Abstract

BackgroundThe APOBEC3G protein represents a novel innate defense mechanism against retroviral infection. It facilitates the deamination of the cytosine residues in the single stranded cDNA intermediate during early steps of retroviral infection. Most poxvirus genomes are relatively A/T-rich, which may indicate APOBEC3G-induced mutational pressure. In addition, poxviruses replicate exclusively in the cytoplasm where APOBEC3G is located. It was therefore tempting to analyze whether vaccinia virus replication is affected by APOBEC3G.ResultsThe replication of vaccinia virus, a prototype poxvirus, was not, however, inhibited in APOBEC3G-expressing cells, nor did other members of the APOBEC3 family alter vaccinia virus replication. HIV counteracts APOBEC3G by inducing its degradation. However, Western blot analysis showed that the levels of APOBEC3G protein were not affected by vaccinia virus infection.ConclusionThe data indicate that APOBEC3G is not a restriction factor for vaccinia virus replication nor is vaccinia virus able to degrade APOBEC3G.

Highlights

  • The APOBEC3G protein represents a novel innate defense mechanism against retroviral infection

  • HeLa-APOBEC3G cells were infected with Vaccinia virus (VACV) of the strain Western Reserve (VACV-WR) at an MOI of 0.05

  • Murine leukemia virus (MLV) and human immunodeficiency virus type 1 (HIV-1)-based vector particles were generated by transient transfections of 293T cells

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Summary

Results

The replication of vaccinia virus, a prototype poxvirus, was not, inhibited in APOBEC3G-expressing cells, nor did other members of the APOBEC3 family alter vaccinia virus replication. HIV counteracts APOBEC3G by inducing its degradation. Western blot analysis showed that the levels of APOBEC3G protein were not affected by vaccinia virus infection

Background
Results and Discussion
Methods
Cullen BR
22. Moss B
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