There are only a few basic ways to fight viruses. A vaccine can prime the immune system to attack them as soon as they invade the body. If a virus manages to establish itself, a doctor may be able to prescribe a drug to slow down its spread. And if all else fails, a doctor may quarantine a patient to head off an epidemic.
Now some scientists are exploring a fundamentally different strategy to fight viruses. They want to wipe them out by luring them to their destruction, like mice to mousetraps.Viruses invade a cell by latching onto certain proteins on its surface. Once attached, they can slip inside the cell and manipulate it into making new copies of themselves. But viruses cannot infect red blood cells. Unlike most other cells in the body, as red blood cells develop in bone marrow they lose their DNA. If a virus ends up inside a red blood cell, there are no genes it can hijack to replicate itself.
“It occurred to us that if a virus bound to a red blood cell, that was a dead end,” said Dr. Robert W. Finberg, a professor at the University of Massachusetts Medical School.
Dr. Finberg and his colleagues decided to turn red blood cells into virus traps. They would bait their traps with a surface protein called CAR. A virus called coxsackie virus B attaches to CAR, using it to invade cells in the pancreas. The new viruses produced by the pancreas stream out through the bloodstream, attaching to CAR proteins in the cells of other organs like the heart and the liver.
The researchers engineered mice to produce CAR on their red blood cells and then compared how they fared against coxsackie virus B compared with normal mice. In the engineered mice, viruses reached only 1 percent to 10 percent of the levels they reached in many organs in normal mice. The normal mice all died within a week of infection. The engineered mice tended to live longer, and after two weeks a third of them were still alive.
Dr. Finberg’s experiments show that virus traps have some promise, but they do not reveal exactly why they failed to eradicate the virus. “What is the threshold for these traps so that they will force the viruses into extinction?” asks Paul E. Turner, an evolutionary biologist at Yale. Dr. Turner and his colleagues are trying to find the answer, but instead of studying mice, they are studying bacteria.
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A mutant form of Pseudomonas grows a lot of extra hairs, which make it an attractive target for viruses. But it cannot retract its hairs, so the viruses cannot get inside it to replicate. Dr. Turner and his colleagues reasoned that these mutants might act as traps for phi-6 viruses, luring them into a dead end.
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Dr. Turner and his colleagues created a mathematical model to predict how phi-6 would fair if they mixed viral traps into a colony of normal Pseudomonas hosts. They predicted that the more virus traps the scientists added, the more the virus population would shrink. Above a threshold of traps, the viruses would not be able replace their lost numbers, and they would disappear completely.
To test the model, the scientists mixed normal bacteria with different levels of mutant traps and then infected them with viruses. After letting the viruses replicate, the scientists took a small sample to start a new colony. They discovered there was indeed a trap threshold above which the virus population could not survive. Above that threshold, the viruses disappeared by the time the scientists started the third round of colonies.
Dr. Turner and his colleagues reported their results this month in the journal Ecology Letters.
Now Dr. Turner and his colleagues are using what they have learned with bacteria to study HIV, the virus that causes AIDS. Normally, HIV infects immune cells called CD4 T cells. Dr. Turner’s team is building red blood cells studded with CD4 proteins on their surface, in the hope of building an HIV trap.
“Once we have those, we can test whether they truly attract HIV,” Dr. Turner said. “And then we can set up experiments like the ones we’ve done with bacteria.”
Source-Bio-Bio Technology
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