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Antiretroviral genotypic resistance in plasma RNA and whole blood DNA in HIV-1 infected patients failing HAART.
J Med Virol. 2008 Oct; 80(10):1695-706.JM

Abstract

The extent to which HIV-1 proviral DNA mutations cause clinically relevant antiretroviral resistance is still controversial. Paired plasma HIV-1 RNA and whole blood DNA were compared in patients failing HAART to investigate if the additional knowledge of archived mutations could improve the selection of potentially active drugs. Seventy-three HIV-1-infected patients with first/second HAART failure were studied before starting a new regimen based on RNA genotyping. Follow-up data after a 12-week therapy were available. DNA genotyping was retrospectively performed on stored whole blood samples and mutational profiles were compared to those from RNA. The mean number of IAS pol mutations was significantly higher in RNA (4.45 +/- 2.76) than in DNA (2.88 +/- 2.47) (P < 0.001). DNA genotyping provided a 6% increase in detection of resistance-associated mutations. Among 64/73 patients showing discordant DNA/RNA profiles, 54 (84%) also differed for predicted active drugs. 16/73 (22%) patients had >or=1 mutation revealed by DNA genotyping alone, probably affecting therapy success in 2/16. However, neither RNA/DNA discordance nor detection of isolated DNA mutations were statistically associated with outcome. In conclusion, plasma RNA remains the elective choice for HIV genotyping in patients with therapy failure, even if the detection of proviral resistance-associated mutations, not simultaneously found in RNA, is a frequent event. Therefore, in some cases DNA plus RNA genotyping might assist in choosing more accurately subsequent antiretroviral regimens.

Authors+Show Affiliations

Clinic of Infectious Diseases, University of Foggia, Foggia, Italy.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18712823

Citation

Saracino, Annalisa, et al. "Antiretroviral Genotypic Resistance in Plasma RNA and Whole Blood DNA in HIV-1 Infected Patients Failing HAART." Journal of Medical Virology, vol. 80, no. 10, 2008, pp. 1695-706.
Saracino A, Gianotti N, Marangi M, et al. Antiretroviral genotypic resistance in plasma RNA and whole blood DNA in HIV-1 infected patients failing HAART. J Med Virol. 2008;80(10):1695-706.
Saracino, A., Gianotti, N., Marangi, M., Cibelli, D. C., Galli, A., Punzi, G., Monno, L., Lazzarin, A., & Angarano, G. (2008). Antiretroviral genotypic resistance in plasma RNA and whole blood DNA in HIV-1 infected patients failing HAART. Journal of Medical Virology, 80(10), 1695-706. https://doi.org/10.1002/jmv.21261
Saracino A, et al. Antiretroviral Genotypic Resistance in Plasma RNA and Whole Blood DNA in HIV-1 Infected Patients Failing HAART. J Med Virol. 2008;80(10):1695-706. PubMed PMID: 18712823.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Antiretroviral genotypic resistance in plasma RNA and whole blood DNA in HIV-1 infected patients failing HAART. AU - Saracino,Annalisa, AU - Gianotti,Nicola, AU - Marangi,Marianna, AU - Cibelli,Donatella C, AU - Galli,Andrea, AU - Punzi,Grazia, AU - Monno,Laura, AU - Lazzarin,Adriano, AU - Angarano,Gioacchino, AU - ,, PY - 2008/8/21/pubmed PY - 2008/10/31/medline PY - 2008/8/21/entrez SP - 1695 EP - 706 JF - Journal of medical virology JO - J Med Virol VL - 80 IS - 10 N2 - The extent to which HIV-1 proviral DNA mutations cause clinically relevant antiretroviral resistance is still controversial. Paired plasma HIV-1 RNA and whole blood DNA were compared in patients failing HAART to investigate if the additional knowledge of archived mutations could improve the selection of potentially active drugs. Seventy-three HIV-1-infected patients with first/second HAART failure were studied before starting a new regimen based on RNA genotyping. Follow-up data after a 12-week therapy were available. DNA genotyping was retrospectively performed on stored whole blood samples and mutational profiles were compared to those from RNA. The mean number of IAS pol mutations was significantly higher in RNA (4.45 +/- 2.76) than in DNA (2.88 +/- 2.47) (P < 0.001). DNA genotyping provided a 6% increase in detection of resistance-associated mutations. Among 64/73 patients showing discordant DNA/RNA profiles, 54 (84%) also differed for predicted active drugs. 16/73 (22%) patients had >or=1 mutation revealed by DNA genotyping alone, probably affecting therapy success in 2/16. However, neither RNA/DNA discordance nor detection of isolated DNA mutations were statistically associated with outcome. In conclusion, plasma RNA remains the elective choice for HIV genotyping in patients with therapy failure, even if the detection of proviral resistance-associated mutations, not simultaneously found in RNA, is a frequent event. Therefore, in some cases DNA plus RNA genotyping might assist in choosing more accurately subsequent antiretroviral regimens. SN - 1096-9071 UR - https://www.unboundmedicine.com/medline/citation/18712823/Antiretroviral_genotypic_resistance_in_plasma_RNA_and_whole_blood_DNA_in_HIV_1_infected_patients_failing_HAART_ L2 - https://doi.org/10.1002/jmv.21261 DB - PRIME DP - Unbound Medicine ER -