Do the new data support the hypothesis that the parasite switched surface glycoproteins once the host immune system responded to the original glycoprotein?

It depends on your data, BUT read explanation

Explanation:

There are two ways to see this question and both are related to the fact that there is a parasite that could change surface glycoproteins at its will. Now, the question is when, and that when is once the host immune system attack it. If you perform an experiment where you have surface glycoproteins of the parasite without any disturb, a situation where the parasite has to respond and a control for this situation ( in this case an attack of the immune system), and the surface glycoproteins after the parasite deals with the situation you can infer some things.

First, if you compare the second surface glycoproteins in both experiments (with immune system attack and with control situation), and you see they are very different yo could say the immune system could have some influence on surface glycoproteins.

Now, you cannot infer completely, you have to see if there is a difference between the initial state of the surface glycoproteins and the final state of them after the immune system attack. There you can see if there is any difference on surface glycoproteins.

BUT you have to see if the comparison between the initial state of the surface glycoproteins and the final state of them after the control situation also changes and in what matter to see if is really the immune system the only one who affects surface glycoproteins.

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the answer is; comparing the frequency of collisions with and without the device

this makes the anti-collision system an independent variable and the collisions a dependent variable. if there are fewer collisions with an anti-collision system that without, then it can be stated that the system is a success. essentially, collisions under an anti-collision system are compared with the frequency of collisions by cars with the human drivers.