Question

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1) Scientists have observed temporary suppression of B cell development in bone marrow during infection with a number of viruses, including hepatitis A, B, and C, influenza, and parvovirus B19.

Given what you know about B cell development, provide 2 hypotheses to explain this phenomenon, one focusing on why the host might suppress B cell development, and the other focusing on why the virus might do this.  

Also, hypothesize why this sort of development suppression is seen with viral infections, but not with bacterial infections, even very severe bacterial blood infections.

(9 points, 3 per hypothesis)

Answer:

A Suppression of the immune system after contaminations or aggravation is a significant procedure that limits immune-mediated pathogenesis and autoimmunity. A few components of immune concealment have gotten a lot of consideration in the previous three decades. These incorporate components identified with suppressive cytokines, and changing development factor (TGF)- β and interleukin (IL)- 10, delivered by administrative cells, and instruments identified with apoptosis mediated by death-ligand

The immune system contains a huge swath of cell types and effectors specific to identify and demolish pathogenic microorganisms and the cells and tissues that harbor them. With this exceptionally lethal defensive capacity comes the requirement for tight guidelines so that once the risk of disease has passed, the system can come back to relative quiet and further harm can be stayed away from. This guideline is mediated by subsets of cells and immunosuppressive particles that are particular to effectively stifle the immune reaction. In a perfect world, immune concealment adjusts the ruinous powers of aggravation while permitting leeway of pathogenic irresistible operators.

General hypothesis why bacteria don’t factor the same response

The bacteria do not have the necessary DNA/RNA controlling abilities as our usually attributed to the viruses. The viruses have the ability to genetically alter the immunity of the victim that they attack, therefore, their effects are long-lasting and are often shown by the triggered immunodeficiency responses (Lundy, 2012). Bacterial infections do not have these characteristics.

Second Hypothesis

Viruses are obligate intracellular parasites. They are wired to take control of the biological machinery of the host. In this regard, it makes sense that their method of infecting is fundamentally different from those of bacterial infections. The bacteria are complete organisms in of themselves, whereas viruses are just proteins or genetic material encased in some protein covering (Laffin, 2001). This difference in their physiology explains why bacterial and viral infections are fundamentally different in their approaches.

Third Hypothesis

The third hypothesis answers the given question, in light of a different perspective. Viral-bacterial co-existence has been known to present for quite some time. Recently, it has been researched extensively, to see if it has any medically useful implications (Almand, Moore, & Jaykus, 2017). But we can take such an example, in order to see how bacteria and viruses are completely different entities and how they work in different spheres altogether. The viruses might even overtake the bacteria to get its own way into the cells of the host. These types of interactions show us the difference in viral and bacterial mechanisms.

Answer 1

A Suppression of the immune system after contaminations or aggravation is a significant procedure that limits immune-mediated pathogenesis and autoimmunity. A few components of immune concealment have gotten a lot of consideration in the previous three decades. These incorporate components identified with suppressive cytokines, and changing development factor (TGF)- β and interleukin (IL)- 10, delivered by administrative cells, and instruments identified with apoptosis mediated by death-ligand

The immune system contains a huge swath of cell types and effectors specific to identify and demolish pathogenic microorganisms and the cells and tissues that harbor them. With this exceptionally lethal defensive capacity comes the requirement for tight guidelines so that once the risk of disease has passed, the system can come back to relative quiet and further harm can be stayed away from. This guideline is mediated by subsets of cells and immunosuppressive particles that are particular to effectively stifle the immune reaction. In a perfect world, immune concealment adjusts the ruinous powers of aggravation while permitting leeway of pathogenic irresistible operators.

General hypothesis why bacteria don’t factor the same response

The bacteria do not have the necessary DNA/RNA controlling abilities as our usually attributed to the viruses. The viruses have the ability to genetically alter the immunity of the victim that they attack, therefore, their effects are long-lasting and are often shown by the triggered immunodeficiency responses (Lundy, 2012). Bacterial infections do not have these characteristics. Bacteria do not take over host's machinery.

Second Hypothesis

Viruses are obligate intracellular parasites. They are wired to take control of the biological machinery of the host. In this regard, it makes sense that their method of infecting is fundamentally different from those of bacterial infections. The bacteria are complete organisms in of themselves, whereas viruses are just proteins or genetic material encased in some protein covering (Laffin, 2001). This difference in their physiology explains why bacterial and viral infections are fundamentally different in their approaches.

Third Hypothesis

The third hypothesis answers the given question, in light of a different perspective. Viral-bacterial co-existence has been known to present for quite some time. Recently, it has been researched extensively, to see if it has any medically useful implications (Almand, Moore, & Jaykus, 2017). But we can take such an example, in order to see how bacteria and viruses are completely different entities and how they work in different spheres altogether. The viruses might even overtake the bacteria to get its own way into the cells of the host. These types of interactions show us the difference in viral and bacterial mechanisms.