CCR5 deficiency predisposes to fatal outcome in influenza virus infection.
Level 3 - non-randomized controlled study
Cohort study comparing mortality across genotypes in influenza-infected patients
PubMed 25918237 · doi:10.1099/vir.0.000165
What was done
Tested 171 respiratory samples from patients infected during the 2009 pandemic influenza for the CCR5-Δ32 mutation (a 32-bp deletion in the CCR5 gene) and analyzed the association between CCR5 genotype and patient mortality.
What was found
Patients with the CCR5-Δ32 mutation exhibited a significantly higher mortality rate of 17.4% compared to 4.7% in wild-type individuals (P = 0.021).
Why it matters
Host genetic factors contributing to severe influenza in previously healthy individuals remain largely unclear; this provides evidence that CCR5 deficiency may increase susceptibility to fatal influenza outcomes.
Limits
The study is limited to a single pandemic cohort of modest sample size (n = 171). The abstract does not specify whether CCR5-Δ32 carriers were heterozygous or homozygous, nor does it report adjustment for potential confounders such as age, comorbidities, or antiviral treatment.
Cited by
- supports CCR5 knockout or null mutations can increase susceptibility to West Nile virus and certain influenza strains.