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Detection of drug resistance mutations as a predictor of subsequent virological failure in patients with HIV-1 viral rebounds of less than 1,000 RNA copies/ml

Chris Verhofstede (UGent) , Filip Van Wanzeele (UGent) , Beatrijs Van Der Gucht (UGent) , Jolanda Pelgrom (UGent) , Linos Vandekerckhove (UGent) , Jean Plum (UGent) and Dirk Vogelaers (UGent)
(2007) JOURNAL OF MEDICAL VIROLOGY. 79(9). p.1254-1260
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Abstract
In order to evaluate the usefulness of resistance testing after a viral rebound with plasma HIV RNA levels of less than 1,000 copies (c)/ml, genotyping was performed on 39 samples from patients on highly active antiretroviral therapy (HAART) showing a viremia of over 50 c/ml up to a maximum of 1,000 c/ml after at least one undetectable viral load result. Protease and reverse transcriptase (RT) sequences were obtained for all 39 samples. In 10 (25.6%) of the samples, mutations not seen before the initiation of the regimen were observed. The M184V/I mutation was the most prevalent but in several patients a combination of multiple mutations was detected. Follow-up samples were available for 34 patients. In six (85.71%) out of seven patients with new mutations, the viral load on the follow-up visit remained detectable, indicating true failure, compared to 6 (31.6%) true failures out of 19 patients in whom only wild type virus was detected (P = 0.02) and three (37.5%) out of eight patients in whom only the mutations already present at the initiation of HAART were seen (P = 0.08). The results indicate that reliable resistance testing can be performed on samples with a viral burden of less than 1,000 c/ml and demonstrate that multiple drug resistance mutations can be selected at low viral load rebounds. Most importantly, detection of resistance mutations in viral rebound samples was predictive of subsequent virological failure.
Keywords
IMMUNODEFICIENCY-VIRUS TYPE-1, ACTIVE ANTIRETROVIRAL THERAPY, DETECTABLE VIREMIA, LOAD, BLIPS, viral rebound, LOW-LEVEL VIREMIA, INFECTED PATIENTS, REVERSE-TRANSCRIPTASE, GENOTYPIC RESISTANCE, TRANSIENT REBOUNDS, viremia, genotyping at low viral load

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Chicago
Verhofstede, Chris, Filip Van Wanzeele, Beatrijs Van Der Gucht, Jolanda Pelgrom, Linos Vandekerckhove, Jean Plum, and Dirk Vogelaers. 2007. “Detection of Drug Resistance Mutations as a Predictor of Subsequent Virological Failure in Patients with HIV-1 Viral Rebounds of Less Than 1,000 RNA Copies/ml.” Journal of Medical Virology 79 (9): 1254–1260.
APA
Verhofstede, C., Van Wanzeele, F., Van Der Gucht, B., Pelgrom, J., Vandekerckhove, L., Plum, J., & Vogelaers, D. (2007). Detection of drug resistance mutations as a predictor of subsequent virological failure in patients with HIV-1 viral rebounds of less than 1,000 RNA copies/ml. JOURNAL OF MEDICAL VIROLOGY, 79(9), 1254–1260.
Vancouver
1.
Verhofstede C, Van Wanzeele F, Van Der Gucht B, Pelgrom J, Vandekerckhove L, Plum J, et al. Detection of drug resistance mutations as a predictor of subsequent virological failure in patients with HIV-1 viral rebounds of less than 1,000 RNA copies/ml. JOURNAL OF MEDICAL VIROLOGY. 2007;79(9):1254–60.
MLA
Verhofstede, Chris, Filip Van Wanzeele, Beatrijs Van Der Gucht, et al. “Detection of Drug Resistance Mutations as a Predictor of Subsequent Virological Failure in Patients with HIV-1 Viral Rebounds of Less Than 1,000 RNA Copies/ml.” JOURNAL OF MEDICAL VIROLOGY 79.9 (2007): 1254–1260. Print.
@article{391690,
  abstract     = {In order to evaluate the usefulness of resistance testing after a viral rebound with plasma HIV RNA levels of less than 1,000 copies (c)/ml, genotyping was performed on 39 samples from patients on highly active antiretroviral therapy (HAART) showing a viremia of over 50 c/ml up to a maximum of 1,000 c/ml after at least one undetectable viral load result. Protease and reverse transcriptase (RT) sequences were obtained for all 39 samples. In 10 (25.6\%) of the samples, mutations not seen before the initiation of the regimen were observed. The M184V/I mutation was the most prevalent but in several patients a combination of multiple mutations was detected. Follow-up samples were available for 34 patients. In six (85.71\%) out of seven patients with new mutations, the viral load on the follow-up visit remained detectable, indicating true failure, compared to 6 (31.6\%) true failures out of 19 patients in whom only wild type virus was detected (P = 0.02) and three (37.5\%) out of eight patients in whom only the mutations already present at the initiation of HAART were seen (P = 0.08). The results indicate that reliable resistance testing can be performed on samples with a viral burden of less than 1,000 c/ml and demonstrate that multiple drug resistance mutations can be selected at low viral load rebounds. Most importantly, detection of resistance mutations in viral rebound samples was predictive of subsequent virological failure.},
  author       = {Verhofstede, Chris and Van Wanzeele, Filip and Van Der Gucht, Beatrijs and Pelgrom, Jolanda and Vandekerckhove, Linos and Plum, Jean and Vogelaers, Dirk},
  issn         = {0146-6615},
  journal      = {JOURNAL OF MEDICAL VIROLOGY},
  language     = {eng},
  number       = {9},
  pages        = {1254--1260},
  title        = {Detection of drug resistance mutations as a predictor of subsequent virological failure in patients with HIV-1 viral rebounds of less than 1,000 RNA copies/ml},
  url          = {http://dx.doi.org/10.1002/jmv.20950},
  volume       = {79},
  year         = {2007},
}

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