Dr. Oliver Fackler, in the Virology Department of the Hygiene Institute of the Heidelberg University Hospital, examined the movement of cells in living zebra fish embryos, and showed that cell mobility is inhibited by the HIV Nef protein.
The researcher said that further experiments on cell cultures showed Nef to cause a short-circuit of two cellular mechanisms, thus inhibiting the reorganization of the cell structure element actin and the cell's ability to move.
Consequently, said Dr. Fackler, the affected immune cells could no longer perform their function.
"We speculate that the negative effect of Nef on the mobility of T-helper cells has far reaching consequences for the efficient formation of antibodies by B-lymphocytes in the patient. The mechanism we have described could be involved in the increasingly observed malfunction of B-lymphocytes in AIDS patients," said Professor Fackler.
Nef has not been a target of antiviral therapy to date.
However, given that one of the first molecular mechanisms has now been decoded and the importance of Nef for the disease has become clearer, the researchers believe that this may change in the future.