Therefore, some suffer worse from deadly bacteria –

Group A strep are common bacteria that can cause strep throat or swine pox, among other things. But if the bacteria becomes invasive, it can become really dangerous. Then it sometimes changes its name to killer bacteria or flesh-eating bacteria. It can lead to life-threatening diseases such as septicemia, septic shock, or soft tissue infections that can lead to amputation, for example, of arms or legs.

Invasive streptococcal infections have increased in recent decades. During the period from July 2021 to July 2022, 220 cases of invasive streptococcus infection were reported in Sweden.

Infection can occur very differently, and it is still not known why some people develop a life-threatening disease while others do not.

interaction between genes

For the past five years, researchers have been studying the underlying biological mechanisms that explain how potentially aggressive streptococcus bacteria affect humans.

– Our hypothesis was that it was caused by an interaction between genes in both humans and bacteria. Previously, very little was known about how different variants of genes in bacteria and our immune system interact and influence the outcome of infectious diseases, says Friedrich Karlsson, a researcher in infectious biology at Lund University.

It turns out that the researchers’ hypothesis is correct – genes are different and this plays a role in the risk of developing serious diseases.

The unfortunate combination increases the risk of serious illnesses

The study shows that the severity of the infection depends on the interaction between a gene — the stinger — in our immune system and a bacterial enzyme found in bacteria that have also plagued the Western world further since the 1980s. The gene can vary between people and this explains why some people get the disease more than others.

A person carrying the “bad” genetic variant of Sting has a 20 percent increased risk of amputation of a body part if infected by an invasive infection by the worst kind of bacteria. For people with a “good” genetic variant, the risk is only three percent.

The proportion of patients who develop septic shock also varies depending on the interaction between human Sting variants and the bacteria’s enzyme activity. The difference is due to a unique combination of genetic material from the host and the pathogen, i.e. the bacteria that causes the disease.

– It has to do in part with the immune system of people with a certain variant of the Sting gene triggering a dangerous and misguided inflammatory response. The outcome depends in part on whether we are infected with a more aggressive bacteria because it has a very active type of enzyme called NADase. Conversely, natural activation of the immune system as a result of another Sting variant and lower bacterial enzyme activity is associated with protection, says Fredrik Carlson.

The risk variant is more common in some parts of the world

The researchers also studied the evolution of different Sting variants in humans. The results show that the Sting risk variant appeared in humans around 35,000 years ago, and that it began spreading differently around the world in connection with the first agricultural revolution 10,000 years ago. The result today is that the Sting risk variant is more common in some parts of the world than others.

Researchers have not studied recent outbreaks of streptococcal infections among children in the United Kingdom and Denmark. But the popular view is that the increase was a result of the pandemic when people in countries with a lockdown strategy were exposed to fewer infections than normal, resulting in lower protection for certain groups afterwards.

The researchers will work further to understand in detail the molecular mechanism by which the bacteria inhibit stinging and the normal inflammatory response.

The study is a collaboration between researchers at Lund University, Karolinska Institutet and Harvard University in the US, among others.

Scientific study:

Interaction between human STING genotype and bacterial NADase activity regulates disease variability between individualsAnd Nature Communications.

communication:

Fredrik Carlson, researcher at Lund University, Frederick Carlson@biol.lu.be seen