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Initial characterization of vaccinia virus B4 suggests a role in virus spread.

Abstract：

:Currently, little is known about the ankyrin/F-box protein B4. Here, we report that B4R-null viruses exhibited reduced plaque size in tissue culture, and decreased ability to spread, as assessed by multiple-step growth analysis. Electron microscopy indicated that B4R-null viruses still formed mature and extracellular virions; however, there was a slight decrease of virions released into the media following deletion of B4R. Deletion of B4R did not affect the ability of the virus to rearrange actin; however, VACV811, a large vaccinia virus deletion mutant missing 55 open reading frames, had decreased ability to produce actin tails. Using ectromelia virus, a natural mouse pathogen, we demonstrated that virus devoid of EVM154, the B4R homolog, showed decreased spread to organs and was attenuated during infection. This initial characterization suggests that B4 may play a role in virus spread, and that other unidentified mediators of actin tail formation may exist in vaccinia virus.

journal_name

Virology

journal_title

Virology

authors

Burles K,Irwin CR,Burton RL,Schriewer J,Evans DH,Buller RM,Barry M

doi

10.1016/j.virol.2014.03.019

subject

Has Abstract

pub_date

2014-05-01 00:00:00

pages

108-20

eissn

0042-6822

issn

1096-0341

pii

S0042-6822(14)00101-9

journal_volume

456-457

pub_type

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