scholarly journals Prevalence of Drug Resistance in Human Immunodeficiency Virus Type 1-Infected Treatment-Naive Children in Pune, India

2014 ◽  
Vol 30 (3) ◽  
pp. 294-298 ◽  
Author(s):  
Mukesh Kumar ◽  
Sourav Sen ◽  
Rakesh K. Gupta ◽  
Devidas Chaturbhuj ◽  
Srikanth P. Tripathy ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Drug Resistance ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Immunodeficiency Virus ◽  
Treatment Naïve

scholarly journals Detection of human immunodeficiency virus type 1 transmitted drug resistance among treatment-naive individuals residing in Jakarta, Indonesia

2020 ◽  
Author(s):  
Siti Qamariyah Khairunisa ◽  
Ni Luh Ayu Megasari ◽  
Retno Pudji Rahayu ◽  
Adiana Mutamsari Witaningrum ◽  
Shuhei Ueda ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Drug Resistance ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Capital City ◽  
Transmitted Drug Resistance ◽  
Immunodeficiency Virus ◽  
Treatment Naïve ◽  
Hiv 1

The presence of transmitted drug resist- ance (TDR) in human immunodeficiency virus type 1 (HIV-1) infected individuals naive to antiretroviral therapy, may affect the effectiveness of treatment. Jakarta, the capital city of Indonesia, recorded the high- est number of cumulative HIV infection cases in the country. This study aimed to identify on the appearance of TDR, as well as to identify HIV-1 subtypes circulating among treatment-naive individuals in Jakarta. Whole blood samples collected from 43 HIV-1 infected, treatment-naive individuals. Viral subtyping and drug resist- ance testing were performed on HIV-1 pol genes amplified using nested polymerase chain reaction. CRF01_AE was detected most frequently in Jakarta (73.08%). Drug resistance-related major mutation was not detected in protease fragments of pol gene, but two major mutations, K103N (6.67%) and Y181C (6.67%), were detected in reverse transcriptase fragments of pol gene. Our results suggest that TDR was emerged in Jakarta at a certain extent, thus further surveillance study to monitor the TDR prevalence and circulating HIV-1 subtypes in this region is considered to be necessary.

scholarly journals Pretreatment human immunodeficiency virus type 1 (HIV-1) drug resistance in transmission clusters of the Cologne-Bonn region, Germany

2019 ◽  
Vol 25 (2) ◽  
pp. 253.e1-253.e4 ◽  
Author(s):  
M. Stecher ◽  
A. Chaillon ◽  
A.M. Eis-Hübinger ◽  
C. Lehmann ◽  
G. Fätkenheuer ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Drug Resistance ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Immunodeficiency Virus ◽  
Hiv 1

scholarly journals Nucleotide and Amino Acid Polymorphisms at Drug Resistance Sites in Non-B-Subtype Variants of Human Immunodeficiency Virus Type 1

2004 ◽  
Vol 48 (8) ◽  
pp. 2993-2998 ◽  
Author(s):  
Dan Turner ◽  
Bluma Brenner ◽  
Daniela Moisi ◽  
Mervi Detorio ◽  
Raymond Cesaire ◽  
...  
Keyword(s):  
Human Immunodeficiency Virus ◽  
Drug Resistance ◽  
Amino Acid ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Subtype B ◽  
Immunodeficiency Virus ◽  
Subtype A ◽  
Silent Substitutions

ABSTRACT We have compared nucleotide substitutions and polymorphisms at codons known to confer drug resistance in subtype B strains of human immunodeficiency virus type 1 (HIV-1) with similar substitutions in viruses of other subtypes. Genotypic analysis was performed on viruses from untreated individuals. Nucleotide and amino acid diversity at resistance sites was compared with a consensus subtype B reference virus. Among patients with non-subtype B infections, polymorphisms relative to subtype B were observed at codon 10 in protease (PR). These included silent substitutions (CTC→CTT, CTA, TTA) and an amino acid mutation, L10I. Subtype A viruses possessed a V179I substitution in reverse transcriptase (RT). Subtype G viruses were identified by silent substitutions at codon 181 in RT (TAT→TAC). Similarly, subtype A/G viruses were identified by a substitution at position 67 in RT (GAC→GAT). Subtype C was distinguished by silent substitutions at codons 106 (GTA→GTG) and 219 (AAA→AAG) in RT and codon 48 (GGG→GGA) in PR. Variations relative to subtype B were seen at RT position 215 (ACC→ACT) for subtypes A and A/E. These substitutions and polymorphisms reflect different patterns of codon usage among viruses of different subtypes. However, the existence of different subtypes may only rarely affect patterns of drug resistance-associated mutations.

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