An international team of scientists has identified genetic differences that increase susceptibility to meningococcal meningitis and sepsis. This article is published in the journal Nature Genetics.
Meningococci, or bacteria of the species Neisseria meningititdis (also known as Meningitis), periodically live in the nasopharynx of most people without causing any disease.
However, in a very small percentage of people, infection with them leads to the development of the so-called invasive meningococcal disease (IPD), which can present as meningitis or sepsis (sepsis), i.e. the invasion of bacteria into the bloodstream. Both complications may also occur.
IChM has a dramatic course. Meningococcal sepsis can be fatal within hours of the onset of symptoms. In many cases, even if the patient is saved, IChM may leave a permanent mark, such as hearing damage, neurological and psychiatric problems, bone and joint damage, kidney failure.
IChM is diagnosed most often in the fall, and among adolescents also in the summer. They are favored by large groups of people and close contacts, e.g. kisses. IChM is a threat primarily to the youngest children, adolescents and young adults (up to 25 years of age). Susceptibility to it may increase in the period of mental and physical stress, in adolescence, when immunity weakens, but often the disease develops in previously completely healthy people.
Therefore, scientists have long suspected that genetic factors must influence susceptibility to IChM.
To identify them, scientists from Imperial College London, together with colleagues from the Institute for Genome Research in Singapore and several research centers in Europe, compared the DNA of more than 1400 patients who had undergone meningococcal meningitis with the DNA of more than 6000 healthy people. The subjects came from Great Britain, the Netherlands, Austria and Spain.
The analysis focused on over 500 the most common differences in single nucleotides, i.e. the structural units of DNA. These differences are referred to as single nucleotide polymorphisms (SNPs).
It turned out that differences in the two genes coding for resistance proteins may determine susceptibility or resistance to meningococcus. It is about the so-called complement factor H (CFH) and related protein 3 (CFHRP3). They regulate the function of the complement system, the protein system that recognizes and destroys pathogenic bacteria.
According to previous studies, meningococci are able to use the H factor to avoid complement attack. It is enough that they attach its molecules to the surface of its cell and the body does not recognize them as foreign. The authors of a recent study speculate that it is easier for bacteria to use certain H-factor variants to hide from the immune system. However, more research is needed to confirm these suspicions.
While most of us carry meningococcus at some point in our lives, only one in 40. people get meningococcal meningitis. Our research was intended to help understand why this small group of people is susceptible to such a severe disease while others remain immune to it. The results obtained by us provide the strongest evidence so far that there are genetic factors predisposing to the development of meningococcal disease – comments Prof. Michael Levin of Imperial College.
In his opinion, this discovery may help in the development of an effective vaccine against meningococcal B group, which, for example, in Poland is mainly responsible for sporadic diseases.
Currently, there are vaccines against meningococcus C, which are the most common cause of outbreaks of IChM in our country. Group A, against which vaccines also exist, is causing epidemics in African countries south of the Sahara. (PAP)