Scientists seek HIV vaccine using monkey model_美文

Scientists seek HIV vaccine using monkey model

“These SIVs that were attenuated, that prevented subsequent infection with the full pathogenic virus, still could cause disease. And people found that if you attenuated them anymore, they didn’t work anymore,” he said.

Picker and his colleagues wanted to understand why the weakened virus offered protection from infection. But at the same time, they needed to prevent it from itself causing disease. They found the answer has to do with T cells, which attack viruses. The weakened, but persistent virus vaccines somehow caused T cells to be ever vigilant. But if the virus was weakened too much, the T cells were not triggered to attack. They concluded that an “effective HIV vaccine might have to persist in the body.”

Picker said, “The unique aspect of the live attenuated vaccines that seem to work was that they were persistent. They weren’t cleared by the host immune system, but they were able to stick around. Of course in the case of HIV/SIV that’s a bad thing, because eventually those live attenuated vaccines would gain strength and cause disease. But probably the fundamental reason, at least what I hypothesized, that they would be able to elicit protection was because of that persistence.”

So, they looked for another persistent virus that was not pathogenic, which might generate T cell immune response.

“The virus that we selected was a virus called cytomegalovirus (CMV), which is actually a virus from a different family of viruses altogether, but it’s one that most people in the world are infected with. But it’s unique in that you can re-infect these people with a virus that now has within its genes HIV genes and then the body would make immune responses to those HIV genes,” he said.