Apologies, this is going to be very technical…
In everyday practice, when there is a tick bite or typical Lyme symptoms, the sample is sent to the laboratory immediately. It is not so important what method is used to examine it there; in most cases, we interpret the result as “gospel”.
We rule out Lyme disease, and then it’s time for steroids or “penguin walking” (shrugging your shoulders) and following protocols. There have been deaths, years of suffering, and ruined lives as a result. The doctor is not responsible because he had the test done. The medical director says that according to publications, this test has 95-100% sensitivity and 100% specificity. Okay, in certain complicated cases, the sensitivity may only be 70%. To some extent, we blame science for this. And science with a capital S says, yes, we designed the clinical research, and this is indeed the result.
A recent study, an article in Nature, pulled the rug out from under this evasion.
In Canada, they studied the genetic groups of Borrelia burgdorferi sensu stricto (the American strain) and formed 12 groups. They studied bacteria isolated from ticks, where the most important protein is different from that in humans. In ticks, OspA is the most important surface protein of Borrelia, and it was found to show the greatest variability, both at the recombination and mutation levels, but the role of mutation was higher.
P41 (flagellin) and OspC, which are not important in ticks but are most commonly measured in humans, as well as the latest “star” p39 (VlsE), showed higher recombination rates with fewer mutations, which is understandable since these proteins are primarily subject to mutation pressure in the human body.
In human serological tests, p41 and OspC most often show a reaction.
So what does this new research say about our serological results?
- The tests developed in America do not work well even there, as a single selected “monoclonal” antigen is only suitable for a few of the 12 variants of the Borrelia strain found there.
- In Europe, there are at least three different strains (and their identified variants, which are sometimes given separate names), which means there is a high degree of variation.
- As a result, a US test that has been validated for Europe (and is most commonly used in laboratories) is unlikely to follow the evolutionary processes (recombination, mutation) of European strains. Thus, it would detect a recombinant protein produced from a “theoretical” gene sequence if it were present in the sample. But it is no longer present…
So, once we have sent the patient’s sample for testing, our work is not done. This change must be initiated from the bottom up, by those who see the patient’s symptoms and know that the picture does not add up with the laboratory. They must force better tests to be developed. As we can see, science with a capital S provides some ammunition, but even then they do not know exactly how their data relates to everyday tests: that the proteins (antigens) that most often show a reaction in tests will only work for a few specific variants. The chances of a reaction are 2/12, 3/12, 4/12. In other cases, Borrelia has long since changed.
But then how can clinical studies show good results? We will discuss this in a future article.
The research mentioned can be found here: https://www.nature.com/articles/s41598-025-24758-2
