Objectives

To determine the impact of the 32bp deletion (CCR5Δ32) in the coding region of the C-C chemokine receptor 5 (CCR5) on the risk of contracting SARS-CoV-2 and severe COVID-19.

Methods

Cross-sectional study among stem cell donors registered with DKMS in Germany. Genetic information was linked to self-reported COVID-19 outcome data. Multivariable regression models were fitted to determine the risk of contracting SARS-CoV-2, severe respiratory tract infection (RTI) and respiratory hospitalization.

Results

CCR5 information was available for 110,544 donors who were tested at least once for SARS-CoV-2. 5,536 participants with CCR5 information reported SARS-CoV-2 infections. For 4,758 donors the COVID-19 disease course was fully evaluable, 498 reported no symptoms, 1,227 described symptoms of severe respiratory tract infections, and 164 of these individuals required respiratory hospitalization. The distribution of CCR5Δ32 genotypes (homozygous wild-type vs. CCR5Δ32 present) did not differ significantly between individuals with or without SARS-CoV-2 infections (OR 0.96, 95%-CI 0.89-1.03, p = 0.21) nor between individuals with or without symptomatic infections (OR 1.13, 95%-CI 0.88-1.45, p = 0.32), severe RTI (OR 1.03, 955-CI 0.88-1.22, p = 0.68) or respiratory hospitalizations (OR 1.16, 95%-CI 0.79-1.69, p = 0.45).

Conclusions

Our data implicate that CCR5Δ32 mutations do not determine the risk of SARS-CoV-2 infections nor the disease course.