Log on / register
BioMed Central home | Journals A-Z | Feedback | Support | My details
Open AccessShort report

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

Eva-K Pauli1 email, Mirco Schmolke1 email, Henning Hofmann2 email, Christina Ehrhardt1 email, Egbert Flory3 email, Carsten Münk2 email and Stephan Ludwig1 email

Institute of Molecular Virology (IMV), Centre of Molecular Biology of Inflammation (ZMBE), Westfaelische-Wilhelms-University Muenster, Münster, Germany

Clinic for Gastroenterology, Hepatology and Infectiology, Heinrich-Heine-University, Duesseldorf, Germany

Paul-Ehrlich-Institute (PEI), Langen, Germany

author email corresponding author email

Retrovirology 2009, 6:38doi:10.1186/1742-4690-6-38

Published: 16 April 2009

Abstract

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-κB dependent, but MAP kinase independent manner. It further turned out that APOBEC expression is part of a general IFNβ response to infection. However, although strongly induced, APOBEC3G does not negatively affect influenza A virus propagation.


© 1999-2010 BioMed Central Ltd unless otherwise stated. Part of Springer Science+Business Media.