Paper Round
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1. What is the primary vector of eastern equine encephalitis (EEE)?
2. What is the best way to protect against EEE? Why?
3. Explain in detail how EEE has impacted the lives of individuals in the towns where it has spread.
4. What are the two phases of EEE?
5. Why were the tissue sections soaked to block endogenous peroxidases before incubation with antibodies?
6. What antibodies were used?
7. Why did they use both a primary and secondary antibody? What purpose do each serve?
8. What general tissue type does the virus spread to before reaching the CNS? What is the more specific tissue subtype?
9. Refer to Figure 2b. Why was IHC staining observed in macrophages, but ISH did not detect viral RNA?
10. Which parts of the CNS were most strongly affected by the virus?
11. Why does simultaneous presence of viral antigen and viral nucleic acids in a cell type indicate viral replication?
12. What is the molecular reason behind EEE causing neurological problems?
13. Give an example of a neurological issue EEE might cause. How?
14. Why is EEE becoming a public health concern?
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