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Last Updated: Oct 11, 2012 - 10:22:56 PM
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Latest Research : Infectious Diseases : AIDS

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HIV-I knocks out immune system faster than thought

Jul 19, 2008 - 1:37:35 PM
In measuring the levels of four products of CD4 T cell death during this period in these samples, they were able to track and establish a timetable of the virus's destructive path.

 
[RxPG] Washington, July 19 - The HIV-I virus virtually knocks out the immune system much faster than previously thought.


The window of opportunity for successful intervention may be only a matter of days - not weeks - after transmission, according to scientists of Duke University Medical Centre.

The finding may compound the problem of the challenge of designing an effective HIV/AIDS vaccine. But it has also yielded a blueprint for what a successful vaccine should look like, and moreover, when such a vaccine would need to work.

Until now, scientists believed that the window of opportunity for intervention lasted three to four weeks between transmission and the development of an established pool of infected CD4 T cells. HIV-1 cripples the immune system by invading and killing CD4 T cells, key infection-fighters in the body.

'But this new study shows that HIV-I does a lot of damage to the immune system very early ... and now we feel that the opportunity to intervene most effectively may range from about five to seven days after infection,' said Barton Haynes, co-author of the study and director, Duke Centre for HIV/AIDS Vaccine Immunology -.

Haynes said the findings suggest that an optimal vaccine strategy would have to pack a double punch: First, establishing as much immunity as possible before infection, much as classic vaccines do, and then following a few days later with a mechanism to provoke a strong, secondary, broad-based antibody response.

'Vaccine candidates to date have pretty much followed a single strategy. Now we know that we need to activate multiple arms of the immune system and we have a better idea of when to do it.'

The conclusion is based on a study of 30 people who were newly-infected with HIV-I. Plasma from these individuals was sampled every three days for several months - before, during, and after the 'ramp-up' phase of infection, when HIV-I is multiplying rapidly and heading toward its peak viral load.

In measuring the levels of four products of CD4 T cell death during this period in these samples, they were able to track and establish a timetable of the virus's destructive path.

These findings will appear in the August issue of the Journal of Virology.





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