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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 the 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 the herpesvirus.
Which of the following, if true, most helps to support the scientists' reasoning?
| Text from Passage | Analysis |
| In response to viral infection, the immune systems of mice typically produce antibodies that destroy the virus by binding to proteins on its surface. |
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| Mice infected with the herpesvirus generally develop keratitis, a degenerative disease affecting part of the eye. |
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| 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 the herpesvirus. |
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The argument starts with how mouse immune systems normally work, then presents a specific problem (herpes causing eye disease), and finally offers a scientific explanation that connects the two through protein similarity.
Scientists believe that keratitis in herpes-infected mice is caused by antibodies that mistake eye cell proteins for virus proteins and attack the eye.
The hypothesis relies on mistaken identity - since eye proteins look like virus proteins, the antibodies that are supposed to fight the virus accidentally attack the eye instead, causing the disease.
Strengthen - We need evidence that increases belief in the scientists' hypothesis that anti-herpesvirus antibodies are causing keratitis through molecular mimicry
The hypothesis makes a specific causal claim about antibodies targeting both herpesvirus proteins AND similar eye cell proteins, leading to eye damage
Look for evidence that confirms the proposed mechanism works as described. We need information showing that the antibody cross-reaction actually happens, that the similarity between proteins is functionally relevant, or that the proposed causal pathway operates in practice
This tells us that other viruses also have surface proteins similar to mouse organs. However, this doesn't help support the specific hypothesis about herpesvirus antibodies causing keratitis. We're not concerned with other viruses - we need evidence specifically about the herpesvirus-keratitis connection. This is irrelevant information that neither strengthens nor weakens the scientists' reasoning.
This suggests that antibody production levels are the same whether mice develop keratitis or not. This actually works against the hypothesis rather than supporting it. If the same amount of antibodies are produced but some mice don't get keratitis, it suggests that antibody quantity isn't the determining factor, which weakens the proposed mechanism.
This provides a perfect controlled experiment that strongly supports the hypothesis. When the herpesvirus has different surface proteins (removing the similarity to eye cell proteins), the mice don't develop keratitis. This directly confirms that the protein similarity is the crucial factor causing the antibody cross-reaction and subsequent eye damage, exactly as the scientists hypothesized.
This tells us that mice can sometimes get keratitis without ever having herpes. This suggests there are other causes of keratitis besides herpesvirus antibodies, which weakens rather than strengthens the scientists' specific hypothesis about herpesvirus-induced keratitis.
This describes mice that can't make antibodies but still get infected with herpes at normal rates. This information is about infection rates, not about keratitis development. Since we don't know whether these antibody-deficient mice develop keratitis or not, this doesn't help us evaluate the scientists' hypothesis about antibody-mediated eye damage.