HIV-1 viral load and phenotypic antiretroviral drug resistance assays based on reverse transcriptase activity in comparison to amplification based HIV-1 RNA and genotypic assays☆
Received 1 July 2009; received in revised form 25 September 2009; accepted 4 October 2009. published online 06 November 2009.
Abstract
Background
Amplification based HIV-1 viral load and genotypic resistance assays are expensive, technologically complex and may be difficult to implement in resource limited settings. Inexpensive, simpler assays are urgently needed.
Objectives
To determine the suitability of the ExaVir™ Load and ExaVir™ Drug assays for use in patient monitoring.
Study design
Specimens from 108 adults were used to compare ExaVir™ Load HIV-1 RT to Amplicor HIV-1 Monitor® HIV-1 RNA, and ExaVir™ Drug phenotype to HIV GenoSure™ genotype.
Results
HIV-1 RT and HIV-1 RNA levels were comparable (Pearson correlation coefficient 0.83). Most (94%) had detectable results in both assays. The mean difference (HIV-1 RT minus HIV-1 RNA) was −0.21log10cps/mLequiv. Relationship between HIV-1 RT and HIV-1 RNA was not affected by RT mutations, CD4 cell count, or efavirenz (EFV) or nevirapine (NVP) use. Phenotypes were generally consistent with genotype findings for EFV, but not for NVP. Most patients (93.9%) with phenotypic EFV resistance had at least one EFV mutation, while 78.0% of patients with phenotypic NVP resistance had at least one NVP mutation. Eleven of 49 samples tested for EFV susceptibility were found resistant (n=2) or with reduced susceptibility (n=9) despite the absence of genotypic resistance. Eleven of 45 samples tested for NVP susceptibility were found resistant (n=9) or with reduced susceptibility (n=2) with no evidence of genotypic mutations.
Conclusions
The ExaVir™ Load assay performed well and may be an alternative to amplification based techniques for HIV-1 RNA quantification. The ExaVir™ Drug assay for phenotypic resistance testing requires further evaluation, especially for NVP.
aThe University of North Carolina at Chapel Hill, Department of Medicine, Chapel Hill, NC, United States
bThe University of North Carolina at Chapel Hill, Department of Microbiology and Immunology, Chapel Hill, NC, United States
cThe University of North Carolina at Chapel Hill, Department of Biostatistics, Chapel Hill, NC, United States
Corresponding author at: Dept of Microbiology & Immunology, University of North Carolina at Chapel Hill, CB # 7290, 709 Mary Ellen Jones Building, Chapel Hill, NC 27599-7290, United States. Tel.: +1 919 966 6872; fax: +1 919 966 9873.
☆ Presented in part at the 13th Conference on Retroviruses and Opportunistic Infections, Denver, CO, February 5–8, 2006, and the 15th Conference on Retroviruses and Opportunistic Infections, Boston, MA, February 3–6, 2008.
ABSTRACT