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|Title: ||Prevalence of Minor Mutations and Natural Polymorphisms at the Protease Gene among Treatment-Naïve Human Immunodeficiency Virus-1 Infected Individual in Jos, Nigeria|
|Authors: ||Okopi, Joseph A. Anejo|
Agaba, Patricia A.
Ugoagwu, Placid O.
Isa, Samson E.
Okwori, Joseph A. E.
Sagay, Solomon A.
Idoko, John A.
Agbaji, Oche O.
Jatau, David E.
Olonitola, Steve O.
|Keywords: ||Human immunodeficiency virus-1 drug resistance|
|Issue Date: ||2013|
|Publisher: ||Journal of HIV & Human Reproduction|
|Series/Report no.: ||Vol. 1;No. 1; Pp 8-14|
|Abstract: ||Background: Minor mutations to protease inhibitors often occur as polymorphisms in the protease gene in non-B human
immunodeficiency virus (HIV)-1 subtype among antiretroviral (ARV) treatment-naïve patients. Aims: This study sought to
determine the prevalence of minor mutations occurring in the protease gene among ARV naïve HIV-1 infected patients in Jos,
Nigeria. Settings and Design: We retrospectively analyzed specimen of 105 patients recruited between October 2010 and April 2011 at the HIV clinic, Jos University Teaching Hospital, Nigeria. Materials and Methods: Genotypic testing was done using
an in-house genotyping system at the Kenya Medical Research Institute HIV-Research Laboratory in Kisumu, Kenya; HIV-1
viral resistance mutations assessed using Stanford HIV drug resistance database and classified using International acquired
immunodeficiency syndrome (AIDS) Society (IAS)-USA list of mutations. In additional, viral subtypes were determined using
REGA subtyping tool v.2.0 and CD4 levels by flow cytometry. Statistical analysis: Prevalence of mutations was computed
and participants’ baseline clinical and biological properties summarized by percentages for categorical variables and mean/ median for quantitative variables. Results: Of the 105 samples, 100 were successfully amplified. HIV-1 subtypes identified were circulating recombinant form (CRF) — CRF02_AG (48.0%), G (41.0%), CRF06_cpx (6.0%) and A1 (5.0%). The most
prevalent minor mutations among the patients occurred at positions L89M (96%), M36I (93%), K20I (77%), V82I (39%), E35Q (29%), L63P (25%) and polymorphisms at I13V (99%), R41K (86%), H69K (86%), K14R (67%). One sample presented with a major PI resistance mutation (Q58E). Conclusions: We found high rates of minor mutations and polymorphisms in circulation, possibly reflecting the drug naivety of participants. In addition, there was an evidence of transmitted drug
resistance, hence targeted genetic resistance testing should be considered in national treatment guidelines.|
|Appears in Collections:||Family Medicine|
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