1. Gene Mutation and Its Pathogenesis (1)/基因突变及其致病性机理
Step 1. The host cells with apparent antibiotics of the same genetic strains are identified during the invasive simulation of a specific bacteria strain (Sample 1);
Step 2. The same bacteria strain is cultivated during radiation, leading to gene mutation (Sample-M) detected by FISH using transmission electron microscopy, as described by other articles of this journal;
Step 3. Invasive simulation by Sample-M targeting the host cells with apparent antibiotics, identified in step 1, is conducted.
Step 4. The disease infection by Sample-M is observed.
Step 5. The bacteria cell division rate (quantify of cells / cultivation time) is observed and compared between cells with gene mutation and cells without gene mutation.
Hypothesis:
The bacteria with gene mutation leads to altered bio-signal which can be difficultly perceived by host cells with specific immunology against their parental bacteria (sample 1), and the infection rate by sample-M is higher than sample 1.
Discussion:
Gene mutation[1], leads to cells with faster cell division rate (DNA or RNA replication rate in virus) than their parental cells (or virus). This explains the sharply epidemic infection caused by bacteria or virus with gene mutation (such as AIV).
2. Gene Mutation and Its Pathogenesis (2)/基因突变及其致病性机理
As discussed previously, gene mutation virus leads to ‘altered’ or distortive bio-signal, which is hardly identified by host cells. Consequently, this section presents a novel method to train the host cells’ ‘memory’ in terms of identifying the invasive virus family with gene mutation.
Step 1. The virus classification on the basis of FISH technology is conducted, which is the morphological markers of genome, as described by other article of this journal.
Step 2. The similar virus families (mild sample) to the pathogenetic virus family with gene mutation (pathogenetic sample) is identified in step 1 on the basis of morphological markers of genome; And the similar virus is less pathogenetic virus (such as becoming dormant in host cells after puncture), which is consequently called as ‘mild’ samples, but is classified into the similar virus family with closed genetic distance to the pathogenetic virus family of gene mutated according to the morphological markers of genome;
Step 3. The specific zymograms of host cells with specific immunology against invasive gene mutation virus is identified, as described above;
Step 4. The biophysical ‘training’ of host cells, described in other article of this journal, is conducted with indication of zymograms in step 3, during the invasive simulation of ‘mild’ samples;
Step 5. This method strengthens the immunology against this gene mutation virus family through similarity invasion simulation.
Discussion:
The pathogenicity of virus invasion in this journal is explained by two process: one is to puncture the host cell membrane, and the other is the virus metabolism in host cells after puncture. Consequently, host cells identify the bio-signal of invasive virus by two stages correspondingly: the first stage is the puncture process, and the morphological bio-signal of invasive virus genome is the main bio-signal (this bio-signal by gene mutation virus is similar to other virus families, rather than its parental virus family); the second stage is the pathogenic metabolism of invasive virus after puncture, and the main bio-signal depends on the gene expression of virus genome (this bio-signal by gene mutation virus is similar to their parental virus). This two process further explains the altered or distortive bio-signal caused by gene mutation virus. This training procedure helps host cells identify the morphological signals of gene mutated virus.
Please note:
If the specific zymograms of host cells with specific immunology against invasive
gene mutation virus is NOT identified by the method described above; then the specific zymograms of host cells with specific immunology against invasive gene mutation virus has to be identified by adjusting the biophysical parameters during invasion simulation of gene mutation virus in lab, as described in other article of this journal. However, it is expected that the specific zymograms of host cells with specific immunology against invasive gene mutation virus is closer to the specific immunology against their parental virus.
However, for the invasive virus (or bacteria) with dormant characters, it is further discussed in other article of this journal.
3. Gene modification of microbial vaccine/微生物疫苗的基因修改技术
Although the gene mutated bacteria or virus has been already commonly used in the production of microbial vaccine in the past [2], the biophysical simulation by adjusting different frequency or intensity of electromagnetic waves, as discussed in my article of this journal, points out a new way of cultivation of microbial vaccine below:
Step 1. Vaccine microbes are cultivated during simulation of electromagnetic wave conditions;
Step 2. Different frequency of electromagnetic wave (or different wavelength) are simulated, and labeled as F1, F2, ..., Fn;
Step 3. Under each simulated frequency of electromagnetic wave, different intensities of electromagnetic wave are simulated, and labeled as I1, I2, ..., and In; Then in total N×N bio-samples are cultivated under biophysical simulation;
Step 4. After sufficient reproduction process, gene mutated vaccine microbes is identified by FISH technology;
Step 5. Finally, this gene-mutated microbial vaccine is inoculated into host cells, and then pathogen invasion simulation is conducted for testing the effectiveness of vaccine.
For the pathogenic bacteria or virus, suitable/accurate gene mutation may reduce the pathogenicity of these pathogens against host cells, but keeps both metabolic and ecological traits which are similar to their parental and pathogenic bacteria or virus. The new strains engineered by this gene modification provides better way of microbial vaccine production than trans-gene microbes. The reasons of this gene mutated technology for gene modification is summarized as below:
The advantages of inoculation of microbial vaccine is not just to cultivate the host cell’s memory in terms of immunology against their parental and pathogenic microbes, but also for the microbial vaccine to be dominant in host environment by competing with their parental and pathogenic microbes’ invasion, because the microbial vaccine compete for the same ‘ecological niche’ with their parental and pathogenic microbes in host cell environment and shows symbiosis with host cells before their parental and pathogenic microbes invade. For example, if the vaccine microbe already ‘occupies’ a host cell with symbiosis, the metabolic substances of symbiotic vaccine microbe, as a kind of bio-signals, eliminates the re-invasion by their parental and pathogenic microbes. This is a common nature of host-invasion interactions. Secondly, the microbial vaccine engineered and created by gene mutation leads to higher cell mutation rate than its parental pathogens so that eliminates the reproduction of parental pathogens which is identified as more pathogenesis against host cell. Consequently, the metabolites of symbiotic vaccine microbe itself are just a kind of effective antibiotics against similar genetic strains, and this competition- exclusion rhythm between different strains of microbes also partly explains that the symbiosis of rhizobium in Leguminosae species leads to antibiotics for biomedicine discussed in other article of this journal.
In this case, the host cells inoculated by symbiotic microbial vaccine can be utilized for exchange transfusion as remediation method, and the symbiosis would not need persist long-termly after cure, because the symbiosis of microbial vaccine may negatively influence the health due to competition for nutrition as well after cure.
Conclusion
Gene mutation is the natural adaptive process of cell evolution in response to environment changes. Moderate gene mutation can be utilized as gene engineering instead of clone Tech due to more nature!