Genetic link to Meningitis
An international study, led by Professor Michael Levin of Imperial College London, has revealed that differences in genetic composition could explain why some people are more likely to contract meningococcal meningitis and/or septicaemia than others.
At some point in time, most of us will carry the meningitis-causing meningococcus bacteria in our noses and throats, but will not go on to develop meningitis. In fact, when exposed to the bacteria, only one in 40,000 people, or 0.0025% of the population, will develop meningitis.
Professor Levin and colleagues set out to investigate why one person becomes ill when 39,999 others, who have been exposed to the same bacteria, do not.
Scientists have long suspected that 'genetics' may be a contributing factor to an increased risk of meningitis but, until now, the specific genes and mechanisms have been largely unknown. In order to address this, scientists began to look for differences between the DNA of people who had experienced meningococcal meningitis and the DNA of those who had not.
The research team analysed the DNA of over 6,000 people from the UK, Holland, Austria and Spain. Over half a million genetic sites, know as 'snips', were analysed. Each 'snip' is made of varying combinations of the following 'nucleobases' (the building blocks of our DNA): cytosine (C), guanine (G), adenine (A) and thymine (T).
For example, the 'snip' of one individual may be as follows:
The equivalent 'snip' of another individual may have a slight variation in the order of nucleobases:
Any variation in the genetic code, even by just one nucleobase (i.e. swapping the position of A and T), can have a significant impact on health, such as increasing an individual's risk of developing meningococcal meningitis.
The research team identified several differences in the DNA of those who had experienced meningococcal meningitis. The most significant variation contributing to an increased risk of meningitis was found in the genes for Factor H and Factor H-related proteins.
Factor H is one of the 25+ proteins that make up the human 'complement system' - part of the immune system that helps, or 'complements', the ability of antibodies to destroy invading pathogens, such as the meningococcus bacteria. Specifically, Factor H and Factor H-related proteins normally ensure that the immune system does not over-react and cause the body to damage its own cells. Professor Levin's research indicates that, when there is aspecific variation in the genetic makeup of the Factor H gene, the invading meningococcus bacteria gain the ability to 'hijack' the body's complement system and cover themselves in Factor H proteins. This Factor H 'coat' enables the bacteria to remain undetected by the human immune system, therefore free to multiply and cause disease. In essence, the variation in the factor H gene permits the meningococcus bacteria to disguise its true identity and cause damage , rather like a wolf in sheep's clothing!
Factor H variations can be detected through simple blood tests and, although not routinely screened for, a referral to an immunologist would be advisable for those who have had meningitis two or more times, or for those with a family history of the disease. However, Professor Levin reassures us that, even with a Factor H variation, the risk of contracting meningococcal meningitis would only increase from a one in 40,000 chance to a ten in 40,000 chance.
The findings of this study are of high scientific significance, as highlighted by Dr Victoria Wright, co-researcher, who said "improving our understanding of why some people get the disease and not others will help to identify those at risk and better develop vaccines".
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