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[Risk of meningococcal infection in children with different hla phenotypes]
Insights
Certain human leukocyte antigen (HLA) phenotypes increase the risk of meningococcal infection in children. Specifically, HLA-Bw16 and HLA-A12 phenotypes are associated with a significantly higher risk compared to HLA-A1.
Area of Science:
- Immunogenetics
- Pediatric Infectious Diseases
Background:
- Meningococcal infections pose a significant health risk, particularly to children.
- Understanding genetic predispositions can aid in risk assessment and prevention strategies.
Purpose of the Study:
- To investigate the association between specific human leukocyte antigen (HLA) phenotypes and the risk of developing meningococcal infection in children.
- To identify HLA antigens that may confer susceptibility or resistance to meningococcal disease.
Main Methods:
- A case-control study involving 104 children with meningococcal infection and 600 healthy controls.
- Determination of 36 histocompatibility antigens across HLA-A, HLA-B, and HLA-C loci using the lymphotoxic test.
Main Results:
- Individuals with the HLA-Bw16 phenotype exhibited a 6-fold increased risk of meningococcal infection.
- Individuals with the HLA-A12 phenotype showed a 3-fold increased risk compared to those with the HLA-A1 phenotype.
Conclusions:
- Specific HLA phenotypes, notably HLA-Bw16 and HLA-A12, are significantly associated with an increased susceptibility to meningococcal infections in children.
- These findings highlight the role of immunogenetics in meningococcal disease risk.
Abstract:
A total of 104 children aged 4 months to 13 years with meningococcal infection were examined. For control 600 healthy donors were used. Histocompatibility antigens were determined by the lymphotoxic test. Altogether 36 antigens of the loci, A, B and C were determined. The data thus obtained indicate that the risk of contacting the infection is 6 times greater for persons with Hl A-Bw16 phenotype and 3 times greater for persons with HL A-A12 phenotype than for persons with Hl A-A1 phenotype.