It should be noted, however, that assay comparisons are to be int

It should be noted, however, that assay comparisons are to be interpreted with caution in the absence of a reference gold diagnostic standard. The most relevant analysis is observing how effective an assay is at predicting virological responses to CCR5 antagonist use. Evidence indicates that GTT (performed and interpreted according to defined parameters) is comparable to the original Trofile assay in predicting virological responses to maraviroc in treatment-experienced patients, and comparable to ESTA in predicting

virological responses to maraviroc in treatment-naïve patients [40, 41]. Thus, in the latter group, both ESTA and GTT performed better than the original Trofile in identifying patients who would respond to maraviroc within the MERIT study. An increasing number of prospective cohort studies in both treatment-naïve and treatment-experienced

find more patients starting maraviroc also indicate that GTT is reliable in terms of positive predictive value [42-44]. One advantage of Selleckchem AZD1208 GTT is the ability to circumvent the high plasma viral load requirement of phenotypic assays, and evaluate tropism in virologically suppressed patients using proviral DNA. There is limited evidence to indicate that GTT of proviral DNA may actually provide better concordance with phenotypic tropism prediction than genotypic analysis of plasma [33, 34, 38, 42-46]. Prospective outcome data for the use of proviral DNA, however, are currently limited to case series [23, 43, 44]. There is limited evidence in

support of the notion that, in treated patients, a tropism test result obtained prior to virological suppression remains usually unchanged during suppression [45, 46] and can be used to guide a subsequent treatment switch when viraemia is suppressed. HIV-1 tropism testing should be performed prior to CCR5 antagonist therapy using a validated phenotypic or genotypic method. Genotypic tropism testing offers a more easily accessible, rapid and inexpensive method for tropism diagnostics than phenotypic testing and is therefore the preferred option (Ib). Laboratories undertaking genotypic tropisms testing should do so under quality assurance schemes and according to the prevailing consensus about not preferred methodology for sampling, testing and interpretation (IV). In treatment-naïve patients, tropism testing should be performed immediately prior to the start of therapy whenever CCR5 antagonist use may be considered in the first-line regimen (unlicensed indication in Europe) (Ia). Alternatively a plasma sample could be stored for future testing if required (IV). In treated patients experiencing virological failure, tropism testing should be performed and the results should become available at the same time as those of drug-resistance testing to ensure all available therapeutic options may be considered (Ia). In treated patients with suppressed viraemia for whom a switch to a CCR5 antagonist is considered (e.g.

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