Updated today 08/26/2024 Spanish time 11:11 PM
When viruses infect cells, they tiny modify the DNA of chromosomes.
When the brain and intelligence correct this tiny fault in the DNA of chromosomes, the virus that created the damage is again attracted by a magnetic field of its genes to the cells.
Depending on the type of virus, not all move through the same magnetic fields and depending on the cells and the tissue, the leukocyte reproduces with certain characteristics.
The leukocyte has a useful life and its DNA is designed to create magnetic fields between leukocyte genes and virus genes and that attracts a type of virus specified in each leukocyte.
All leukocytes in the blood can be differentiated by some genes in their DNA, depending on the species of virus or bacteria that they attack.
It can also be said that the useful life of the leukocyte is when it runs out of virus food specified in its DNA and dies from malnutrition.
It may also happen that leukocytes attack cells, as is the case with psoriasis. This is because tumor cells or giant cells are inhabited by microorganisms such as viruses that do not leave the cells and hide inside the cells. In this case, it is necessary to reduce cellular inflammation and the resources that make it possible for this microorganism to survive inside the cell, modifying the DNA of chromosomes, genes or proteins and causing it to go out into the bloodstream and the leukocyte has the protein or gene that magnetically attracts the microorganism, in this case the virus that causes the psoriasis tumor.
In this case, where leukocytes attack cells, it may happen that a virus infects the possible cell and by gene attraction, the leukocyte attacks the cell by attraction of a gene of the cell or of the virus that is inside the cell.
The easiest thing in this case may be to eliminate the gene from the tumor cells that deadly attract the leukocyte, but the virus could create it again.
A possible solution to this problem is to reproduce a gene in the tumor cells, which causes the exit door of the virus, the opposite effect to the gene implanted by the virus that causes the entry and its stay, a gene that could be useful for the leukocyte to attract the virus.
This magnetic field of the genes, can hide secrets such as breathing and heart rate, the cell needing two genes, one for low atmospheric pressures and another for high atmospheric pressures.
Tumor or giant cells can orbit outside the optimal atmospheric measurements, causing difficulty in breathing or these two genes for the virus to malfunction and the leukocyte could only contain one gene for high pressures, which is when the viruses descend from the atmosphere or pass into the blood.
Through gases or magnetic fields of genes, a high pressure gene in this case is the entry door of the virus, such as the flu. That is why every time giant cells are reduced, through modifications of chromosome DNA, it causes the cells to orbit correctly and the viruses to activate.
In the case of the leukocyte that attacks the tumor cells, it could happen that the gene for the magnetic field exit gate or the gene for low atmospheric pressure and respiratory rate of the cell is not formed in the tumor cell or is not working properly.
It is a bit complicated, but for the gene to form, which forms the low pressure or storm in the atmosphere and for the virus to leave the cell and not let the gas that enters through the genes be lost, the tumor cell has to form a molecule with its digestive system, which makes the gas of the gene that formed the virus stable and this molecule that forms the cell, is the key that closes the other gene and forms low pressures or storms, making the cellular radiation descend from the atmosphere and the formed molecule asphyxiates until it opens the other high pressure gene and that is when the tumor cell begins to breathe through the high pressure gene and the faster the cell does this operation, the tumor tissue could improve, but it must be taken into account that, the change in rhythm of these tumor cells need a modification in the DNA of the chromosome that adapts to the heart rate.
