CCR5 deficiency is a risk factor for early clinical manifestations of West Nile virus infection but not for viral transmission.
Level 4 - case-series / case-control
Case-control study comparing genotype distribution and symptoms between infected cases and uninfected controls
PubMed 20025530 · doi:10.1086/649426
What was done
Investigators evaluated CCR5Delta32 homozygous mutation distribution among US blood donors identified from a nationwide screening program (34,766,863 donations screened between 2003 and 2008). The study compared 634 true-positive West Nile virus (WNV) cases against 422 WNV-negative false-positive screening controls. Participants self-reported clinical symptoms occurring within the 2 weeks following blood donation using a standardized questionnaire.
What was found
Homozygous CCR5Delta32 frequency did not differ between WNV-positive cases and WNV-negative controls. However, among WNV-positive cases, CCR5Delta32 homozygosity was significantly associated with developing clinical symptoms consistent with WNV infection (P = .002), an association absent in uninfected controls.
Why it matters
This clarifies that CCR5 deficiency does not alter initial susceptibility to viral infection or transmission, but rather impairs host control of disease progression, predisposing infected individuals to symptomatic illness.
Limits
Symptom assessment relied on self-reported questionnaires over a 2-week post-donation recall window. Precise allele frequencies, odds ratios, and confidence intervals were not reported in the abstract. The cohort was restricted to individuals eligible to donate blood, potentially introducing a healthy-donor selection effect.
Cited by
- supports CCR5 knockout or null mutations can increase susceptibility to West Nile virus and certain influenza strains.