ArticleJournal of acquired immune deficiency syndromes (1999)2010
HIV replication capacity is an independent predictor of disease progression in persons with untreated chronic HIV infection.
Article in Journal of acquired immune deficiency syndromes (1999), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed.
- Article
- Dissecting HIV Virulence: Heritability of Setpoint Viral Load, CD4+ T-Cell Decline, and Per-Parasite Pathogenicity.Molecular biology and evolution · 2018Article
- Factors Associated With the Control of Viral Replication and Virologic Breakthrough in a Recently Infected HIV-1 Controller.EBioMedicine · 2017Article
- Lack of a significant impact of Gag-Protease-mediated HIV-1 replication capacity on clinical parameters in treatment-naive Japanese individuals.Retrovirology · 2015Article
- HIV type 1 polymerase gene polymorphisms are associated with phenotypic differences in replication capacity and disease progression.The Journal of infectious diseases · 2014Article
- Treatment-associated polymorphisms in protease are significantly associated with higher viral load and lower CD4 count in newly diagnosed drug-naive HIV-1 infected patients.Retrovirology · 2012Article
- Early virologic failure and the development of antiretroviral drug resistance mutations in HIV-infected Ugandan children.Journal of acquired immune deficiency syndromes (1999) · 2011Article
Corrections and comments
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Authors and funding
11 authors.
Funding
Abstract
objectiveTo assess the effect of pol replication capacity (RC) on the hazard ratio of progression to a composite endpoint of time to progression to <350 CD4+ cells per microliter, initiation of therapy, or death.
methodspol RC assays were performed after study closure in baseline samples obtained from 316 enrollees in a prospectively monitored cohort of treatment-naive adults with >or=450 CD4+ cells per microliter and >or=1000 HIV-1 RNA copies per milliliter.
resultsThe median RC was 79%. Patients with a lower RC had a lower median viral load (4.0 vs 4.2 Log HIV-1 RNA copies/mL, P = 0.026) and a lower rate of protease inhibitor resistance 2% vs 8%, P = 0.03). Otherwise, baseline demographic and laboratory characteristics were similar. The hazard ratio of progression to the composite endpoint was 0.73 (P = 0.041) for persons with lower RC, 2.07 per 1.0 log10 higher viral load (P < 0.001), and 0.86 per 50 cells per microliter higher CD4+ cell count (P < 0.001). The effect of lower RC was also significant in a separate analysis of time to initiation of therapy (P = 0.04).
conclusionsThese results show that untreated patients with lower vs higher RC had a slower rate of progression as assessed by a composite outcome of time to CD4+ count <or=350 cells per microliter, treatment initiation, or death.
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