The world's first wiki where authorship really matters (Nature Genetics, 2008). Due credit and reputation for authors. Imagine a global collaborative knowledge base for original thoughts. Search thousands of articles and collaborate with scientists around the globe.

wikigene or wiki gene protein drug chemical gene disease author authorship tracking collaborative publishing evolutionary knowledge reputation system wiki2.0 global collaboration genes proteins drugs chemicals diseases compound
Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

The presence of tat protein or tumor necrosis factor alpha is critical for herpes simplex virus type 1-induced expression of human immunodeficiency virus type 1.

Tat-independent transcription of human immunodeficiency virus type 1 (HIV-1) plays an important role in virus life cycle before biologically significant levels of Tat protein have been accumulated. Using a latently infected T-cell line containing an integrated Tat-defective HIV-1 provirus, we examined whether factors known to up-regulate the HIV-1 expression in vitro can replace the requirement for a functional Tat protein and induce the expression of the Tat-defective HIV-1 provirus. Both tumor necrosis factor alpha (TNF-alpha) and herpes simplex virus type 1 (HSV-1) infection stimulated transcription of the Tat-defective HIV-1 provirus to comparable levels, but in HSV-1-infected cells, the cytoplasmic HIV-1 transcripts were not efficiently translated in the absence of Tat protein and were excluded from the large polysomes. However, HSV-1 infection did not affect the distribution of cellular gamma-actin RNA or 28S RNA in the polysomal fractions. The translational block of HIV-1 RNA was not mediated by the virion-associated host cell shutoff protein (vhs); dissociation of HIV-1 transcripts from the polysomes and inefficient translation was also observed in cells infected with the vhs-defective mutant of HSV-1 (vhs-1). Overexpression of Rev protein did not rescue the synthesis of HIV-1 proteins in these cells; however, the observed inhibition of HIV-1 RNA translation was efficiently overcome in the presence of Tat protein or TNF-alpha. These findings suggest that, in contrast to TNF-alpha, HSV-1 infection is not able to induce a full cycle of HIV-1 replication and that cytokines and Tat have a critical role in the activation of HIV-1 provirus by HSV-1.[1]

References

 
WikiGenes - Universities