Sickle cell disease is associated with decreased HIV but higher HBV and HCV comorbidities in US hospital discharge records: A cross-sectional study
Center for Sickle Cell Disease, Howard University, Washington, DC, USA.Sexually transmitted infections (Impact Factor: 3.4). 05/2012; 88(7). DOI: 10.1136/sextrans-2011-050459
OBJECTIVE: Some studies suggest that HIV infection progresses slowly in patients with sickle cell disease (SCD). The authors aimed to determine the relationships between SCD and HIV infection. METHODS: National Hospital Discharge Survey data from adult African-Americans in the period of 1997-2009 were analysed. The comorbidities of SCD with HIV infections in hospital discharges were analysed. Multiple logistic regression was used to test the association between SCD and HIV. For comparative purposes, the relationships of SCD with hepatitis B virus (HBV) and hepatitis C virus (HCV) were also assessed. RESULTS: 423 431 records were divided into two time periods 1997-2003 (53% of records) and 2004-2009 (47% of records). The frequency of HIV diagnosis was lower in patients with SCD (1.5% vs 3.3% in patients without SCD). In logistic regression, SCD diagnosis was associated with an OR of 0.24 (95% CI 0.18 to 0.32) for HIV diagnosis in the first period and with an OR of 0.31 (95% CI 0.22 to 0.42) in the second period. In contrast, SCD was associated with higher risk of HCV (OR=2.01, 95% CI 1.56 to 2.59 in the first period and OR=2.12, 95% CI 1.71 to 2.63 in the second period). SCD was also associated with a higher risk of HBV (OR=1.15, 95% CI 0.72 to 1.83 in the first period and OR=1.82, 95% CI 1.24 to 2.68 in the second period). CONCLUSIONS: The lower risk of HIV comorbidity, but not HCV and HBV, with SCD is consistent with the possibility that SCD has a unique effect in altering the risk of HIV infection or progression. Investigation of how the haemolytic and immunological changes of SCD influence HIV might lead to new therapeutic or preventive approaches.
- Sexually transmitted infections 06/2012; 88(7). DOI:10.1136/sextrans-2012-050613 · 3.40 Impact Factor
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ABSTRACT: Despite efficient antiretroviral therapy, eradication of HIV-1 infection is challenging and requires novel biological insights and therapeutic strategies. Among other physiological and environmental factors, intracellular iron greatly affects HIV-1 replication. Higher iron stores were shown to be associated with faster progression of HIV-1 infection and to inversely correlate with the survival of HIV-1 infected patients. Iron is required for several steps in the HIV-1 life cycle, including reverse transcription, HIV-1 gene expression and capsid assembly. Here, the authors present a comprehensive review of the molecular mechanisms involved in iron- and oxygen-mediated regulation of HIV-1 replication. We also propose key intracellular pathways that may be involved in regulating HIV-1 replication, via protein kinase complexes, CDK9/cyclin T1 and CDK 2/cyclin E, protein phosphatase-1 and other host factors.Future Virology 03/2013; 8(3):301-311. DOI:10.2217/fvl.13.6 · 1.01 Impact Factor
- Retrovirology 09/2013; 10(Suppl 1):P63-P63. DOI:10.1186/1742-4690-10-S1-P63 · 4.19 Impact Factor
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