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1) Scientists have observed temporary suppression of B celldevelopment in bone marrow during infection with a number ofviruses, including hepatitis A, B, and C, influenza, and parvovirusB19.

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

Also, hypothesize why this sort of developmentsuppression is seen with viral infections, but not with bacterialinfections, even very severe bacterial bloodinfections.

(9 points, 3 per hypothesis)

Answer:

A Suppression of the immune system after contaminations oraggravation is a significant procedure that limits immune-mediatedpathogenesis and autoimmunity. A few components of immuneconcealment have gotten a lot of consideration in the previousthree decades. These incorporate components identified withsuppressive cytokines, and changing development factor (TGF)- β andinterleukin (IL)- 10, delivered by administrative cells, andinstruments identified with apoptosis mediated by death-ligand

The immune system contains a huge swath of cell types andeffectors specific to identify and demolish pathogenicmicroorganisms and the cells and tissues that harbor them. Withthis exceptionally lethal defensive capacity comes the requirementfor tight guidelines so that once the risk of disease has passed,the system can come back to relative quiet and further harm can bestayed away from. This guideline is mediated by subsets of cellsand immunosuppressive particles that are particular to effectivelystifle the immune reaction. In a perfect world, immune concealmentadjusts the ruinous powers of aggravation while permitting leewayof pathogenic irresistible operators.

General hypothesis why bacteria don’t factor the sameresponse

The bacteria do not have the necessary DNA/RNA controllingabilities as our usually attributed to the viruses. The viruseshave the ability to genetically alter the immunity of the victimthat they attack, therefore, their effects are long-lasting and areoften 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 totake control of the biological machinery of the host. In thisregard, it makes sense that their method of infecting isfundamentally different from those of bacterial infections. Thebacteria are complete organisms in of themselves, whereas virusesare just proteins or genetic material encased in some proteincovering (Laffin, 2001). This difference in their physiologyexplains why bacterial and viral infections are fundamentallydifferent in their approaches.

Third Hypothesis

The third hypothesis answers the given question, in light of adifferent perspective. Viral-bacterial co-existence has been knownto present for quite some time. Recently, it has been researchedextensively, to see if it has any medically useful implications(Almand, Moore, & Jaykus, 2017). But we can take such anexample, in order to see how bacteria and viruses are completelydifferent entities and how they work in different spheresaltogether. The viruses might even overtake the bacteria to get itsown way into the cells of the host. These types of interactionsshow us the difference in viral and bacterial mechanisms.