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[Association of class I HLA antigens with invasive meningococcal disease]
M Holub1, J Hobstová, J Prazák
1Infekcní klinika, Fakultní nemocnice na Bulovce, Praha.
Background:
The majority of meningococcal infections are characterized by nasopharyngeal carriership. In some patients invasive disease with a mild course develops, while some cases have a lethal outcome. The reasons of this wide variation range are not clear. The objective of the present work was to assess whether the development of invasive meningococcal disease or its prognosis are associated with HLA class I.
Methods And Results:
The group of patients was formed by 40 patients (29 females, 11 males, mean age 16 years, range 8 months to 52 years). In 28 patients the disease was caused by N. meningitidis group C, in 9 cases group B, in three cases the serotype was not assessed. The etiology was confirmed by cultivation or latex agglutination. Twenty-three patients had a mild course of the disease, 8 a medium severe one, 9 patients a severe clinical course (score according to Stiehme, Damrosch and Rosenblat). The patients were compared with 227 non-related blood donors (114 women, 113 men, 18 to 50 years old). In patients and controls 24 lymphocytic HLA antigens class I were identified as to type. Typing was done using the standard microlymphocytotoxic test in the NIH modification. The results were processed by statistical methods using Fisher's exact test and the 2 x 2 test with Yates correction. In patients with a mild course HLA antigens B7 and B12 predominate (p = 0.03; p = 0.02), in medium severe cases antigen A11 (p = 0.03), in patients with the most severe course antigen A9 (p = 0.04). In invasive infections caused by N. meningitidis serotype B antigen B17 predominates (p = 0.05).
Conclusions:
The severity of meningococcal invasive infections is associated with HLA class I. Invasive disease caused by N. meningitidis serotype B are more likely to occur in carriers of HLA B17. No relationship was found between HLA class I and invasive disease caused by N. meningitidis regardless of serotype and with serotype C.
Insights
Human Leukocyte Antigen (HLA) class I variations influence the severity of meningococcal infections. Specific HLA antigens are associated with different disease severities and serotypes, particularly N. meningitidis serotype B.
Area of Science:
- Immunogenetics
- Infectious Diseases
- Microbiology
Background:
- Meningococcal infections commonly present as nasopharyngeal carriership, with variable disease severity.
- The underlying reasons for the wide range in disease outcomes remain unclear.
- This study investigates the association between Human Leukocyte Antigen (HLA) class I and the development or prognosis of invasive meningococcal disease.
Purpose of the Study:
- To determine if HLA class I antigens are associated with the development of invasive meningococcal disease.
- To assess the relationship between HLA class I and the prognosis (severity) of meningococcal infections.
- To explore potential links between specific HLA class I alleles and N. meningitidis serotypes.
Main Methods:
- Compared HLA class I antigen types in 40 patients with invasive meningococcal disease against 227 healthy blood donors.
- Utilized standard microlymphocytotoxic test for HLA typing.
- Employed Fisher's exact test and 2x2 test with Yates correction for statistical analysis.
Main Results:
- Specific HLA class I antigens were linked to disease severity: B7 and B12 in mild cases, A11 in medium-severe cases, and A9 in severe cases.
- HLA antigen B17 was predominant in invasive infections caused by N. meningitidis serotype B (p=0.05).
- No significant association was found between HLA class I and overall invasive disease or serotype C infections.
Conclusions:
- HLA class I plays a role in the severity of invasive meningococcal infections.
- Carriers of HLA B17 may be more susceptible to invasive disease caused by N. meningitidis serotype B.
- No correlation was observed between HLA class I and invasive disease regardless of serotype or specifically with serotype C.