Because the covid-19 virus is amazingly mutating, we urgently need a lot of articles in this area. In light of recent events, we have been writing an article on the mutagenicity of the covid-19 virus and treatment with morphine. The covid-19 virus is an exception due to its non-segmented genome, its mutagenicity. Also in this article morphine is a suitable drug because it neutralizes most of the symptoms of the covid-19 virus. Morphine increases immunity against the virus due to the presence of mu3 receptors on the surface of immune cells. Morphine also counteracts symptoms such as shortness of breath, pain, and even diarrhea. Diarrhea has been reported in cases of the covid-19 virus.

Background: Clostridioides difficile infection (CDI) has been primarily associated with the toxin B (TcdB), which can activate the intestinal immune system and lead to pathological damage. Even though the biological functions of intestine epithelial cell- derived extracellular vesicles (I-Evs) have been well documented, the role of I-Evs in the process of CDI is still unknown. Results: We isolated I-Evs ranging from 100–200 nm in mean diameter, with a density of 1.09-1.17 g/mL. These I-Evs expressed the extracellular vesicle-associated specific surface markers, CD63 and TSG101. In vitro, 50 µg I-Evs decreased the expression of IL-6, TNF- ß, IL-1ß, and IL-22 in MC38 induced by 0.8 ng/mL C. difficile TcdB, and increased expression of TGF- ß1. In vivo, I-Evs also promoted regulatory T cell induction, which improved inflammation of mice up to 80% relative to C. difficile TcdB infected mice, depending on the TGF- ß1 signal pathway. Conclusion: Our study firstly demonstrated that I-Evs originated from intestine epithelial cells is potentially a novel treatment endogenous candidate to effectively reduce the local infection induced by C. difficile TcdB.

The world over artificial respiration is employed as one of the intensive care treatment measures in severe cases of COVID-19 because of the significant respiratory distress patients develop. Nevertheless, the outcome is poor. Lethality varies from country to country and clinic to clinic between 50% and 90%. So the question arises as to whether the use of oxygen can be a risk factor in the treatment of acute inflammatory diseases in general and of COVID-19 in particular. Oxidative stress is the first and oldest step of cellular defense and starts before the activation of the immune system. This leads to an increase of intracellular oxygen in the mitochondria, followed by an elevated electron flow and the formation of superoxide as well as other reactive oxygen species and reactive nitrogen species. Superoxide reacts with nitric oxide, which is always present in inflammation, forming peroxynitrite, the strongest inducer of oxidative stress. This step induces the activation of nuclear factor kB, followed by the production of proinflammatory cytokines. The elevated levels of inducible nitric oxide synthase keep this cycle running. High amounts of superoxide have to be compensated and catabolized by manganese-superoxide dismutase 2 into hydrogen peroxide and in a second step by catalase into water. When using artificial respiration, these steps are accelerated considerably in the inflamed tissue of the lung, leading to a significant increase of the electron flow as well as an elevation of superoxide, oxidative stress, and water. As SARS-CoV-2 generally induces the production of proteins (and not only those necessary for viral reproduction), the water will remain in the tissue, causing edema and thus a wet lung syndrome associated with a growing oxygen diffusion distance to red blood cells. Ultimately, patients do not suffocate in spite of, but because of, the presence of high levels of oxygen. The limited number of patients who survive this deleterious treatment describe it as having had a sensation of drowning. The reasons will be discussed.