The AIDS-causing HIV specifically counteracts the mechanisms of human cells that protect these against viral infections a special viral protein marks protective cellular proteins for their rapid destruction and thus diminishes the cell's supply. A team of researchers in Heidelberg under supervision of virologist Dr. Oliver Keppler demonstrated this mechanism for the first time in cell cultures, thus discovering a target for a novel treatment strategy.
Another important discovery of the Heidelberg virologists this strategy of the human HIV is not effective in a rat model for AIDS. The protective protein in rats is immune to HIV counteraction. Consequently, HIV cannot propagate itself as easily in the animal model as in humans one limitation of the current rat model. However, this new knowledge may enable an improvement of the small animal model developed by the Heidelberg researchers. The study was published in the journal Cell Host & Microbe in March 2009.
Newly formed viruses are retained at the cell surface
In addition to the immune system, the body can activate other protective mechanisms to fight or stop virus infections the infected cells themselves dispose of several proteins that inhibit various steps of virus reproduction. In the presence of the protective protein CD317, newly formed viruses are tethered to the cell surface when they are in the process of leaving the cell and this prevents them from infecting other cells of the body. HIV overcomes this restriction by its protein Vpu by specifically counteracting this protective mechanism, which, interestingly, is effective against many types of viruses.
Dr. Keppler's team of virologists from the Department of Virology at the Hygiene Institute of Heidelberg University Hospital (Medical Director: Professor Dr. Hans-Georg Krusslich) studied how Vpu disrupts protection by CD317. They determined that in human cells in which Vpu was formed after infe
|Contact: PD Dr. med. Oliver T. Keppler|
University Hospital Heidelberg