an inhibitor of folate uptake.
FUNDING BACKGROUND
This project has been funded with Federal funds from the Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Department of Health and Human Services, under Contract No. HHSN275201800001I.

Identifiants

pubmed: 33341441
pii: S2352-3964(20)30543-0
doi: 10.1016/j.ebiom.2020.103167
pmc: PMC7753150
pii:
doi:

Substances chimiques

HIV Integrase Inhibitors 0
Heterocyclic Compounds, 3-Ring 0
Oxazines 0
Piperazines 0
Pyridones 0
dolutegravir DKO1W9H7M1

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

103167

Subventions

Organisme : NICHD NIH HHS
ID : HHSN275201800001C
Pays : United States
Organisme : NICHD NIH HHS
ID : HHSN275201800001I
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2020 The Authors. Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interest The authors have no competing interests relating to this study. AJC acts as consultant for ViiV Healthcare Limited, with any fees going to support his research program. LS received personal support for participating in a ViiV organized Think Tank.

Auteurs

Haneesha Mohan (H)

Toronto General Hospital Research Institute, Princess Margaret Cancer Research Tower (PMCRT), University Health Network, 101 College Street, 10th Floor, Room 359, Toronto, Ontario M5G 1L7, Canada.

Monica Guzman Lenis (MG)

Toronto General Hospital Research Institute, Princess Margaret Cancer Research Tower (PMCRT), University Health Network, 101 College Street, 10th Floor, Room 359, Toronto, Ontario M5G 1L7, Canada.

Evelyn Y Laurette (EY)

Toronto General Hospital Research Institute, Princess Margaret Cancer Research Tower (PMCRT), University Health Network, 101 College Street, 10th Floor, Room 359, Toronto, Ontario M5G 1L7, Canada.

Oscar Tejada (O)

Toronto General Hospital Research Institute, Princess Margaret Cancer Research Tower (PMCRT), University Health Network, 101 College Street, 10th Floor, Room 359, Toronto, Ontario M5G 1L7, Canada.

Tanvi Sanghvi (T)

Toronto General Hospital Research Institute, Princess Margaret Cancer Research Tower (PMCRT), University Health Network, 101 College Street, 10th Floor, Room 359, Toronto, Ontario M5G 1L7, Canada.

Kit-Yi Leung (KY)

Developmental Biology & Cancer Department, UCL Great Ormond Street Institute of Child Health, University College London, London, UK.

Lindsay S Cahill (LS)

Mouse Imaging Centre, The Hospital for Sick Children, Toronto, Ontario, Canada; Department of Chemistry, Memorial University of Newfoundland, St John's, Newfoundland and Labrador, Canada.

John G Sled (JG)

Mouse Imaging Centre, The Hospital for Sick Children, Toronto, Ontario, Canada; Department of Medical Biophysics, University of Toronto, Toronto, Ontario, Canada; Translational Medicine, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada.

Paul Delgado-Olguín (P)

Translational Medicine, The Hospital for Sick Children, Toronto, Ontario M5G 0A4, Canada; Department of Molecular Genetics, University of Toronto, Toronto, Ontario M5S 1A8, Canada; Heart & Stroke Richard Lewar Centre of Excellence, Toronto, Ontario M5S 3H2, Canada.

Nicholas D E Greene (NDE)

Developmental Biology & Cancer Department, UCL Great Ormond Street Institute of Child Health, University College London, London, UK.

Andrew J Copp (AJ)

Developmental Biology & Cancer Department, UCL Great Ormond Street Institute of Child Health, University College London, London, UK.

Lena Serghides (L)

Toronto General Hospital Research Institute, Princess Margaret Cancer Research Tower (PMCRT), University Health Network, 101 College Street, 10th Floor, Room 359, Toronto, Ontario M5G 1L7, Canada; Department of Immunology and Institute of Medical Sciences, University of Toronto, Toronto, Ontario, Canada; Women's College Research Institute, Women's College Hospital, Toronto, Ontario, Canada. Electronic address: lena.serghides@utoronto.ca.

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Classifications MeSH