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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
pene
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