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Open access, freely available online Synopses of Research Articles Virus Proteins Prevent Cell Suicide Long Enough to Establish Latent Infection DOI: 10.1371/journal.pbio.0030430 Little more than a small genome encased in protein, a virus can’t reproduce without help from the cell it may ultimately destroy. After attaching to the cell membrane, a virus slips inside the cell, then co-opts its transcription and replication machinery to reproduce. Some viruses, such as the Epstein-Barr virus (EBV), enter a latent stage before they start to reproduce. During latency, the virus expresses its own genes, which help maintain the viral genome until replication begins. In many viral life cycles, including EBV, reproduction continues until the cell bursts and releases a new crop of viruses. As a defense, cells undergo programmed cell death, or apoptosis, which protects other cells by containing the invader. But just as the host depends on apoptosis to survive, viral survival depends on preventing apoptosis.To do this, many viruses use relatives of a protein called DOI: 10.1371/journal.pbio.0030430.g001 Bcl-2 (the viral version is called vBcl- 2).Though many vBcl-2–like proteins, or homologs, can trigger apoptosis, all the viral Bcl-2 homologs identi?ed so far inhibit apoptosis during viral reproduction. This electron microscopic image of two Epstein Barr Virus virions (viral particles) shows round capsids—protein-encased genetic material—loosely surrounded by the membrane envelope. This unexpected temporal regulation of gene expression suggested that BHRF1 andBAFL1 activity might initially regulate apoptosis in the infected functional gene, the virus regained its ability to transform the cells.Thus, the two genes are redundant—if one is disabled, the other can take its place. Altogether, these results show that BHRF1 andBAFL1 play a critical role in establishing latent infection by preventing apoptosis until the latency genes can be activated. After the virus penetr