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AIDS vaccine research offers new insights on survival

e replicating.

"While this vaccine approach cannot actually prevent an infection, it can tamp down the AIDS virus, resulting in the development of a much milder form of the disease in vaccinated monkeys that subsequently become infected," he adds. "We know this because the loss of helper T-cells is much less dramatic, the amount of virus replication is much less and the infected animals go on to live longer."

Until now, the success or failure of this type of T-cell vaccine has been determined by measures of virus levels and total counts of CD4+ helper T-cells, which are indicative of infection control in monkeys infected with the AIDS virus.

As in previous studies, this new research found that among monkeys infected with the simian immunodeficiency virus (SIV) -- 24 of which were vaccinated and six of which were not -- the immunity generated by the vaccine controlled infection for approximately 100 days before levels of virus increased and T-cell counts dropped.

But instead of ending the experiment at this point -- assuming that the vaccine conferred protection for only 100 days -- Letvin and his VRC colleagues decided to follow the monkeys for an additional 750 days, a total of 850 days or nearly three years.

"We found that the vaccinated monkeys lived significantly longer than the unvaccinated monkeys following infection and that levels of memory CD4+ cells remained significantly higher in the vaccinated animals," explains Letvin. "This suggests that the initial protection that the vaccine provides in the early weeks following infection gives the monkeys a long-term survival advantage, and that this protection is associated with a significantly higher level of memory CD4+ cells."

In another aspect of the study, Letvin and his colleagues at the VRC found that measurements of a subset of memory CD4+ T cells -- central memory CD4+ T cells -- could help predict how the vaccinated monkeys would fare over the long run. <
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Source:Harvard Medical School


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