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In response to viral infection, the immune systems of mice typically

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In response to viral infection, the immune systems of mice typically  [#permalink]

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In response to viral infection, the immune systems of mice typically produce antibodies that destroy the virus by binding to proteins on its surface. Mice infected with a herpesvirus generally develop keratitis, a degenerative disease affecting part of the eye. Since proteins on the surface of cells in this part of the eye closely resemble those on the herpesvirus surface, scientists hypothesize that these cases of keratitis are caused by antibodies to herpesvirus.

Which of the following, if true, gives the greatest additional support to the scientist's hypothesis?



(A) Other types of virus have surface proteins that closely resemble proteins found in various organs of mice.

(B) There are mice that are unable to form antibodies in response to herpes infections, and these mice contract herpes at roughly the same rate as other mice.

(C) Mice that are infected with a herpesvirus but do not develop keratitis produce as many antibodies as infected mice that do develop keratitis.

(D) There are mice that are unable to form antibodies in response to herpes infections, and these mice survive these infections without ever developing keratitis.

(E) Mice that have never been infected with a herpesvirus can sometimes develop keratitis.


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Originally posted by pb_india on 16 May 2005, 09:10.
Last edited by Bunuel on 27 Sep 2018, 00:14, edited 1 time in total.
Renamed the topic and edited the question.
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Re: QOTD: In response to viral infection, the immune systems of mice typic  [#permalink]

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New post 05 Feb 2018, 10:56
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Start with the scientists' hypothesis. We are told that mice infected with a herpesvirus generally develop keratitis. The hypothesis is that "these cases of keratitis (those in mice infected with herpesvirus) are caused by antibodies to herpesvirus".

Now that we've identified the hypothesis, let's look at how the scientists arrived at this hypothesis:

  • When mice are infected by a virus, their immune systems produce antibodies to fight the infection.
  • These antibodies are supposed to destroy the virus by binding to proteins on its surface.
  • So if a mouse is infected with herpesvirus, we would expect the mouse's immune system to produce antibodies that would bind to proteins on the virus's surface. Great!
  • Unfortunately, mice with herpesvirus generally develop keratitis, a degenerative disease affecting part of the eye. Interesting... why does that happen?
  • Well, proteins on the surface of cells in this part of the eye closely resemble those on the herpesvirus surface. Uh oh... maybe the antibodies that are supposed to bind to the herpesvirus proteins are ALSO binding to proteins in the eye, since those proteins closely resemble those of the virus.
  • So the antibodies are supposed to be attacking the virus, but, if the hypothesis is correct, then those antibodies are also attacking cells in the eye.

This hypothesis seems to make sense, but we need an answer choice that gives it the greatest additional support:

Quote:
A. Other types of virus have surface proteins that closely resemble proteins found in various organs of mice.

In order for this statement to support the hypothesis, we would need additional information. What happens when mice are infected with those other types of virus? Do the organs with similar proteins suffer any damage? If so, then the hypothesis would be supported. But without further evidence, choice (A) doesn't help. Eliminate (A).

Quote:
B. There are mice that are unable to form antibodies in response to herpes infections, and these mice contract herpes at roughly the same rate as other mice.

These poor mice won't be able to fight the herpesvirus. If these mice also did NOT develop keratitis once infected with the herpesvirus, then we would have some solid support for the hypothesis. Unfortunately, we are not given such information.

All we know is that the mice who can't fight the herpesvirus contract the virus at about the same rate as other mice. We aren't interested in herpesvirus contraction rates. We are interested in the cause of the keratitis that generally develops in the infected mice. Eliminate (B).

Quote:
C. Mice that are infected with a herpesvirus but do not develop keratitis produce as many antibodies as infected mice that do develop keratitis.

This statement probably weakens the hypothesis. The scientists argue that the keratitis is caused by the antibodies. If these mice produce the same levels of antibodies and the antibodies cause the keratitis, then why wouldn't those mice also develop keratitis? This suggests that the antibodies aren't actually causing the keratitis.

If infected mice that do not develop keratitis did NOT produce as many antibodies as infected mice that do develop keratitis, then we would have support for the hypothesis. But this is not what statement (C) says, so eliminate (C).

Quote:
D. There are mice that are unable to form antibodies in response to herpes infections, and these mice survive these infections without ever developing keratitis.

Ah ha! This is what we were looking for in choice (B). The mice are unable to form antibodies in response to herpes infections. These poor mice cannot fight the virus, but they also do not develop keratitis. No antibodies, no keratitis. This certainly supports the scientists' hypothesis, so hang on to (D).

Quote:
E. Mice that have never been infected with a herpesvirus can sometimes develop keratitis.

Notice that the hypothesis specifically refers to "THESE CASES of keratitis." Which cases? Those that develop in mice infected with herpesvirus. So the scientists are not trying to explain causes of ALL cases of keratitis. Instead, they are only trying to explain the cases that develop in mice infected with herpesvirus.

Choice (E) does suggest that there are other ways to develop keratitis (besides the way proposed by the scientists). If anything, this slightly weakens the hypothesis by implying that something else (besides the antibodies to herpesvirus) could be causing these cases of keratitis. At best, choice (E) is irrelevant. At worst, it weakens the hypothesis, so eliminate (E).

Choice (D) is the best answer.
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Re: In response to viral infection, the immune systems of mice typically  [#permalink]

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New post 06 Nov 2005, 21:55
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Antibodies kill both VIRUS and EYE.

No antibodies, no eye damage.

D. There are mice that are unable to form antibodies in response to herpes infections, and these mice survive these infections without ever developing keratitis.
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Re: In response to viral infection, the immune systems of mice typically  [#permalink]

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New post 24 Nov 2005, 01:56
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It should be D

conlclusion: these cases of keratitis are caused by antibodies to herpesvirus.

Premise1: Mice infected with a herpesvirus generally develop keratitis

Premise2: the immune systems of mice typically produce antibodies that destroy the virus by binding to proteins on its surface.

Premise3:proteins on the surface of cells in this part of the eye closely resemble those on the herpesvirus surface.

we need an evidence to strengthen the conclusion.
the evidence need to show that if a mouse cannot produce antibodies in respose to herpesvirus but did not develop keratitis, the conclusion will be further strengthen.

so D is the right choice.
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Re: In response to viral infection, the immune systems of mice typically  [#permalink]

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New post 01 Feb 2016, 19:28
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The correct answer is D.

When X is thought to cause Y, it's important to consider whether Y occurs even when X is absent: if it does not, that strengthens the notion that X is causing Y in those cases where they occur together (OG)
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Re: In response to viral infection, the immune systems of mice typically  [#permalink]

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New post 16 Dec 2016, 17:09
Dear all,

I have a different angle of view about this argument. I think the ones who select E may have the same thought as me. Could anyone give me a detailed explanation for my reasons below if you see it is flawed?

Based on the last sentence, the hypothesis of the scientists should be: (1) As the some eyes' cells are resemble to that of herpes, keratitis are mistakenly generated on those eyes' cell as a response of antibodies to herpes.
The hypothesis cannot be: (2) Keratitis are generated by antibodies to herpes.

If so, answer E strengthens (1) the best. It demonstrates keratitis can appear without herpes. It provides a signal for further studies that the antibodies mis-recognize eyes' cells as herpes in those cases.
Meanwhile answer D just strengthens (2). But I don't think (2) is a good interpretation of the scientists' hypothesis.
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Re: In response to viral infection, the immune systems of mice typically  [#permalink]

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New post 17 Dec 2016, 09:59
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nathalie1107 wrote:
Dear all,

I have a different angle of view about this argument. I think the ones who select E may have the same thought as me. Could anyone give me a detailed explanation for my reasons below if you see it is flawed?

Based on the last sentence, the hypothesis of the scientists should be: (1) As the some eyes' cells are resemble to that of herpes, keratitis are mistakenly generated on those eyes' cell as a response of antibodies to herpes.
The hypothesis cannot be: (2) Keratitis are generated by antibodies to herpes.

If so, answer E strengthens (1) the best. It demonstrates keratitis can appear without herpes. It provides a signal for further studies that the antibodies mis-recognize eyes' cells as herpes in those cases.
Meanwhile answer D just strengthens (2). But I don't think (2) is a good interpretation of the scientists' hypothesis.


Choice E doesn't strengthen the argument.

E. Mice that have never been infected with a herpesvirus can sometimes develop keratitis.

If choice E is true, then the argument may be wrong. If mice that have never been infected with a herpesvirus can sometimes develop keratitis, keratitis could be caused by other reasons rather than antibodies to herpesvirus. How could we know that keratitis is caused by those antibodies in case that the mice aren't even infected with herpesvirus?
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Re: In response to viral infection, the immune systems of mice typically  [#permalink]

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New post 13 Nov 2017, 21:15
I have a simple query. I understand the no cause no effect situation.
My understanding - Antibodies bind on proteins (found on antibodies' surface) to destroy viruses. Similar proteins are found on the surface of herpesvirus. Herpesvirus leads to keratitis. Thus Antibodies cause keratitis.
Now, when the function of the antibodies is to destroy the virus as given in the question, therefore, they are only reducing the chances of keratitis by fighting herpesvirus. Therefore, how can they cause keratitis? They lead to lower cases of keratitis.

Lets see it this way - More herpes more keratitis. Antibodies fight herpes. Thus, less chance of keratitis.

Kindly help...
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Re: In response to viral infection, the immune systems of mice typically  [#permalink]

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New post 14 Nov 2017, 03:58
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kingb wrote:
In response to viral infection, the immune systems of mice typically produce antibodies that destroy the virus by binding to proteins on its surface. Mice infected with a herpesvirus generally develop keratitis, a degenerative disease affecting part of the eye. Since proteins on the surface of cells in this part of the eye closely resemble those on the herpesvirus surface, scientists hypothesize that these cases of keratitis are caused by antibodies to herpesvirus.

Which of the following, if true, gives the greatest additional support to the scientists’ hypothesis?

A. Other types of virus have surface proteins that closely resemble proteins found in various organs of mice.
B. There are mice that are unable to form antibodies in response to herpes infections, and these mice contract herpes at roughly the same rate as other mice.
C. Mice that are infected with a herpesvirus but do not develop keratitis produce as many antibodies as infected mice that do develop keratitis.
D. There are mice that are unable to form antibodies in response to herpes infections, and these mice survive these infections without ever developing keratitis.
E. Mice that have never been infected with a herpesvirus can sometimes develop keratitis.


Nice question. Here goes my understanding in a dramatic and hopefully in a comprehensible way:

1. Virus attacks the mice.
2. The mice fights back using its soldiers(antibodies) to destroy the crew of enemy (proteins of the virus).
3. This time Herpesvirus attacked mice. Assume that herpesvirus is a strong enemy whose soldiers (proteins) coincidentally look like the people(proteins) on the surface of a part of mice eye.
4. The soldiers of mice(antibodies), unable to identify the difference, also attacked his own people ( proteins on that part of the eye) by binding with them and thus causing keratitis.

Scientists hypothesize that keratitis in such cases is caused by the soldiers (antibodies) of the mice that were sent to attack the virus. You are asked to support this.
option D says-
There are mice that did not send its soldiers(antibodies) to fight herpes and such mice did not develop keratitis after surviving the invasion by Herpes. - This clearly shows that Keratisis was caused by the soldiers (antibodies) of the mice in the earlier case when the mice had actually sent antibodies to fight herpes. When the mice sent no soldiers to fight, there was no keratitis.

Hope it brought Thor into your mind. (Bahubali for Indians) :)
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Re: In response to viral infection, the immune systems of mice typically  [#permalink]

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New post 16 Nov 2017, 13:54
Quote:
In response to viral infection, the immune systems of mice typically produce antibodies that destroy the virus by binding to proteins on its surface. Mice infected with a herpesvirus generally develop keratitis, a degenerative disease affecting part of the eye. Since proteins on the surface of cells in this part of the eye closely resemble those on the herpesvirus surface, scientists hypothesize that these cases of keratitis are caused by antibodies to herpesvirus.

Which of the following, if true, gives the greatest additional support to the scientists’ hypothesis?

A. Other types of virus have surface proteins that closely resemble proteins found in various organs of mice.
B. There are mice that are unable to form antibodies in response to herpes infections, and these mice contract herpes at roughly the same rate as other mice.
C. Mice that are infected with a herpesvirus but do not develop keratitis produce as many antibodies as infected mice that do develop keratitis.
D. There are mice that are unable to form antibodies in response to herpes infections, and these mice survive these infections without ever developing keratitis.
E. Mice that have never been infected with a herpesvirus can sometimes develop keratitis.

talismaaniac wrote:
I have a simple query. I understand the no cause no effect situation.
My understanding - Antibodies bind on proteins (found on antibodies' surface) to destroy viruses. Similar proteins are found on the surface of herpesvirus. Herpesvirus leads to keratitis. Thus Antibodies cause keratitis.
Now, when the function of the antibodies is to destroy the virus as given in the question, therefore, they are only reducing the chances of keratitis by fighting herpesvirus. Therefore, how can they cause keratitis? They lead to lower cases of keratitis.

Lets see it this way - More herpes more keratitis. Antibodies fight herpes. Thus, less chance of keratitis.

Kindly help...

The first red flag is that this analysis contradicts information given in the passage: "Mice infected with a herpesvirus generally develop keratitis." So we KNOW that mice infected with herpesvirus generally develop keratitis, and we have to support a hypothesis explaining WHY that happens.

Let's think about the cycle:

  • A mouse gets infected with herpesvirus.
  • Antibodies are produced to fight the infection.
  • WHILE the antibodies are fighting the infection, they are also destroying the cells in the eye (CAUSING keratitis).
  • MAYBE the antibodies successfully eliminate the herpesvirus (or maybe not... we don't know whether the antibodies will win the fight). In that case, the antibodies would no longer be produced. Regardless, the keratitis has ALREADY developed by that point. Maybe the keratitis would then go away too, but we don't know (or care) about that. All that matters is that the antibodies caused the keratitis in the first place.

I hope that helps!
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