Bouazzaoui, A.A.BouazzaouiKreutz, M.M.KreutzEisert, V.V.EisertBracharz, S.S.BracharzDinauer, N.N.DinauerHeinzelmann, A.A.HeinzelmannHallenberger, S.S.HallenbergerStrayle, J.J.StrayleWalker, R.R.WalkerRübsamen-Waigmann, H.H.Rübsamen-WaigmannAndreesen, R.R.AndreesenBriesen, H. vonH. vonBriesen2022-03-032022-03-032006https://publica.fraunhofer.de/handle/publica/21180110.1016/j.virol.2006.07.0252-s2.0-33750990479In order to identify cellular genes which interfere with HIV-1 replication in monocyte-derived macrophages (MAC), cells were stimulated with interferon (IFN) or lipopolysaccharide (LPS) leading to a pronounced inhibition of HIV-1 infection in these cells, and the resulting gene expression was analyzed. Using the microarray technology we identified a gene named Stimulated Trans-Acting Factor of 50 kDa (Staf50), which is known to repress the activity of the HIV-1 LTR. Analysis of the Staf50 expression by real-time PCR showed an overexpression in IFN? (up to 20-fold) and LPS (up to 10-fold)-stimulated MAC as well as in infected cells (up to 3-fold). For stable overexpression, 293 T cells and primary macrophages were transduced with Staf50-IRES-GFP bicistronic pseudotype viruses. After transduction, 293 T CD4/CCR5 and MAC were infected with HIV-1, and virus replication was monitored by p24 ELISA. Overexpression of Staf50 inhibited the HIV-1 infection between 50% and 90% in 293 T CD4/CCR5 as well as in MAC. Our findings suggest that host genetic effects in combination with viral properties determine the susceptibility of an appropriate target cell for HIV-1 infection as well as the replication potential of the virus in the cell resulting in an overall productive infection.en610620579journal article