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Efavirenz
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Alan C. Street, Irani Thevarajan
Characteristic mutations in the reverse transcriptase gene are associated with development of resistance to efavirenz (Stanford University HIV Drug Resistance Database, 2014; Wensing et al., 2015). That these mutations truly cause efavirenz resistance has been proven in experiments in vitro in which the mutations are introduced into the reverse transcriptase gene of drug-sensitive HIV-1 strains by site-directed mutagenesis; when these mutated strains are assayed for reverse transcriptase activity and viral replicative capacity, they are no longer inhibited by efavirenz (Bacheler et al., 2001).
Use of whole genome sequencing in surveillance of drug resistant tuberculosis
Published in Expert Review of Anti-infective Therapy, 2018
Ruth McNerney, Matteo Zignol, Taane G Clark
TB would not be the first disease to utilize sequencing for surveillance. Precedence has been established in the field of HIV where genotyping is used to assess resistance to antiretroviral drugs. The Stanford HIV Drug Resistance Database was established in 2007 to serve as a public repository for genotypic, phenotypic, and clinical data facilitating the development of consensus guidelines on nomenclature and data interpretation. WHO guidelines on HIV drug resistance surveillance were updated in 2015 [71], and a global network of testing centers and genotyping laboratories has been established [72]. Other conditions that also utilize NGS for surveillance include flu, polio and malaria, and some foodborne diseases.
Frequency of cross-resistance to rilpivirine and etravirine among HIV-1 subtype C infected individuals failing nevirapine/efavirenz based ART regimen
Published in Infectious Diseases, 2019
V. V. Ramalingam, J. P. Demosthenes, B. C. Ghale, P. Rupali, G. M. Varghese, O. C. Abraham, R. Kannangai
This observational study was conducted at the Clinical Virology and Infectious Disease departments of a tertiary care hospital in South India. Samples were collected from 100 consecutive patients who were failing first line ART regimen (tenofovir/zidovudine and lamivudine with nevirapine/efavirenz) and subjected to routine HIV-1 genotypic resistance testing during 2012–2017. In this cohort of patients close to 90% of the patients acquired HIV through heterosexual contact. No cases of prevention of mother to child transmission or cases of patients who were on mono or dual therapy were included in the study. The genotypic resistance assay was carried out in 100 HIV-1 infected individuals towards patient management by amplification of pol gene from plasma followed by sequencing as described earlier [3]. Briefly, the HIV-1 pol gene was amplified by a nested PCR from extracts of plasma RNA using QIAamp viral RNA extraction kit (QIAGEN GmbH, Hilden, Germany). Initially, QIAGEN One Step RT PCR assay (cDNA synthesis and first round PCR) was carried out followed by a second round PCR to amplify specific 1800bp pol gene [3]. The sequencing of the amplified products was done with three sets (forward and reverse) of the sequencing primers using Big dye terminator assay with the ABI PRISM 310 genetic analyzer (PE Applied Bio-System, CA). The sequences were aligned using the Bioedit software (www.mbio.ncsu.edu/bioedit/bioedit.html) and subsequently submitted to the Stanford HIV drug resistance database (http://hivdb.stanford.edu) for analysis and interpretation. In this study, mutations score of 30 and above was considered as high/intermediate resistance, 10–29 mutation score was taken as low/potential low level resistance and 0–9 was considered as susceptible as per the Stanford HIV drug resistance database.
Letter to the editor: switching treatment to lamivudine plus boosted atazanavir or darunavir in virologically suppressed HIV-infected patients – evidence from a large observational cohort
Published in Infectious Diseases, 2019
D. F. Bavaro, D. Di Carlo, P. Zuccalà, F. Bai, F. Incardona, A. Battisti, S. Giachè, E. Salomoni, R. Gagliardini, S. Di Giambenedetto, M. Pecorari, M. Zazzi, A. De Luca, A. Bezenchek, S. Lo Caputo
Cumulative drug resistance to NRTIs, NNRTIs and PIs (according to Stanford HIV Drug resistance database https://hivdb.stanford.edu/assets/media/resistance-mutation-handout-Feb2017.516aee6f.pdf 2017 lists) was evaluated in patients with at least one plasma genotypic resistance test (GRTs) available before switching. Patients were stratified according to the number of drug classes resistance. Finally, for patients with a GRT both before switching and at virological failure, drug resistance evolution was evaluated.