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Does sickle cell disease protect against HIV/AIDS?
  1. Stephen Obaro
  1. Correspondence to Dr Stephen Obaro, Department of Pediatrics and Human Development, Michigan State University, East Lansing, MI 48824, USA; stephen.obaro{at}hc.msu.edu

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Understanding the interaction between genetic diseases and systemic disorders can stimulate advances in therapeutics, disease pathogenesis and prevention strategies. For example, the rarity of pulmonary tuberculosis in patients with cystic fibrosis,1 protection against Epstein Barr viral infection in X linked agamaglobulinemia2 and amelioration of common variable immune deficiency by acquisition of HIV3 contributed significantly to the understanding of genetic and mechanistic pathogenesis of tuberculosis and HIV.

In this edition of STI, Nouraie and colleagues4 analysed hospital discharge data over a 13-year period from adult African American patients and described the association between Sickle cell disease and co-morbid viral infections such as HIV, hepatitis B and C infections. They reviewed 423 431 records over two time periods of 7 and 6 years and observed lower frequency of HIV diagnosis in patients with sickle cell disease (SCD) (1.5% vs 3.3% in patients without SCD). In contrast, SCD was associated with higher risk of HCV (OR=2.01, 95% CI 1.56 to 2.59 in the first and 2.12, 95% CI 1.71 to 2.63 in the second period) and HBV (OR=1.15, 95% CI 0.72 to 1.83 in the first and 1.82, 95% CI 1.24 to 2.68 in the second period).

The differential risks of infection in SCD to these viral infections, all of which are bloodborne and generally associated with similar behavioural risk factors, are intriguing. Several plausible explanations exist for their observations, including the inhibition of HIV viral replication due to the persistent up regulation of inflammation, iron metabolism and immunologic changes in SCD.

As is typical with any retrospective, hospital-based study, there is a selection bias, as cases with severe disease are more likely to present for hospitalisation; observations from a community-based surveillance may be different. Co-morbid conditions were retrieved from hospital records and not by active screening, thus there may be over-representation of SCD, a condition that is routinely diagnosed through newborn screening and under representation of HIV, for which there is no routine population screening. The study focused primarily on adults and thus selected for survivors of both conditions and did not correct for multiple hospitalisations in individuals and may have over-sampled for conditions that are typically associated with multiple hospital admissions. These limitations notwithstanding, their observations and other limited case report series in the literature should prompt more detailed population-based studies in regions with high endemicity for both SCD and HIV to confirm this association and probe underlying mechanistic explanations.

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  • Competing interests None.

  • Provenance and peer review Commissioned; internally peer reviewed.

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