TY - JOUR
T1 - Analyses of HIV-1 integrase gene sequences among treatment-naive patients in the Eastern Cape, South Africa
AU - Onoriode Digban, Tennison
AU - Chucks Iweriebor, Benson
AU - Chikwelu Obi, Larry
AU - Nwodo, Uchechuwku
AU - Ifeanyi Okoh, Anthony
N1 - Publisher Copyright:
© 2019 Wiley Periodicals, Inc.
PY - 2020/8/1
Y1 - 2020/8/1
N2 - Drug resistance has been recognized in all available therapeutic class of medications for the management of human immunodeficiency virus-1 (HIV-1) infected patients. This makes the continuous study of HIV drug resistance and new treatment options pertinent to patients and researchers globally. The aim of this study is to analyze the complete HIV-1 integrase gene for the possible occurrence of resistance mutations or polymorphisms. We performed genetic analyses on 48 treatment-naive HIV-1-infected patients using nested polymerase chain reaction. Integrase drug-related resistance mutation (DRMs) analysis was performed on all generated sequences according to Stanford HIV drug interpretation program and the International AIDS Society-USA guidelines while phylogenetic analysis was inferred using MEGA 6. The study revealed no major resistance-associated mutation. However, E157Q (2.1%), L74M/I (4.2%), and P142T (2.1%) were the observed accessory and polymorphic mutations. Naturally occurring polymorphism observed were E11D, K14R, D25E, V31I, M50I, V72I, P90T, F100Y, L101I, T124A, T125A, K136Q, D167E, V201I, L234I, A265V, A269K, D278A, and S283G. Phylogenetic analysis delineated all the sequences as HIV-1 subtype C. The study revealed the absence of major integrase inhibitors associated resistance mutations in a setting where integrase inhibitor is administered as salvage therapy in patients developing resistance to first and second-line antiretroviral treatment. However minor and natural polymorphisms were observed and thus may influence the outcome of each treatment regimen. However, additional studies are required to precisely evaluate the impact of these mutations on integrase inhibitors in the Eastern Cape of South Africa.
AB - Drug resistance has been recognized in all available therapeutic class of medications for the management of human immunodeficiency virus-1 (HIV-1) infected patients. This makes the continuous study of HIV drug resistance and new treatment options pertinent to patients and researchers globally. The aim of this study is to analyze the complete HIV-1 integrase gene for the possible occurrence of resistance mutations or polymorphisms. We performed genetic analyses on 48 treatment-naive HIV-1-infected patients using nested polymerase chain reaction. Integrase drug-related resistance mutation (DRMs) analysis was performed on all generated sequences according to Stanford HIV drug interpretation program and the International AIDS Society-USA guidelines while phylogenetic analysis was inferred using MEGA 6. The study revealed no major resistance-associated mutation. However, E157Q (2.1%), L74M/I (4.2%), and P142T (2.1%) were the observed accessory and polymorphic mutations. Naturally occurring polymorphism observed were E11D, K14R, D25E, V31I, M50I, V72I, P90T, F100Y, L101I, T124A, T125A, K136Q, D167E, V201I, L234I, A265V, A269K, D278A, and S283G. Phylogenetic analysis delineated all the sequences as HIV-1 subtype C. The study revealed the absence of major integrase inhibitors associated resistance mutations in a setting where integrase inhibitor is administered as salvage therapy in patients developing resistance to first and second-line antiretroviral treatment. However minor and natural polymorphisms were observed and thus may influence the outcome of each treatment regimen. However, additional studies are required to precisely evaluate the impact of these mutations on integrase inhibitors in the Eastern Cape of South Africa.
KW - RNA extraction
KW - Research and Analysis Methods
KW - antiviral agents
KW - infection
KW - integrase inhibitors
KW - resistance
UR - http://www.scopus.com/inward/record.url?scp=85078275011&partnerID=8YFLogxK
U2 - 10.1002/jmv.25661
DO - 10.1002/jmv.25661
M3 - Article
C2 - 31889319
AN - SCOPUS:85078275011
SN - 0146-6615
VL - 92
SP - 1165
EP - 1172
JO - Journal of Medical Virology
JF - Journal of Medical Virology
IS - 8
ER -