Vaccine controls HIV infection
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Vaccine controls HIV infection

03.01.2013 - Spanish and French researchers have found a therapeutic vaccine strategy to boost the immune response to HIV.

A therapeutic vaccine that uses heat-inactivated HIV appears to boost the immune response to the virus in people, reports Science Translational Medicine. The findings pave the way for the development of vaccines that could potentially control HIV replication without the need for life-long antiretroviral medication. The vaccine is made from treated dendritic cells or DCs.

When a microorganism like HIV invades the body, cells called phagocytes chop up the virus and break it into small fragments. Some of these pieces find their way into the membranes of DCs. The DCs then present the pieces of HIV to lymphocytes, white blood cells that then launch a specific immune response against the virus. The problem is that DCs can also carry a part of the infectious virus on their outer membrane. Consequently, the white blood cells can get infected and die instead of developing an immune response.

To avoid this problem, Felipe García from University of Barcelona and colleagues from CRNS Paris primed the DCs of 36 patients with heat-inactivated HIV and then delivered the DCs back into patients as a therapeutic vaccine. The exposure to inactivated HIV allows the DCs to deliver their message to the white blood cells without harming them. The researchers found that vaccine was able to stimulate a noticeable degree of immune response against HIV, and that higher responses correlated with better control of virus replication. However, it is not yet clear how much of an immune response is needed to make an effective vaccine. Importantly, the vaccine appeared to be safe and well-tolerated. The results offer evidence that future HIV vaccines could help control the virus.

Earlier in December another research team from Barcelona had presented a different strategy to prevent HIV infection of human CD4 lymphocytes. By blocking HIV entry into DCs they were able to prevent CD4 cells from viral invasion.



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