Abstract
We analysed data from 80 patients who tested positive for SARS‐CoV‐2 RNA who had previously been HLA typed to support transplantation. Data were combined from two adjacent centres in Manchester and Leeds to achieve a sufficient number for early analysis. HLA frequencies observed were compared against two control populations: first, against published frequencies in a UK deceased donor population (n = 10,000) representing the target population of the virus, and second, using a cohort of individuals from the combined transplant waiting lists of both centres (n = 308), representing a comparator group of unaffected individuals of the same demographic. We report a significant HLA association with HLA‐ DQB1*06 (53% vs. 36%; p < .012; OR 1.96; 95% CI 1.94–3.22) and infection. A bias towards an increased representation of HLA‐A*26, HLA‐DRB1*15, HLA‐DRB1*10 and DRB1*11 was also noted but these were either only significant using the UK donor controls, or did not remain significant after correction for multiple tests. Likewise, HLA‐A*02, HLA‐B*44 and HLA‐C*05 may exert a protective effect, but these associations did not remain significant after correction for multiple tests. This is relevant information for the clinical management of patients in the setting of the current SARS‐CoV‐2 pandemic and potentially in risk‐assessing staff interactions with infected patients.
Highlights
The capacity of an individual to mount an effective immune response to infection is entirely dependent upon their inherited complement of human leucocyte antigens (HLA) which present pathogenic peptides to T and B lymphocytes
This study investigated HLA profiles of patients admitted with PCR-confirmed SARS-CoV-2 infection to identify any potential HLA bias which might indicate an impaired capacity to mount an effective immune response to the infection
For HLA Class I, HLAA*26 was significantly increased in the patients compared with Group A controls (11.3% vs. 4.0%; p = .0049, pc = .0198; OR = 3.04 confidence intervals (CI) 1.50–6.13, 0.0019, pc = .0076). These data need to be interpreted cautiously as the associations reaching significance against Group A controls are based on comparison with a UK population and HLADRB1*10 and HLA-A*26 are known to be represented at higher frequency in the BAME populations
Summary
The capacity of an individual to mount an effective immune response to infection is entirely dependent upon their inherited complement of human leucocyte antigens (HLA) which present pathogenic peptides to T and B lymphocytes. The repertoire of the viral peptides bound by each individual is dependent upon sequence variation within the antigen recognition site of their HLA molecules This has recently been underlined in the twin study of Williams et al (2020). A number of in silico studies have defined the potential for immune responsiveness based on differential viral peptide binding to HLA alleles (Fast, Altman, & Chen, 2020; Nguyen et al, 2020). These are useful in vaccine design but do not represent the situation in natural infection where the full HLA type of the individual, comprising up to twelve alleles across six loci, informs the capacity for immune response. The information is of value towards risk stratification and clinical management of patients and potentially in risk-assessing staff interactions with infected patients
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