You may have heard in the media or read in my last post how difficult it is to develop drugs or even a vaccine against a new virus like Corona SARS CoV2. However, we must not forget in all our concern about this situation that the strongest weapon against viruses and also against new viruses like Corona SARS CoV2 is our own immune system – and we should not underestimate its capabilities.
Because just as viruses have optimally adapted to host organisms over the course of evolution, so has our immune system been optimized over the course of evolution to defend against microorganisms. Our immune system therefore consists of two defense lines – the first line of defense is the so-called innate immune system (innate immunity), the second – even more powerful defense line – is the so-called adaptive immunity (adaptive immunity), which is mediated by B and T lymphocytes.
As a reminder – viruses invade body cells and use the host’s synthesis machinery for their own reproduction. Virus replication (proliferation) disrupts normal cellular function and leads to loss of function and ultimately death of the infected cell. Our immune system is designed to eliminate infected cells and block further infections. This happens initially very quickly and efficiently through the activation of the innate immune system, which is supported in the course by the mechanisms of adaptive immunity, which reacts slower, but contributes even more specifically to virus elimination.
The main mechanisms of innate immunity against viruses are the inhibition of infection by the release of type I interferons (interferon alpha and interferon beta – the latter is also used for the therapy of multiple sclerosis) and the NK cell-mediated killing of virus-infected cells (NK stands for “natural killer cells”).
There are various mechanisms by which a viral infection triggers the production of interferons – often the viral genetic material (the RNA or DNA) is recognized by certain intracellular receptors, which then stimulate the body’s own production of type I interferons in the infected cells. Type I IFNs inhibit virus replication both in infected and in non-infected cells- thus they also protect neighboring (still) healthy cells of a tissue. Perhaps now you also understand why we consider the use of interferon-beta preparations absolutely uncritical. I wouldn’t go so far as to claim that they could even be protective against a corona infection, but the use of interferons is currently not problematic in any case.
NK cells are the second crucial mechanism of immunity against viruses at the beginning of the infection, before an adaptive immune response, mediated by B and T lymphocytes, develops. The term “natural killer” arises from the fact that their main function is to kill infected cells (similar to the killer cells of the adaptive immune system, the cytotoxic T lymphocytes (CTLs), which I will report on in the next post), without having to differentiate further (hence natural). NK cells make up about 5% to 15% of the lymphocytic cells in the blood and spleen, they contain cytotoxic granules (cell toxins) that can destroy infected target cells. The fascinating thing about NK cells is that they can distinguish infected (stressed) cells from healthy cells – they do this with the help of certain surface receptors. Because of this ability to distinguish, NK cells are also very important in suppressing and eliminating tumor cells.
Perhaps it reassures you in the context of the corona epidemic that none of the currently used MS therapies have a significant effect on the components of innate immunity. This is probably also the reason why, despite the use of immunotherapeutics, normal infection defense continues to work pretty well – because a functioning innate immunity is already (at least) “half the battle”. Most MS drugs interfere in one way or another with the processes of adaptive immunity – and these mechanisms are even more complex and varied.
Nevertheless, we will take a closer look at the adaptive immunity in the next post to understand the function in basic terms. Then it will also be easier to assess the risks and side effects of individual MS drugs.
