1. Restate the tradeoff hypothesis in your own words. How does it differ from th

Question

1. Restate the tradeoff hypothesis in your own words. How does it differ from the avirulence hypothesis?

2. How can we use evolution of cooperation theories to explain Helicobacter evolution?

3. What factors affect the way virulence of a pathogen evolves? How could you manipulate your pathogen's environment to maintain maximum virulence?

4. What are the relative roles of point mutations, horizontal gene transfer, phage, and genome rearrangements in the evolution of pathogens?

5. What is R? How does R evolve when a pathogen switches to a new host? If R is less than 1, will the pathogen survive? Greater than 1?

6. for your pathogen for world domination: How could you design your pathogen to avoid the tradeoff between virulence and transmission?  

Explanation / Answer

The 'trade-off' hypothesis states that parasitic transmission of a pathogen into a host will definitely lead to an increase and effect of the pathogen that has been transmitted.

Avirulence hypothesis states that there are specific genes in living organisms which can 'recognise' the pathogen with the help of a pathogen avirulence determinant encoded by an avirulence gene. This triggers the immune system.

2] Coperation theories in evolution suggest that unrelated individuals cooperate for their mutial benefit and evolve

to occupy their niche in the ecosystem.

Helicobacter is a genus of Gram -negative bacteria. It has a characteristic helical shape. This genus contains about 35 species of which H.pylori is the most common one which occupies the upper gastrointestinal tract and liver of mammals and some birds.

H.pylori commonly cause peptic ulcers, gastritis and even stomach cancer in humans. They have evolved to survive in the highly acidic surroundings in the stomach by producing large quantities of an enzyme called urease. This enzyme raises the pH in the stomach fron 2 to as high as about 6 or even 7. Research shows that in the course of evolution , helicobacter aquires Hpn and Hpn-2 proteins which help it to control the secretion of urease which is crucial for the survival of the helicobacter in the strongly acidic medium of the stomach.

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