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A little flight through the world of immunology and virology

otherwise a travel agency for microscopic warfare




The following few lines are intended to raise awareness among the public. I will try to present and embellish it with the help of admittedly limited, but publicly available, resources so that even a layman willing to further self-educate can understand how it all works. In the words of an unnamed medium, "Understand how" immunity works…


This article will only cover the parts necessary to understand the function of the spread of coronaviruses (there are hundreds of them commonly among humans) and the body's defences, i.e. it will not go into the details essential for other forms of pathogens. Of course, I would also like to address experts who have successfully forgotten the following basic facts from school, because they either never used them or they are specialized in other activities, which in neither case unfortunately prevented them from fitting into the role of advisors to politicians. At the same time, it has to be written in such a simple way that it can be understood by everyone, even from non-medical disciplines.


Let's get to it. Step one, meeting the source of the infection, the infected. This person is spreading the infection in his environment by means of droplets containing the virus. The droplets are also released through normal speech, up to a distance of 1m, and even further for loud talkers. This can also be verified by our own experiment, where we sit opposite a person with a strong light behind him (typically, e.g., low evening sun) and in this light the flying droplets are clearly visible. These virus-containing droplets can enter our body through two routes. The easier way (for the virus) is by inhalation and therefore by respiration through the mucous membranes of the respiratory tract. The more difficult, but generally also quite common, route is through the mucous membranes in the digestive tract, where the droplet has e.g. fallen into food or drink, or the droplet has stuck to the surface and before the virus has had time to die (which can take hours) we have touched it with our hand, which we then e.g. serve food with. Of course, there is also the possibility of direct introduction of the virus into the mucous membranes of the hand, for example, if we wipe our eye with a contaminated hand. This is why protection of the nose and mouth is so important (droplets also come out of the nose when breathing, albeit in smaller quantities).



That was boring, wasn't it? Let's make it better - step two, contagion. So if we get a virus in our body, the first line of defense is the mucous membranes. The virus invades the mucosal cells and begins to multiply. This starts the spread of the disease in the body, and the person becomes contagious, as he releases mucous (i.e. droplets, whether in the form of coughing or even plain talking, see previous paragraph) containing the virus into his environment. The time between infection and symptomatic manifestation of the disease is called the incubation period. Already during the incubation period a person gradually becomes infectious. This is a very important fact, since an infected person is therefore contagious before the first symptoms of the disease appear. Each disease has a different incubation period.




Still bored? Then we go to war - step three, acute defense of the organism. It takes time for the human body's immune system to react. During this time, the virus multiplies uncontrollably on the mucous membranes. Logically, the larger the initial dose received, the more the virus has time to multiply in the body before the first immune reaction occurs. Logically, the immune system starts to defend itself at the point of penetration of the virus, i.e. at the mucous membranes. The defence is triggered by the production of antibodies with the help of immune system cells called Lymphocytes. In this case, with the help of B-type Lymphocytes on the mucosa to form specific mucosal type A antibodies (immunoglobulins A, IgA for short, general info HERE and HERE).

Specific antibodies are those that are specifically produced against a particular virus, non-specific antibodies are universal (typically anti-inflammatory, but e.g. children produce large amounts of non-specific antibodies in general, because the immune system is still actively learning through contact with the environment). The first contact with a given virus type can take several days for the Lymphocytes to "develop specialization", i.e. specificity, of the antibodies (more on specificity HEREuse translator please, i cant find relevant simple medical document in public source in english), the antibodies produced gradually improve (become more specific). However, after this time, when the virus is fully understood, antibodies are already produced efficiently and tailored to the virus. The IgA antibodies in the mucous mucus, among other things, prevent further multiplication of the virus on the mucous membranes and, thanks to their action, the person gradually ceases to be infectious. This is the second very important fact, because until sufficient IgA antibodies are produced to neutralise the virus in the mucous membranes, the person will be contagious. If IgA antibodies are not produced (e.g. by a defect in the immune system), human will be contagious throughout the course of the disease (Note: no IgA antibodies are produced by vaccination). IgA antibodies disappear from the body after about 1-2 weeks. The immune system has a memory of the diseases experienced (it may even be hereditary in some cases). The way it works is that some of the B Lymphocytes become memory (say "teachers" for new Lymphocytes), for possible faster production of antibodies during the next attack on the organism. The next time the organism is attacked, IgA specific for this type of virus are then produced much faster, during higher number of hours (but not days as it was when the virus was first encountered).


After the first line of defense on the mucous membranes comes "heavy artillery" in military terminology. IgM antibodies are very active and are the main form of defence of the organism in the acute phase of the disease. Their independent source is largely the spleen, but they are also partly part of the B-lymphocytes. Excess or hyperactivity of IgM antibodies leads to severe autoimmune diseases. On the other hand, as a point of interest, there is a certain percentage of people who do not make IgM antibodies at all or only minimally (they make do with IgA and IgG, which they then make at a higher level). IgM antibodies are intended to be a vigorous response by the body and are primarily used to cure the disease. The production of these antibodies begins after the pathogen has penetrated from the mucous membranes into the body. Thus, usually in the case of respiratory diseases, this is when the pathogen has already successfully invaded the organism and is present inside and begins to invade organ cells and use them to replicate itself. Thus, there is a temporal overlap in the production of IgA and IgM and we can detect both types of antibodies at the same time. IgM antibodies last longer in the body than IgA, but usually disappear only shortly after the disease is eradicated, in the lower order of weeks. Interestingly, IgM antibodies do not have the ability to label for phagocytosis (phagocytosis is simply put, cleaning up dead bodies and virus debris), they are merely "disease killers".




That was already more interesting, wasn't it? Let's move on - step three, cleaning up after the war, learning from the crisis situation and preventive defence. It sounds almost political, but that's exactly what it is. Our body, or rather our immunity, can learn and remember how to defend itself against a virus. Towards the end of a successful fight against the disease, IgG antibodies start to be produced (IgG are called long term antibodies - CAUTION not to be confused with "memory cells" / "memory immunity" as the political "experts" call and like to call it, that's different - we'll explain that in a moment). IgG antibodies are produced by immune cells called plasmocytes, which are made from B lymphocytes, which we have already become familiar with in fending off the first attack. Thus, the antibody produced is specifically optimized for the particular virus it is meant to address. As mentioned above, some of the B Lymphocytes become memory cells. Thus, this is simply put, the aforementioned "memory immunity", or more correctly, immune memory. This is the third very important fact. The existence of IgG antibodies, therefore, implies the existence of B lymphocytes (which must have produced them) and therefore logically the existence of memory cells. It's akin to someone with a chicken egg in their hand claiming that it's not proof of the existence of a chicken. Silly, isn't it.


IgG antibodies are very small and long lasting. They can mark waste for phagocytosis (disposal, to give a simple idea phagocytes are like ash collectors in the body), they pass through the placenta (i.e. they can pass to the fetus) and can persist in the body for years. Their production starts the moment the immunity recognizes a successful attack. There is usually a temporal overlap with IgM antibodies.



Endnote: The immune system can be stimulated to produce more antibodies with now commonly available drugs (e.g. the recently widely mentioned Isoprinosine). Dosage experience is important especially at the beginning and end of the disease and should be taken with caution, especially in young people who have a healthy immune system. Overproduction (called cytokine storm) can occur and antibodies very simply put start to attack the body similar to some autoimmune diseases).



How the course of the disease differs in vaccinated people



Beforehand, it is important to understand at least the minimum basics of how vaccination works. The principle of any vaccination is to increase the body's defences (quite generally speaking). There are several ways to achieve this. In more or less gentle ways. Classical vaccination consists of introducing a weakened or dead virus as a whole into a muscle or under the skin. This gives the organism the opportunity to become familiar with its structure and to produce IgG antibodies against it, with all the consequences mentioned above. Unfortunately, the production of such vaccines in large quantities is lengthy (not for development, but for production), so modern methods originally intended for other purposes are being promoted (see e.g.
HERE and HERE , and pay attention to the resources in the footer, they contain very interesting facts from very recent history). Simply put, vaccinations using mRNA or vector technologies damage the cell and "grow" recognizable characteristic proteins of the pathogen in the cell that the immune system attacks. These damaged cells should then be destroyed by the immune system and the Lymphocytes will then remember the part of the virus that the cells have grown. When the virus is attacked and after it has successfully penetrated the body, it should then be eliminated more quickly (virtually immediately if antibodies exist, or after they have been produced by the immune system) - in theory.


Whatever the method, the immune system will only create IgG antibodies. Moreover, in the case of modern vaccines, somewhat less perfect, since the antibody thus artificially created "knows" only the characteristic protein (usually a spike) grown, not the pathogen as a whole. Moreover, due to the ability of viruses to mutate, usually the vaccination contains an "outdated" model. These shortcomings are eliminated by higher stimulation of the immune system (e.g., multiple doses) and thus higher antibody counts.



Let's fast-forward through the course of infection in a vaccinated human.



At the moment of infection, the virus starts to multiply on the mucous membranes. Just as in the unvaccinated, for the same length of time, the person is infectious and therefore contagious to his or her surroundings in the same way. If, as a public official (or his advisor), someone publicly declares that a vaccinated person is not worth testing, this could obviously be classified as aiding the spread of a contagious disease.



The course is therefore more or less similar. The B lymphocytes are the first to kick in and start making IgA antibodies. When the virus enters the body from the mucous membranes, IgM antibodies are produced and IgG antibodies from the stocks (if available) are also used. If the virus is the same as that contained in the vaccination, immediate production of new IgG antibodies follows. However, this is usually not the case with corona viruses. The new mutation is more or less altered and the antibodies do not function quite so ideally after vaccination, but still, because of the higher quantity (if available), they inhibit the multiplication of the virus.


This could be good news because the course of the disease will not be so severe, but it has important pitfalls. Mutations occur during virus multiplication, but because the antibodies inhibit the "old model" the mutations are more successful in escaping these "old" antibodies. Vaccinated is a better source of mutations for rapidly mutating viruses (just typically corona viruses) than unvaccinated for the same amount of viral production. If the organism is attacked by a significantly different mutation, there is of course no difference between vaccinated and unvaccinated protozoa. The entire pathogen (not just the outdated spike protein) is only learned to be recognized by the lymphocytes during the course of infection, just as in the unvaccinated. Thus, control of the infection is only slightly faster and there is a chance that the disease will break out without symptoms or with mild symptoms.
Important fact: In order to manage the infection, the Lymphocytes must learn to recognize the mutation in exactly the same way as in the unvaccinated, and only then does immunity become comprehensive. In the context of the above, a vaccinated patient is just as infectious as an unvaccinated one, and has a higher propensity to generate additional mutations.







Vaccination against rapidly mutating viruses is therefore practically only suitable for vulnerable populations where it is assumed that their own immunity will not cope with the disease. Preventive vaccination is a matter of weighing the benefits and risks, and vaccination after a disease is unnecessary and in many ways dangerous. Vaccination (of any kind) should always be preceded by antibody testing (in case there is a possibility that the patient may have encountered the disease - there is probably no point in testing someone who has never been outside Europe for Zika antibodies, nor for a strain of influenza only estimated for a future season). If we vaccinate a person with a supply of their own antibodies, they will be consumed extremely quickly and the production of more antibodies will start just as quickly. The immune system becomes very stressed and can easily be damaged in various ways.




No vaccination is generally risk-free. Vaccinations using dead or weakened pathogens as a natural irritant to the immune system have been with us for about 200 years (i.e. 200 years of documented, informal traced back to antiquity), and in that time they have undergone a relatively large number of studies and tests, and their long-term effects and possible side effects can be accurately defined. The same cannot be said, however, of modern mRNA, vector or protein methods, which have a history of less than a few decades (even taking into account the theory described in the laboratory) and whose method consists of artificially irritating the immune system.



Update on the vaccination against COV-19, not yet verified by a large targeted study (09/2021): these "artificially" produced antibodies, however, besides being imperfect and thus promoting mutations, also seem to disappear very quickly compared to natural antibodies. They seem to disappear completely in low numbers of months, but studies have so far been carried out on extremely small numbers of people (the study is not easy, requiring regular measurements of antibodies - at least as follows: before vaccination, 1 week after the first dose, 3 weeks after the second dose - i.e. before the second dose, 3 weeks after the second dose, and then every month later). This would of course explain the situation in Israel and other countries with high vaccination rates.



Sorry for imperfect english (but still better then googlenglish), Translated with www.DeepL.com/Translator (free version)




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