The full name of the corona or covid virus is SARS-CoV-2 (severe acute respiratory syndrome coronavirus type 2) and it is a so-called beta coronavirus, which first appeared in late 2019 and was identified as the cause of the disease COVID-19 (acronym; English: coronavirus disease 2019) in early 2020. Coronaviruses have a wide distribution among mammals and birds. In humans, infection results primarily in mild colds but also in severe pneumonia. The SARS-CoV-2 uses a specific enzyme (ACE-2) as a receptor to enter the body. Potential host cells for the virus, with the appropriate docking sites, are found not only in the respiratory tract, but especially in the intestine, vascular cells, kidney, heart muscle, and other organs. This is why, for example, diarrhea – in contrast to the common cold – is often one of the symptoms of an infection. And in contrast to the “harmless” corona viruses, it can lead to severe kidney disease with kidney failure or cardiovascular disease, among other things.
One of the most frequently mentioned arguments against vaccination or wearing a mask as self-protection is: a good immune system. Of course, a well-functioning and stable immune system is an important component in preventing disease. However, just like adequate sleep, a healthy diet or plenty of exercise, it is no guarantee of health. Cancers strike even health ascetics. A strong immune system does not protect against viral diseases. The HIV virus, herpes or hepatitis viruses don’t give a damn about the athletic fitness of the host. Bacterial infections like typhoid eliminate healthy people. Be that as it may, the covid virus is of course much less dangerous than the pathogens just mentioned, but even extremely healthy and fit athletes are not immune.
With the immune system there is no black and white and no shades of gray. There are no clearly defined categories “good”, “bad” or “mediocre”. The immune system consists of many factors, it is colorful. It is not for nothing that we choose our partners – consciously or unconsciously – also with the help of our nose. Women in particular have a very well-developed sense of smell to determine oligofactorily which partner suits them biologically. Here it is above all a question of potential offspring getting as “good” and extensive an immune system as possible. Thus, the woman sniffs out the immune system of her counterpart (men, as mentioned, also, but less intensively). If a man has a complementary immune system to the woman, he smells particularly seductive for this woman. Similar immune systems tend to cause rejection in the woman before the man’s own smell. Just blood relatives and especially father and daughter usually “can’t smell” each other, which also acts as a protection against inbreeding. So, however, a woman can “reject” a man although he has a “very good” immune system. If there were an absolute “value” for the goodness of an immune system, the characteristics for it would generally be desired by potential partners during reproduction in the course of evolution. However, this is not so and every immune system has strengths and weaknesses. Some people have immune systems that can more easily fight off SARS-CoV-2. However, we do not (yet) know what characteristics indicate this. The immune system contains many components. Among the many different cells of our immune system are the well-known “killer cells ” such as the T-lymphocytes. Certain proteins of our immune system function as messenger substances or serve to defend against pathogens. But the psyche also plays a role. Thus, the nervous system, hormonal system and immune system interact with our psyche. Depression is not just “bad thoughts and feelings”, but measurable metabolic changes in the brain. Depression causes us sleep problems and lack of sleep can lead to depression. This complexity of our immune system shows how vulnerable avoidably healthy people can be once the Achilles heel of their otherwise strong immune system is hit.
A special feature of corona is that, in addition to acute disease, there may also be cases of protracted symptomatology following infection. Colloquially, this is called long-covid, although the term is somewhat misleading. The acute covid symptoms have usually disappeared, yet affected individuals still suffer from post-covid infection symptoms. This post-covid syndrome manifests itself differently. According to the Robert Koch Institute RKI, common complaints include fatigue, exhaustion, shortness of breath, concentration and memory problems, sleep disturbances, muscle weakness and pain, and psychological problems such as depressive symptoms and anxiety. Furthermore, a worsening of the lung function as well as liver and kidney function restrictions, heart muscle inflammations and the new occurrence of diabetes mellitus can also be seen. The latter point in particular has also caught the attention of some scientists. Diabetes type 2 is not a primary problem of the pancreas like diabetes type 1. In the case of diabetes type 2, it becomes apparent that those affected are no longer able to activate their fat burning sufficiently, even under relatively low physical stress. A substantial part of the energy is obtained from the breakdown of sugar, producing lactate. Even healthy, high-performing athletes without pre-existing conditions have been hit hard by post-covid. Performance tests with affected athletes revealed frightening results. Their values resembled those of type 2 diabetics. Their fat burning was disturbed. Energy production from fatty acids takes place via the power plants in our cells, the mitochondria. Other symptoms of Long-Covid also point to a disturbance of mitochondrial function. The exhaustion that can accompany sufferers for months is similar to chronic fatigue syndrome (CFS), the exact cause of which has not yet been clarified. The list of possible triggers is long. Chronic fatigue syndrome CFS occurs in connection with various viral diseases such as three-day fever, herpes viruses, enteroviruses, influenza, but also after bacterial diseases triggered by intracellular bacteria such as Chlamydia, Legionella or Coxiellen. A persistent activation of the immune system can be detected, even if no viruses can be detected and the disease seems to have subsided. A disturbance of the mitochondrial function can be detected. Some viruses and bacteria use mitochondria to modify the cellular environment for their own purposes. Thus, such a change in mitochondrial metabolism could also occur in COVID-19 and be the cause of long-covid. Exercise increases the size of mitochondria, their number in cells and improves their functionality. However, it does not protect against long-covid. Just as each person has his or her individual genetic material in the form of DNA in his or her cells, mitochondria also have their own mDNA. This mitochondrial genetic material sometimes influences how susceptible mitochondria are to attack by viruses or bacteria. Although scientific studies show that coronavirus infection is less likely after vaccination and that COVID-19 is less severe on average, there are no consistent results to date regarding protection against long-covid.
What is the bottom line? Panic or fear of infection is certainly not the answer. “Respect” for COVID-19 as a serious disease is appropriate, however. As with protection from other infectious diseases, active and passive protection must be upheld. Of course, the rules of passive protection remain: sufficient sleep, a healthy diet and sufficient sport or exercise. There is no universal recipe, but only the individual optimum. Active protection against covid means e.g. keeping your distance and regularly ventilating closed rooms.
_________
Further literature:
Robert-Koch-Institut RKI: Gesundheitliche Langzeitfolgen (Stand: 19.4.2022) https://www.rki.de/SharedDocs/FAQ/NCOV2019/FAQ_Liste_Gesundheitliche_Langzeitfolgen.html
Robert-Koch-Institut RKI: Epidemiologischer Steckbrief zu SARS-CoV-2 und COVID-19 https://www.rki.de/DE/Content/InfAZ/N/Neuartiges_Coronavirus/Steckbrief.html;jsessionid=54F691D56B01586DD48412C3EFFD27F6.internet062?nn=13490888#doc13776792bodyText1
de Boer E, Petrache I, Goldstein NM, Olin JT, Keith RC, Modena B, Mohning MP, Yunt ZX, San-Millán I, Swigris JJ. Decreased Fatty Acid Oxidation and Altered Lactate Production during Exercise in Patients with Post-acute COVID-19 Syndrome. Am J Respir Crit Care Med. 2022 Jan 1;205(1):126-129. doi: 10.1164/rccm.202108-1903LE. PMID: 34665688; PMCID: PMC8865580.
Saima Ajaz, Mark J. McPhail, Keshav K. Singh, Salma Mujib, Francesca M. Trovato, Salvatore Napoli, and Kosh Agarwal. Mitochondrial metabolic manipulation by SARS-CoV-2 in peripheral blood mononuclear cells of patients with COVID-19. American Journal of Physiology-Cell Physiology 2021 320:1, C57-C65
Srinivasan K, Pandey AK, Livingston A, Venkatesh S. Roles of host mitochondria in the development of COVID-19 pathology: Could mitochondria be a potential therapeutic target? Mol Biomed. 2021 Nov 23;2:38. doi: 10.1186/s43556-021-00060-1. PMID: 34841263; PMCID: PMC8608434.
Thomas Boehm: Qualitätskontrolle im Immunsystem. (Steuerung der Partnerwahl). Max-Planck-Institut für Immunbiologie, Freiburg 2005, Beteiligte Abteilungen: Entwicklung des Immunsystems.
Ryback, Ralph, and Alfonso Eirin. “Mitochondria, a Missing Link in COVID-19 Heart Failure and Arrest?.” Frontiers in cardiovascular medicine vol. 8 830024. 17 Jan. 2022, doi:10.3389/fcvm.2021.830024
Ledford H. Do vaccines protect against long COVID? What the data say. Nature. 2021 Nov;599(7886):546-548. doi: 10.1038/d41586-021-03495-2. PMID: 34815580.
Fang H, Tu S, Sheng J, Shao A. Depression in sleep disturbance: A review on a bidirectional relationship, mechanisms and treatment. J Cell Mol Med. 2019 Apr;23(4):2324-2332. doi: 10.1111/jcmm.14170. Epub 2019 Feb 7. PMID: 30734486; PMCID: PMC6433686.
SCHEIBENBOGEN, C., H.-D. VOLK, P. GRABOWSKI, K. WITTKE, C. GIANNINI, B. HOFFMEISTER und L. HANITSCH: Chronisches Fatigue-Syndrom. Heutige Vorstellung zur Pathogenese, Diagnostik und Therapie tägl. prax. 55, 567–574 (2014) Hans Marseille Verlag GmbH München
