April, 2008: 3 (4)
"Salmonella-Secreted Protein AvrA Inhibits Apoptosis"
[Cover Caption]
Browse Archive
 Previews | Pages |
|---|---|
| Linking Inflammasome Activation and Phagosome Maturation Vanja Lazarevic and Fabio Martinon | 199 |
| (C)Re-Combining Textbook Models of Virus Spread within the Host Erik S. Barton and Douglas W. White | 201 |
| Commentary | Pages |
| Identifying Host Targets for Drug Development with Knowledge from Genome-wide Studies: Lessons from HIV-AIDS Cheryl A. Winkler | 203 |
| Review | Pages |
| P Bodies, Stress Granules, and Viral Life Cycles Carla J. Beckham and Roy Parker | 206 |
| Articles | Pages |
| Diet-Induced Obesity Is Linked to Marked but Reversible Alterations in the Mouse Distal Gut Microbiome Peter J. Turnbaugh, Fredrik Bäckhed, Lucinda Fulton, and Jeffrey I. Gordon | 213 |
| Mycobacterium tuberculosis Prevents Inflammasome Activation Sharon S. Master, Silvana K. Rampini, Alexander S. Davis, Christine Keller, Stefan Ehlers, Burkhard Springer, Graham S. Timmins, Peter Sander, and Vojo Deretic | 224 |
| Salmonella AvrA Coordinates Suppression of Host Immune and Apoptotic Defenses via JNK Pathway Blockade Rheinallt M. Jones, Huixia Wu, Christy Wentworth, Liping Luo, Lauren Collier-Hyams, and Andrew S. Neish | 233 |
| The Interferon-Induced Protein BST-2 Restricts HIV-1 Release and Is Downregulated from the Cell Surface by the Viral Vpu Protein Nanette Van Damme, Daniel Goff, Chris Katsura, Rebecca L. Jorgenson, Richard Mitchell, Marc C. Johnson, Edward B. Stephens, and John Guatelli | 245 |
| Human Cytomegalovirus Protein UL38 Inhibits Host Cell Stress Responses by Antagonizing the Tuberous Sclerosis Protein Complex Nathaniel J. Moorman, Ileana M. Cristea, Scott S. Terhune, Michael P. Rout, Brian T. Chait, and Thomas Shenk | 253 |
| The Major Virus-Producing Cell Type during Murine Cytomegalovirus Infection, the Hepatocyte, Is Not the Source of Virus Dissemination in the Host Torsten Sacher, Jürgen Podlech, Christian A. Mohr, Stefan Jordan, Zsolt Ruzsics, Matthias J. Reddehase, and Ulrich H. Koszinowski | 263 |
Cover Caption
On the cover: In this issue, Jones et al. (p. 233) report that AvrA, a protein secreted by Salmonella typhimurium during epithelial host invasion, has repressive effects on conserved cellular pro-apoptotic responses. Using both transgenic Drosophila and murine models, the authors show that AvrA mediates potent inhibition of JNK pathway signaling. The cover image depicts a Drosophila larva imaginal eye disk used to provide precise spatial and temporal control of AvrA expression. AvrA (green) inhibits the phosphorylation of JNK (red) in response to constitutive expression of the Drosophila tumor necrosis factor ortholog Eiger.
Featured Article
- The Major Virus-Producing Cell Type during Murine Cytomegalovirus Infection, the Hepatocyte, Is Not the Source of Virus Dissemination in the Host
Torsten Sacher, Jürgen Podlech, Christian A. Mohr, Stefan Jordan, Zsolt Ruzsics, Matthias J. Reddehase, and Ulrich H. Koszinowski
[Summary] [Full Text] [PDF] [Supplemental Data] - The course of systemic viral infections is determined by the virus productivity of infected cell types and the efficiency of virus dissemination throughout the host. Here, we used a cell-type-specific virus labeling system to quantitatively track virus progeny during murine cytomegalovirus infection. We infected mice that expressed Cre recombinase selectively in vascular endothelial cells or hepatocytes with a murine cytomegalovirus for which Cre-mediated recombination would generate a fluorescently labeled virus. We showed that endothelial cells and hepatocytes produced virus after direct infection. However, in the liver, the main contributor to viral load in the mouse, most viruses were produced by directly infected hepatocytes. Remarkably, although virus produced in hepatocytes spread to hepatic endothelial cells (and vice versa), there was no significant spread from the liver to other organs. Thus, the cell type producing the most viruses was not necessarily the one responsible for virus dissemination within the host.
