Festschrift: Peter Beighton

Evaluating the contribution of APOBEC3G haplotypes, on influencing HIV infection in a Zimbabwean paediatric population

K Mhandire, K Duri, D Mhandire, C Musarurwa, B Stray-Pedersen, C Dandara

Abstract


Background. Apolipoprotein B mRNA-editing catalytic polypeptide like-3G (APOBEC3G) is an antiviral enzyme that reduces viral fitness by introducing uracil to thymidine hypermutations in viral genomes. Thus, polymorphisms in the APOBEC3G gene have been implicated in differential outcomes of HIV infection and disease progression. However, there is insufficient evidence on the role of APOBEC3G gene variants on HIV infection, especially in African populations. This study therefore describes polymorphisms in the APOBEC3G gene in a Zimbabwean paediatric population and evaluates their effects on susceptibility to HIV infection among children born to HIV-infected mothers. 

Methods. A total of 104 children aged between 7 and 9 years, comprising 68 perinatally exposed to HIV (32 born infected (EI) and 36 born uninfected (EU)) and 36 unexposed and uninfected (UEUI) controls were recruited. Allelic variants (n=5) in the APOBEC3G gene were characterised. 

Results. Frequencies for minor APOBEC3G alleles in the HIV-uninfected groups (EU and UEUI) were c.557G (40%), g.-90C (32%), g.-571C (12%), c.467-85C (42%), and c.582-162G (6%). APOBEC3G c.467-85C frequency was statistically significantly different when compared to the Masai of Kinyawa, Kenya population (42% v. 18%). None of the single nucleotide polymorphisms individually or as part of haplotypes were significantly associated with HIV infection when comparing the EI and EU groups. 

Conclusions. Our findings suggest that APOBEC3G polymorphisms alone may not have significant predictive power for inferring genetic susceptibility to vertical transmission of HIV in children perinatally exposed to HIV.


Authors' affiliations

K Mhandire, Division of Human Genetics, Department of Pathology, Institute of Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town; Department of Chemical Pathology, University of Zimbabwe, Harare; and Letten Foundation Research House, Harare, Zimbabwe

K Duri, Department of Immunology, University of Zimbabwe, Harare, Zimbabwe

D Mhandire, Department of Chemical Pathology, University of Zimbabwe, Harare, Zimbabwe; and Letten Foundation Research House, Harare, Zimbabwe

C Musarurwa, Department of Chemical Pathology, University of Zimbabwe, Harare, Zimbabwe

B Stray-Pedersen, Letten Foundation Research House, Harare, Zimbabwe; Division of Obstetrics and Gynecology, Rikshospitalet, University of Oslo, Norway

C Dandara, Division of Human Genetics, Department of Pathology, Institute of Infectious Disease and Molecular Medicine, Faculty of Health Sciences, University of Cape Town, South Africa

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Cite this article

South African Medical Journal 2016;106(6):S119. DOI:10.7196/SAMJ.2016.v106i6.11013

Article History

Date submitted: 2016-05-06
Date published: 2016-05-25

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