aThe upper two panel fiq tce of mice orally inoculated with norovirus, then trea
ID: 200854 • Letter: A
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aThe upper two panel fiq tce of mice orally inoculated with norovirus, then treated 21 days later with a single u (labeled D) shows the results of an experiment with Cor IF or saline (PBS). Shedding of virus was monitored for 35 days post-injection dose The lower ection in 3 tes of mice. Are the results shown in the upper and lower figures single pan el figure shows the level of microorganism as a function of the duration of S or NO? Explain your answer. (6 pts) Control PBS Ragt PBS 6 5 2 20 22 23 24 30 40 50 60 20 21 22 23 24 30 40 50 PBS or IFN PBS or IFN). Mouse (human) lacking innate immunity Mouse (human) lacking adaptive immunity Normal mice and humans Duration of infectionExplanation / Answer
V(D)J recombination activation gene RAG-1 is involved in the V(D)J recombination reaction of immunoglobulin and T cell receptor genes. RAG-1-deficient mice have small lymphoid organs lacking mature B and T lymphocytes and have an immune system similar to non leaky SCID mice. These mice lack adaptive immunity.
In panels D, the number of noviruses in the stool of control and Rag-/- mice treated with PBS was the same at all time points. Hence, PBS had no effect in reducing viral load in chronic novirus infection. However, treatment of both types of mice infected with noviruses, with interferon lambda (IFNl) results in reduction of noviruses from stool of the organism. Days 21-35 represent a chronic stage of infection.
This is surprising as Rag-/- mice lack adaptive immunity. Adaptive immunity reduces the number of pathogens in chronic infection by producing specific T and B cells (lower panel). The lower panel indicates that in absence of adaptive immunity (mouse lacking adaptive immunity) are not capable of reducing pathogen number in chronic infection. The number of microorganisms remains constant after longer duration of time (chronic infection). In normal mice with functional adaptive immunity, the pathogen load will decrease when adaptive immunity is stimulated in chronic infection.
IFNls exert antiviral effects by inducing expression of IFN-stimulated genes. They cause macrophage and dendritic cell polarization. This effect is required to prime helper T-cell activation and proliferation. IFNl are known to increase Th1- and reduce Th2-cytokines. Hence, theoretically, IFNl should not be able to reduce the novirus numbers in the stool sample of Rag-/- mice due to lack of ability to activate T cells, which would kill the virus.
Hence, the results shown in upper D panel and lower panel do not match.
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