Matsumoto conducted thorough eye examinations of 45 Chagas disease patients with heart problems. She found that under bright conditions, the Chagas patients performed comparably to 50 healthy control individuals. But in the dark, 37 of 45 (82 percent) Chagas patients had trouble seeing with at least one eye, and 19 of 45 (42 percent) had trouble with both eyes. Matsumoto then approached Paveto, and both contacted Levin, whose laboratory was well-stocked with antibodies from Chagas patients and who had already developed the tests needed to study molecular mimicry.
In previous research, Levin and colleagues showed that the immune systems of patients infected by T. cruzi generate antibodies that attack the parasite but also cause damage to heart cells. Levin suspected "molecular mimicry" as the cause of the misguided attack. Molecular mimicry occurs when a molecule that is part of an infectious agent resembles a molecule native to the body. Eventually, the immune system begins to mistake the native molecule for the invader. Levin's investigations revealed that an intra-cellular T. cruzi protein resembles the beta1-adrenergic receptor on the surface of heart cells, a finding that helped explain why Chagas patients develop certain heart problems.
Now, it turns out, molecular mimicry can also upset the delicate machinery inside retinal cells. Levin and his team found that antibodies geared to attack T. cruzi also block rhodopsin, a molecule that converts light into electrical impulses sent to the brain. "Rhodopsin takes light and transforms it ?that's its function," said Levin.
To demonstrate molecular mimicry in the retina, Paveto extracted rhodopsin from cow's eyes. Through a series of tests, the team showed that cow rhodopsin, which is similar to the human
Source:Howard Hughes Medical Institute