Folate deficiency increases the incidence of dolutegravir-associated foetal defects in a mouse pregnancy model.


Journal

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

Informations de publication

Date de publication:
Sep 2023
Historique:
received: 26 04 2023
revised: 26 07 2023
accepted: 03 08 2023
medline: 18 9 2023
pubmed: 16 8 2023
entrez: 16 8 2023
Statut: ppublish

Résumé

Dolutegravir (DTG) is a recommended first-line regimen for all people with Human Immunodeficiency Virus (HIV) infection. Initial findings from Botswana, a country with no folate fortification program, showed an elevated prevalence of neural tube defects (NTDs) with peri-conceptional exposure to DTG. Here we explore whether a low folate diet influences the risk of DTG-associated foetal anomalies in a mouse model. C57BL/6 mice fed a folate-deficient diet for 2 weeks, were mated and then randomly allocated to control (water), or 1xDTG (2.5 mg/kg), or 5xDTG (12.5 mg/kg) both administered orally with 50 mg/kg tenofovir disoproxil fumarate 33.3 mg/kg emtricitabine. Treatment was administered once daily from gestational day (GD) 0.5 to sacrifice (GD15.5). Foetuses were assessed for gross anomalies. Maternal and foetal folate levels were quantified. 313 litters (103 control, 106 1xDTG, 104 5xDTG) were assessed. Viability, placental weight, and foetal weight did not differ between groups. NTDs were only observed in the DTG groups (litter rate: 0% control; 1.0% 1xDTG; 1.3% 5xDTG). Tail, abdominal wall, limb, craniofacial, and bleeding defects all occurred at higher rates in the DTG groups versus control. Compared with our previous findings on DTG usage in folate-replete mouse pregnancies, folate deficiency was associated with higher rates of several defects, including NTDs, but in the DTG groups only. We observed a severe left-right asymmetry phenotype that was more frequent in DTG groups than controls. Maternal folate deficiency may increase the risk for DTG-associated foetal defects. Periconceptional folic acid supplementation could be considered for women with HIV taking DTG during pregnancy, particularly in countries lacking folate fortification programs. This project has been funded by 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 and award #R01HD104553. LS is supported by a Tier 1 Canada Research Chair in Maternal-Child Health and HIV. HM is supported by a Junior Investigator award from the Ontario HIV Treatment Network.

Sections du résumé

BACKGROUND BACKGROUND
Dolutegravir (DTG) is a recommended first-line regimen for all people with Human Immunodeficiency Virus (HIV) infection. Initial findings from Botswana, a country with no folate fortification program, showed an elevated prevalence of neural tube defects (NTDs) with peri-conceptional exposure to DTG. Here we explore whether a low folate diet influences the risk of DTG-associated foetal anomalies in a mouse model.
METHODS METHODS
C57BL/6 mice fed a folate-deficient diet for 2 weeks, were mated and then randomly allocated to control (water), or 1xDTG (2.5 mg/kg), or 5xDTG (12.5 mg/kg) both administered orally with 50 mg/kg tenofovir disoproxil fumarate 33.3 mg/kg emtricitabine. Treatment was administered once daily from gestational day (GD) 0.5 to sacrifice (GD15.5). Foetuses were assessed for gross anomalies. Maternal and foetal folate levels were quantified.
FINDINGS RESULTS
313 litters (103 control, 106 1xDTG, 104 5xDTG) were assessed. Viability, placental weight, and foetal weight did not differ between groups. NTDs were only observed in the DTG groups (litter rate: 0% control; 1.0% 1xDTG; 1.3% 5xDTG). Tail, abdominal wall, limb, craniofacial, and bleeding defects all occurred at higher rates in the DTG groups versus control. Compared with our previous findings on DTG usage in folate-replete mouse pregnancies, folate deficiency was associated with higher rates of several defects, including NTDs, but in the DTG groups only. We observed a severe left-right asymmetry phenotype that was more frequent in DTG groups than controls.
INTERPRETATION CONCLUSIONS
Maternal folate deficiency may increase the risk for DTG-associated foetal defects. Periconceptional folic acid supplementation could be considered for women with HIV taking DTG during pregnancy, particularly in countries lacking folate fortification programs.
FUNDING BACKGROUND
This project has been funded by 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 and award #R01HD104553. LS is supported by a Tier 1 Canada Research Chair in Maternal-Child Health and HIV. HM is supported by a Junior Investigator award from the Ontario HIV Treatment Network.

Identifiants

pubmed: 37586112
pii: S2352-3964(23)00328-6
doi: 10.1016/j.ebiom.2023.104762
pmc: PMC10450420
pii:
doi:

Substances chimiques

dolutegravir DKO1W9H7M1
Folic Acid 935E97BOY8

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

104762

Informations de copyright

Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of interests The authors have no conflicts of interest relating to this study.

Auteurs

Haneesha Mohan (H)

Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.

Jessica Nguyen (J)

Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.

Ben MacKenzie (B)

Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.

Audrey Yee (A)

Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.

Evelyn Yukino Laurette (EY)

Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.

Tanvi Sanghvi (T)

Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.

Oscar Tejada (O)

Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.

Valeriya Dontsova (V)

Toronto General Hospital Research Institute, University Health Network, Toronto, Ontario, Canada.

Kit-Yi Leung (KY)

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

Cameron Goddard (C)

Mouse Imaging Center, The Hospital for Sick Children, Toronto, Ontario, Canada.

Taylor De Young (T)

Mouse Imaging Center, The Hospital for Sick Children, Toronto, Ontario, Canada.

John G Sled (JG)

Mouse Imaging Center, 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, 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, University Health Network, Toronto, Ontario, Canada; Department of Immunology and Institute of Medical Sciences, University of Toronto, Toronto, Ontario, Canada. Electronic address: lena.serghides@utoronto.ca.

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