Authors
Simon Bannison Bani
Kwabena Owusu Danquah
Christian Obirikorang
William K. B. A. Owiredu
Lawrence Quaye
Edmund Muonir Der
Emmanuel Acheampong, Edith Cowan UniversityFollow
Yussif Adams
Peter Paul M. Dapare
Moses Banyeh
Enoch Odame Anto, Edith Cowan UniversityFollow
Samuel Asamoah Sakyi
Document Type
Journal Article
Publication Title
Scientific Reports
Volume
10
Issue
1
Publisher
Springer Nature
School
School of Medical and Health Sciences / Graduate Research School
RAS ID
35347
Abstract
© 2020, The Author(s). Highly active antiretroviral therapy (HAART) is known to cause lipid abnormalities such as dyslipidaemia in HIV-infected individuals. Yet, dyslipidaemia may not independently occur as it may be worsened by single nucleotide polymorphisms (SNPs) in lecithin cholesterol acyltransferase (LCAT) and lipoprotein lipase (LPL). This case–control study was conducted in three-selected hospitals in the Northern part of Ghana. The study constituted a total of 118 HIV-infected participants aged 19–71 years, who had been on HAART for 6–24 months. Dyslipidaemia was defined based on the NCEP-ATP III criteria. HIV-infected individuals on HAART with dyslipidaemia were classified as cases while those without dyslipidaemia were grouped as controls. Lipid profile was measured using an automatic clinical chemistry analyzer and genomic DNA was extracted for PCR (GeneAmp PCR System 2700). Overall, the prevalence of dyslipidaemia was 39.0% (46/118). High levels of low-density lipoprotein cholesterol (LDL-C), total cholesterol (TC), and reduced levels of high-density lipoprotein cholesterol (HDL-C) were observed in all cases. A total of 256 selected PCR amplicons comprising 137 LPL (exons 3, 5 and 6) and 119 LCAT (exons 1, 4, and 6) were sequenced in 46 samples (Inqaba Biotech). Six (6) clinically significant SNPs were identified in exons 1 and 4 for LCAT whereas 25 non-clinically significant SNPs were identified for LPL in exons 5 and 6. At position 97 for LCAT exon 1, there was a deletion of the nucleotide, ‘A’ in 32.5% (13/40) of the sampled population while 67.5% (27/40) of the sample population retained the nucleotide, ‘A’ which was significantly associated with dyslipidaemic outcomes in the study population (p = 0.0004). A total of 25 SNPs were identified in exons 5 and 6 of LPL; 22 were substitutions, and 3 were insertions. However, none of the 25 SNPs identified in LPL exon 5 and 6 were statistically significant. SNPs in LCAT may independently contribute to dyslipidaemia among Ghanaian HIV-infected individuals on HAART, thus, allowing genetic and/or functional differential diagnosis of dyslipidaemia and creating an opportunity for potentially preventive options.
DOI
10.1038/s41598-020-76113-2
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
Comments
Bani, S. B., Danquah, K. O., Obirikorang, C., Owiredu, W. K. B. A., Quaye, L., Der, E. M., ... Sakyi, S. A. (2020). Single nucleotide polymorphisms in LCAT may contribute to dyslipidaemia in HIV-infected individuals on HAART in a Ghanaian population. Scientific Reports, 10, article 19419. https://doi.org/10.1038/s41598-020-76113-2