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Meningitis susceptibility linked to genetic makeup, experts claim

16 August 2010
Appeared in BioNews 571

Researchers have discovered genetic factors that they believe are associated with an increased susceptibility to the bacterial form of Meningitis.

This is a serious condition that can lead to swelling of the brain and blood poisoning that is caused by Neisseria meningitidis. But the authors report that the ‘genes responsible for disease development are largely unknown’.

The scientists conducted a genome-wide association scan (GWAS) on 475 people with meningococcal disease and over 4,700 ‘healthy’ individuals in the UK. They found that SNPs (single nucleotide polymorphisms) in a region involved with the immune system were strongly associated with increased susceptibility. 

One of the strongest associations was found in SNPs in the complement factor region, and in particular those around complement Factor H (CFH).

The complement pathway plays an important role in the immune response. But the organism that causes meningococcal disease is thought to be able to evade this by binding to the hosts CFH.

Genetic variation in this region therefore makes it easier or harder for the organism to attack the host, and means that some people are more susceptible than others.

The BBC reported that Professor Michael Leven, a vaccine expert from Imperial College (London) said that ‘the findings would be particularly useful in developing a vaccine against meningitis B’.

In a further comment on the research, Sue Davie from the Meningitis Trust said: ‘This exciting work has thrown new light on factors that play a part in determining why some people get meningococcal disease and others do not’.

The research is published in the journal Nature Genetics.

Gene link to meningitis infection
BBC News |  8 August 2010
Genome-wide association study identifies variants in the CFH region associated with host susceptibility to meningococcal disease
Nature Genetics |  8 August 2010
Meningitis Trust media statement
Meningitis Trust |  8 August 2010
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