HAART produces a positive and sustained effect on neurocognitive impairment in HIV-infected patients. A reduction of plasma viral load was associated with the regression of neuropsychological test abnormalities.

Background: Neurocognitive impairment (NCI) and HIV-associated neurocognitive disorders (HAND) remain prevalent despite HAART. We examined sensitivity, specificity, positive predictive value (PPV), negative predictive value (NPV), and correct classification rate (CCR) of screening tools for the detection of NCI and HAND in HAART treated patients. Methods: We examined 101 unselected HAART-treated patients. Patients were administered the self-reported three questions (EACS Guidelines), the International HIV-Dementia Scale (IHDS), the Mini-Mental Status Examination (MMSE), and a comprehensive 6-domain (17-test) neuropsychological (NP) battery (120 minutes) that included, among others, the Digit Symbol (DS), the Trail Making Modalities (TM), and the Grooved Pegboard (GP) tests. NCI was defined according to the AAN criteria. HAND was diagnosed after exclusion of confounding conditions. Results: Our cohort was relatively healthy (mean CD4 count: 575 cells/mm3, undetectable plasma HIV RNA 85%). Prevalence of NCI and HAND were 39.6% (40 of 101) and 30.7% (31 of 101), respectively. Mean scores of IHDS (9.9 vs 10.8; p<0.001) and MMSE (26.8 vs 28.2; p=0.004) differed significantly between impaired and unimpaired patients, while mean three-questions scores (8.0 vs 7.0; p=0.23) did not. The three questions showed also poor sensitivity for the detection of both NCI (20%) and HAND (22%). The IHDS showed fairly good sensitivity (55%) and NPV (73.5%). Adding to the IHDS some easy to administer NP tests, i.e. TM, DS, and GP, resulted in an increase in sensitivity and NPV for the detection of NCI (table). Similar results were obtained regarding the detection of HAND (not shown in table). Conclusions: Both NCI and HAND are still very prevalent in HAART-treated patients. Among screening tools the self-reported three question show poor sensitivity. The IHDS performed better in terms of sensitivity, PPV, and NPV. Combinations of easy-to-administer NP tests with the IHDS resulted in increased sensitivity and NPV. Combining IHDS with one or two simple NP test may represent an improvement in the screening approach to the detection of both NCI and HAND

Background The V118I mutation is included in the nucleoside analogue mutations (NAMs) set. It contributes to thymidine-analogue resistance and, consequently, to resistance to the whole nucleoside reverse transcriptase inhibitor (NRTI) class. We focused on the V118I mutation in order to evaluate factors associated with its detection and its relationship with HIV progression. Methods Clinical and laboratory data at genotypic resistance test (GRT) of highly active antiretroviral therapy-failing patients were collected and their association with the V118I mutation was analysed. Patients were also followed over time to determine factors related to progression to a new AIDS-related event or death. Results Of the 792 patients included, 114 (14.4%) carried the V118I mutation. In univariate analysis, the V118I mutation was significantly associated with a higher HIV RNA level, lower CD4+ T-cell count, Centers for Disease Control and Prevention (CDC) stage C, higher number of pre-GRT regimens and class-wide resistance (CWR) to NRTIs, protease inhibitors and non-nucleoside reverse transcriptase inhibitors. Higher numbers of pre-GRT regimens and NRTI CWR were also associated in the multivariable analysis. Within the post-GRT observation period of up to 6 years (median: 72 months; interquartile range: 33–109) 107 events (58 new AIDS-related diseases and 49 deaths) were observed. Using the Cox proportional hazard model and the major clinical, behavioural and laboratory data, the V118I mutation was found to be associated with the endpoint (hazard ratio: 1.93, 95% confidence interval: 1.06–3.50; P=0.031). Other factors associated with disease progression were CDC stage C and lower CD4+ T-cell count at GRT. Conclusions The analysis of our observational database suggests that the onset of the V118I mutation after treatment failure is unfavourable for the patient and can be considered a strong marker of disease progression.

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