Author | Oliveira, Marta Iglis | |
Author | Souza Junior, Valter Romão de | |
Author | Vidal, Claudia Fernanda de Lacerda | |
Author | Araújo, Paulo Sérgio Ramos de | |
Access date | 2019-04-04T14:03:51Z | |
Available date | 2019-04-04T14:03:51Z | |
Document date | 2018 | |
Citation | OLIVEIRA, M. I. et al. Virologic Suppression in Response to Antiretroviral Therapy despite Extensive Resistance within HIV-1 Reverse Transcriptase after the First Virologic Failure. BMC Infectious Diseases, v. 18, n. 1, p. 1-11, Oct. 2018. | pt_BR |
ISSN | 1471-2334 | pt_BR |
URI | https://www.arca.fiocruz.br/handle/icict/32364 | |
Language | eng | pt_BR |
Rights | open access | pt_BR |
Title | Virologic suppression in response to antiretroviral therapy despite extensive resistance within HIV-1 reverse transcriptase after the first virologic failure | pt_BR |
Type | Article | pt_BR |
DOI | 10.1186/s12879-018-3400-6 | |
Abstract | Background: Incomplete virologic suppression results in mutations associated with resistance and is a major
obstacle to disease control. We analyzed the genotypic profiles of HIV-1 patients at the time of the first virologic
failure and the response to a salvage regimen after 48 weeks.
Methods: This work was a cross-sectional, retrospective, analytical study based on data collected from medical
records and genotyping tests between 2006 and 2016. The sample consisted of data on individuals living with HIV
(PLWH) from three major reference centers.
Results: A total of 184 patients were included in the data analysis. Viral subtype B was the most common (81.3%)
as well as M184 V/I (85.3%) and K103 codon mutations (65.8%). Forty-eight weeks after switching to a salvage
regimen, 67.3% of patients achieved an undetectable viral load.
Discussion: The number of mutations associated with nucleos(t)ide reverse transcriptase inhibitors (NRTI(t)s) did
not affect virologic suppression (9.3% for zero NRTI(t)-associated mutations vs 48.6% for 1–2 NRTI(t)-associated
mutations vs 42.1% for ≥3 NRTI(t)-associated mutations, p = 0.179). An ARV time (the beginning of the first ARV
regimen up to genotyping) of > 36 months was a protective factor for detectable viral load (PR = 0.60, 95% CI
= 0.39–0.92, p = 0.020) and a risk factor for developing ≥3 NRTI(t)-associated mutations (PR = 2.43, 95% CI
1.38–4.28, p = 0.002).
Conclusions: We found that extensive resistance to NRTI(t)s at the time of the first virologic failure did not impact
virologic suppression at 48 weeks after switching to a second-line therapy based on NRTI(t)s plus protease inhibitors. | pt_BR |
Affilliation | Universidade Federal de Pernambuco. Programa de Pós-graduação em Ciências da Saúde. Recife, PE, Brasil. | pt_BR |
Affilliation | Universidade Federal de Pernambuco. Faculdade de Medicina do Recife. Recife, PE, Brasil. | pt_BR |
Affilliation | Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil. | pt_BR |
Affilliation | Universidade Federal de Pernambuco. Programa de Pós-graduação em Ciências da Saúde. Recife, PE, Brasil / Fundação Oswaldo Cruz. Instituto Aggeu Magalhães. Recife, PE, Brasil. | pt_BR |
Subject | HIV-1 drug resistance | pt_BR |
Subject | Genetic diversity | pt_BR |
Subject | Subtypes | pt_BR |
Subject | Antiretroviral therapy | pt_BR |
DeCS | Adulto | pt_BR |
DeCS | Anti-retrovirais / uso terapêutico | pt_BR |
DeCS | Estudos Transversais | pt_BR |
DeCS | Resistência a Medicamentos Virais / genética | pt_BR |
DeCS | Fêmea | pt_BR |
DeCS | Genótipo | pt_BR |
DeCS | Infecções por HIV / quimioterapia | pt_BR |
DeCS | Transcriptase Reversa do HIV / genética | pt_BR |
DeCS | HIV-1 / genética | pt_BR |
DeCS | HIV-1 / isolamento e purificação | pt_BR |
DeCS | Humanos | pt_BR |
DeCS | Masculino | pt_BR |
DeCS | Meia idade | pt_BR |
DeCS | Mutação | pt_BR |
DeCS | Estudos retrospectivos | pt_BR |
DeCS | Fatores de risco | pt_BR |
DeCS | Terapia de Salvamento | pt_BR |
DeCS | Falha no tratamento | pt_BR |
DeCS | Carga viral | pt_BR |
DeCS | Adulto jovem | pt_BR |
xmlui.metadata.dc.subject.ods | 10 Redução das desigualdades | |