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• W2023121370 abstract "Integrated HIV-1 proviruses in resting CD4 T cells are believed to be a significant barrier to HIV eradication. The activation of latent HIV infection using a histone deacetylase inhibitor (sodium valproate) and the intensification of antiretroviral therapy (ART) with enfuvirtide accelerated HIV-1 clearance from CD4 memory T cells isolated from patients with HIV-1 infection [1], and was widely reported to be a potential milestone in the cure of this disease [2]. We report a case of a single patient, in whom long-term combination therapy with ART and sodium valproate did not significantly alter the rebound kinetics of viral replication after the cessation of ART. A 54-yearold Armenian Iranian man was diagnosed with HIV-1 in 2001 when he presented with cerebral toxoplasmosis; his CD4 T-cell count was 44 cells/μl and viral load was 1 280 000 copies/ml. He was treated with ART (efavarenz, abacavir and lamivudine) for HIV-1 infection and sodium valproate for recurrent grand mal seizures since 2001. Since 2003 his plasma viral load has always been less than 75 copies/ml, using the branched DNA assay v3.0 (Chiron Corp., Emeryville, California, USA), and his CD4 T-cell count has ranged from 467 to 1115 cells/μl. Sodium valproate levels have been in the therapeutic range (50–100 mg/l). After the publication of the recent Lancet report [1], the patient attended our clinic requesting help in establishing whether he was cured of HIV-1 infection. Baseline blood samples for viral load, lymphocyte subsets, valproate levels, episomal complementary DNA circles [3], and CD8+CD38++ immune activation were taken (Table 1). Antiretroviral therapy was modified to prevent the risk of viral resistance, and 2 weeks later all ART was stopped. Serial measures of HIV-1 viral load, lymphocyte subsets and immune activation were performed. Within 3 weeks of stopping ART there was a rapid rebound of the HIV-1 viral load, with a concomitant marked increase in CD8+CD38++ immune activation and a fall in the CD4 T-cell count. Episomal cDNA circles were negative at day 0 and day 20. HAART was recommenced 28 days after the cessation of therapy with good effect. At the last follow-up 66 days after restarting HAART, the viral load was 1761 copies/ml and the CD4 T-cell count was 697 cells/ml.Table 1: Serial measurements of CD4 and CD8 T-cell counts, viral loads (branched DNA assay) and CD8 CD38 immune activation.The addition of long-term valproate therapy did not significantly increase the time to virological relapse after the stopping ART [4], nor did it alter the kinetics of viral relapse, with linear regression analysis demonstrating a viral rebound rate constant 0.34 per day, which falls within the range previously reported: 0.12–0.91 per day [4]. Our patient had well-controlled disease, with a viral load below the limit of detection for over 2 years. He had normal percentages of CD8 T cells expressing CD38, suggestive of a plasma viral load less than 7 copies/ml (unpublished observations). Our data suggest that sodium valproate had only a modest effect on the eradication of HIV-1 infection from latently infected CD4 T cells. The intensification of ART can decrease the t1/2 of latent HIV-1 cellular reservoirs [5]. We suggest that further controlled studies are needed to establish the relative contribution of the intensification of pre-existing ART and sodium valproate in the clearance of HIV-1 from CD4 memory T cells." @default.
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• W2023121370 date "2006-08-01" @default.
• W2023121370 modified "2023-09-26" @default.
• W2023121370 title "No change to HIV-1 latency with valproate therapy" @default.
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• W2023121370 doi "https://doi.org/10.1097/01.aids.0000238421.36313.fa" @default.
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