Resistance Mutations in Subtype C HIV Type 1 Isolates from Indian Patients of Mumbai Receiving NRTIs Plus NNRTIs and Experiencing a Treatment Failure: Resistance to AR

Deshpande, Alaka; Jauvin, Valérie; Magnin, Noël; Recordon-Pinson, Patrícia; Faure, Muriel; Masquelier, Bernard; Aurillac-Lavignolle, Valérie; Fleury, Hervé

doi:10.1089/aid.2006.0183

Cited by 52 publications

(59 citation statements)

References 12 publications

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“…In our study, 53.3 % of the patients (16 of 30 non-responsive patients) were on a treatment regimen containing 3TC, and none of them exhibited the Q151M mutation. Similar findings have been reported in previous publications from India [26,42]. One of the drug-naive patients in the current study, however, showed the Q151M mutation, which again suggests transmitted resistance.…”

Section: Discussionsupporting

confidence: 93%

“…In our study, the majority of the sequences obtained from the patients, all but four, were identified as subtype C (96 %) based on the reverse transcriptase gene sequence and phylogenetic analysis. As in our study, along with subtype C, subtype A1 has been reported in other studies to be a minor subtype [3,13,26,42]. The pattern of clustering shows evolutionary relatedness among the sequences.…”

Section: Discussionsupporting

confidence: 85%

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Comparative analysis of drug resistance mutations in the human immunodeficiency virus reverse transcriptase gene in patients who are non-responsive, responsive and naive to antiretroviral therapy

et al. 2016

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Drug resistance mutations in the Pol gene of human immunodeficiency virus 1 (HIV-1) are one of the critical factors associated with antiretroviral therapy (ART) failure in HIV-1 patients. The issue of resistance to reverse transcriptase inhibitors (RTIs) in HIV infection has not been adequately addressed in the Indian subcontinent. We compared HIV-1 reverse transcriptase (RT) gene sequences to identify mutations present in HIV-1 patients who were ART non-responders, ART responders and drug naive. Genotypic drug resistance testing was performed by sequencing a 655-bp region of the RT gene from 102 HIV-1 patients, consisting of 30 ART-non-responding, 35 ART-responding and 37 drug-naive patients. The Stanford HIV Resistance Database (HIVDBv 6.2), IAS-USA mutation list, ANRS_09/2012 algorithm, and Rega v8.02 algorithm were used to interpret the pattern of drug resistance. The majority of the sequences (96 %) belonged to subtype C, and a few of them (3.9 %) to subtype A1. The frequency of drug resistance mutations observed in ART-non-responding, ART-responding and drug-naive patients was 40.1 %, 10.7 % and 20.58 %, respectively. It was observed that in non-responders, multiple mutations were present in the same patient, while in responders, a single mutation was found. Some of the drug-naive patients had more than one mutation. Thymidine analogue mutations (TAMs), however, were found in non-responders and naive patients but not in responders. Although drug resistance mutations were widely distributed among ART non-responders, the presence of resistance mutations in the viruses of drug-naive patients poses a big concern in the absence of a genotyping resistance test.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 85%

Comparative analysis of drug resistance mutations in the human immunodeficiency virus reverse transcriptase gene in patients who are non-responsive, responsive and naive to antiretroviral therapy

et al. 2016

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“…Previous publications from India have highlighted the absence or low prevalence of the Q151M mutation. [4,5] Based on data from the West from previously published studies, M184V was the most commonly observed mutation in patients on NRTIs. [9] We have very limited data but the mutational patterns observed appear similar to published data.…”

Section: Discussionmentioning

confidence: 99%

“…[9] We have very limited data but the mutational patterns observed appear similar to published data. [4,5,11] One of the worrying factors is a recent report from western India which documented M41L, D67N, M184V, and A98G in the RT gene of treatment naïve individuals. [15] Mutations conferring resistance to NNRTIs were also seen, with one strain showing resistance only to NNRTIs.…”

Section: Discussionmentioning

confidence: 99%

Drug Resistant Mutations Detected by Genotypic Drug Resistance Testing in Patients Failing Therapy in Clade C Hiv-1 Infected Individuals From India

Kandathil

Kannangai

Verghese

et al. 2009

Indian Journal of Medical Microbiology

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Purpose: There has been an increase in the number of individuals administered antiretroviral therapy (ART) in India but treatment outcome is hampered by increasing development of drug resistance. Previous reports from India have shown M184V as the commonest mutation in treated individuals. However, there is no evidence for any protease mutations in these reports. This study was done to observe the common/unique mutational patterns observed in reverse transcriptase (RT) and protease (Pr) genes of clade C HIV-1 strains from individuals showing treatment failure in India. Materials and Methods: The assay was done by sequencing the Pr and RT genes of the HIV-1 strains from 18 individuals failing ART. Analysis was carried out using Stanford HIV drug resistance database (SHDB). The sequences were also submitted to the calibrated population resistance tool of SHDB and Rega HIV-1 sub typing tool. Phylogenetic analysis and quality control were performed with Mega 4. Results: Among the 20 strains, 19 showed resistance to both nucleoside reverse transcriptase inhibitors (NRTIs) and non-nucleoside reverse transcriptase inhibitors (NNRTIs), one strain to NNRTIs and five strains showed protease inhibitors (PI) resistance and 3-class resistance. The most common mutation conferring NRTI resistance was M184V (90%) while K103N (45%) was the most common mutation conferring NNRTI resistance. The M46I mutation was seen in 20% of the Pr sequences. Conclusion: Resistance testing to check the prevalence of drug resistance mutations that arise following failure of the first line regimen to establish guidelines for second line regimens in India is a must. Studies are needed to confirm if mutation patterns that arise among clade C following failure of ART are the same as for clade B strains.

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“…This suggested that subtype C could have a lower genetic barrier to resistance to NNRTIs than subtype B, and that this V106M mutation could be more frequent in subtype C infected patients failing therapy, than in subtype B infected patients. Indeed, the clinical importance of the V106M mutation in non-B subtypes has been confirmed in several studies showing that V106M is more frequently seen in subtype C (and CRF01_AE) after therapy with EFV or NVP (Deshpande et al, 2007;Hsu et al, 2005;Marconi et al, 2008;Rajesh et al, 2009). The G190A mutation was also relatively more frequent in subtype C Indian and Israeli patients failling NNRTI-based regimens than in subtype B (Deshpande et al, 2007;Grossman et al, 2004).…”

Section: Impact Of Hiv-1 Diversity In Drug Resistancementioning

confidence: 87%

HIV-1 Diversity and Its Implications in Diagnosis, Transmission, Disease Progression, and Antiretroviral Therapy

Bártolo¹,

Taveira²

2012

Genetic Diversity in Microorganisms

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Resistance Mutations in Subtype C HIV Type 1 Isolates from Indian Patients of Mumbai Receiving NRTIs Plus NNRTIs and Experiencing a Treatment Failure: Resistance to AR

Cited by 52 publications

References 12 publications

Comparative analysis of drug resistance mutations in the human immunodeficiency virus reverse transcriptase gene in patients who are non-responsive, responsive and naive to antiretroviral therapy

Comparative analysis of drug resistance mutations in the human immunodeficiency virus reverse transcriptase gene in patients who are non-responsive, responsive and naive to antiretroviral therapy

Drug Resistant Mutations Detected by Genotypic Drug Resistance Testing in Patients Failing Therapy in Clade C Hiv-1 Infected Individuals From India

HIV-1 Diversity and Its Implications in Diagnosis, Transmission, Disease Progression, and Antiretroviral Therapy

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