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Development of HIV with drug resistance after CD4 cell count-guided structured treatment interruptions in patients treated with highly active antiretroviral therapy after dual-nucleoside analogue treatment.
Clin Infect Dis. 2005 Mar 01; 40(5):728-34.CI

Abstract

BACKGROUND

For patients with human immunodeficiency virus (HIV) infection, structured treatment interruption (STI) is an attractive alternative strategy to continuous treatment, particularly in resource-restrained settings, because it reduces both side effects and costs. One major concern, however, is the development of resistance to antiretroviral drugs that can occur during multiple cycles of starting and stopping therapy.

METHODS

HIV genotypic drug resistance was investigated in 20 HIV-infected Thai patients treated with highly active antiretroviral therapy (HAART) and CD4 cell count-guided STI after dual nucleoside reverse-transcriptase inhibitor (NRTI) treatment. Resistance was tested at the time of the switch from dual-NRTI treatment to HAART and when HAART was stopped during the last interruption.

RESULTS

After STI, one major drug-resistance mutation occurred (T215Y), and, in the 4 samples with preexisting major mutations (D67N [n=2], K70R [n=2], T215Y [n=2], and T215I [n=1]), the mutations disappeared. All mutations in the HIV protease gene were minor mutations already present, in most cases, before STI was started, and their frequency was not increased through STI, whereas the frequency of reverse-transcriptase gene mutations significantly decreased after the interruptions. After the 48-week study period, no patients had virological failure. Long-term follow-up (108 weeks) showed 1 case of virological failure in the STI arm and 1 in the continuous arm. No virological failure was seen in patients with major mutations.

CONCLUSIONS

Major HIV drug-resistance mutations were not induced through CD4 cell count-guided treatment interruptions in HIV-infected patients successfully treated with HAART after dual-NRTI therapy.

Authors+Show Affiliations

HIV Netherlands, Australia, Thailand Research Collaboration (HIV-NAT), Thai Red Cross AIDS Research Centre, Bangkok, Thailand.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)

Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

15714420

Citation

Nuesch, Reto, et al. "Development of HIV With Drug Resistance After CD4 Cell Count-guided Structured Treatment Interruptions in Patients Treated With Highly Active Antiretroviral Therapy After Dual-nucleoside Analogue Treatment." Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America, vol. 40, no. 5, 2005, pp. 728-34.
Nuesch R, Ananworanich J, Sirivichayakul S, et al. Development of HIV with drug resistance after CD4 cell count-guided structured treatment interruptions in patients treated with highly active antiretroviral therapy after dual-nucleoside analogue treatment. Clin Infect Dis. 2005;40(5):728-34.
Nuesch, R., Ananworanich, J., Sirivichayakul, S., Ubolyam, S., Siangphoe, U., Hill, A., Cooper, D., Lange, J., Phanuphak, P., & Ruxrungtham, K. (2005). Development of HIV with drug resistance after CD4 cell count-guided structured treatment interruptions in patients treated with highly active antiretroviral therapy after dual-nucleoside analogue treatment. Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America, 40(5), 728-34.
Nuesch R, et al. Development of HIV With Drug Resistance After CD4 Cell Count-guided Structured Treatment Interruptions in Patients Treated With Highly Active Antiretroviral Therapy After Dual-nucleoside Analogue Treatment. Clin Infect Dis. 2005 Mar 1;40(5):728-34. PubMed PMID: 15714420.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Development of HIV with drug resistance after CD4 cell count-guided structured treatment interruptions in patients treated with highly active antiretroviral therapy after dual-nucleoside analogue treatment. AU - Nuesch,Reto, AU - Ananworanich,Jintanat, AU - Sirivichayakul,Sunee, AU - Ubolyam,Sasiwimol, AU - Siangphoe,Umaporn, AU - Hill,Andrew, AU - Cooper,David, AU - Lange,Joep, AU - Phanuphak,Praphan, AU - Ruxrungtham,Kiat, Y1 - 2005/02/04/ PY - 2004/07/28/received PY - 2004/10/11/accepted PY - 2005/2/17/pubmed PY - 2006/8/10/medline PY - 2005/2/17/entrez SP - 728 EP - 34 JF - Clinical infectious diseases : an official publication of the Infectious Diseases Society of America JO - Clin Infect Dis VL - 40 IS - 5 N2 - BACKGROUND: For patients with human immunodeficiency virus (HIV) infection, structured treatment interruption (STI) is an attractive alternative strategy to continuous treatment, particularly in resource-restrained settings, because it reduces both side effects and costs. One major concern, however, is the development of resistance to antiretroviral drugs that can occur during multiple cycles of starting and stopping therapy. METHODS: HIV genotypic drug resistance was investigated in 20 HIV-infected Thai patients treated with highly active antiretroviral therapy (HAART) and CD4 cell count-guided STI after dual nucleoside reverse-transcriptase inhibitor (NRTI) treatment. Resistance was tested at the time of the switch from dual-NRTI treatment to HAART and when HAART was stopped during the last interruption. RESULTS: After STI, one major drug-resistance mutation occurred (T215Y), and, in the 4 samples with preexisting major mutations (D67N [n=2], K70R [n=2], T215Y [n=2], and T215I [n=1]), the mutations disappeared. All mutations in the HIV protease gene were minor mutations already present, in most cases, before STI was started, and their frequency was not increased through STI, whereas the frequency of reverse-transcriptase gene mutations significantly decreased after the interruptions. After the 48-week study period, no patients had virological failure. Long-term follow-up (108 weeks) showed 1 case of virological failure in the STI arm and 1 in the continuous arm. No virological failure was seen in patients with major mutations. CONCLUSIONS: Major HIV drug-resistance mutations were not induced through CD4 cell count-guided treatment interruptions in HIV-infected patients successfully treated with HAART after dual-NRTI therapy. SN - 1537-6591 UR - https://www.unboundmedicine.com/medline/citation/15714420/Development_of_HIV_with_drug_resistance_after_CD4_cell_count_guided_structured_treatment_interruptions_in_patients_treated_with_highly_active_antiretroviral_therapy_after_dual_nucleoside_analogue_treatment_ L2 - https://academic.oup.com/cid/article-lookup/doi/10.1086/427878 DB - PRIME DP - Unbound Medicine ER -