High level expression of the anti-retroviral protein APOBEC3G is induced by influenza A virus but does not confer antiviral activity

Human APOBEC3G is an antiretroviral protein that was described to act via deamination of retroviral cDNA. However, it was suggested that APOBEC proteins might act with antiviral activity by yet other mechanisms and may also possess RNA deamination activity. As a consequence there is an ongoing debat...

Full description

Saved in:
Bibliographic Details
Published in:Retrovirology 2009-04, Vol.6 (1), p.38-38, Article 38
Main Authors: Pauli, Eva-K, Schmolke, Mirco, Hofmann, Henning, Ehrhardt, Christina, Flory, Egbert, Münk, Carsten, Ludwig, Stephan
Format: Article
Language:English
Subjects:
Animals
Antiviral agents
Antiviral Agents - metabolism
Antiviral Agents - pharmacology
APOBEC-3G Deaminase
Cell Line
Control
Cytidine Deaminase - genetics
Cytidine Deaminase - metabolism
Cytidine Deaminase - pharmacology
Development and progression
Genetic aspects
Humans
Immune response
Influenza
Influenza A virus - drug effects
Influenza A virus - pathogenicity
Influenza A virus - physiology
Influenza A Virus, H1N1 Subtype - drug effects
Influenza A Virus, H1N1 Subtype - pathogenicity
Influenza A Virus, H1N1 Subtype - physiology
NF-kappa B - genetics
NF-kappa B - metabolism
RNA, Viral - metabolism
RNA, Viral - pharmacology
Short Report
Up-Regulation
Virus Replication - drug effects
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Human APOBEC3G is an antiretroviral protein that was described to act via deamination of retroviral cDNA. However, it was suggested that APOBEC proteins might act with antiviral activity by yet other mechanisms and may also possess RNA deamination activity. As a consequence there is an ongoing debate whether APOBEC proteins might also act with antiviral activity on other RNA viruses. Influenza A viruses are single-stranded RNA viruses, capable of inducing a variety of antiviral gene products. In searching for novel antiviral genes against these pathogens, we detected a strong induction of APOBEC3G but not APOBEC3F gene transcription in infected cells. This upregulation appeared to be induced by the accumulation of viral RNA species within the infected cell and occurred in an NF-kappaB dependent, but MAP kinase independent manner. It further turned out that APOBEC expression is part of a general IFNbeta response to infection. However, although strongly induced, APOBEC3G does not negatively affect influenza A virus propagation.
ISSN:1742-4690
1742-4690
DOI:10.1186/1742-4690-6-38