An Adenovirus Traffic Update: From Receptor Engagement to the Nuclear Pore

Abstract

Adenoviruses have a bipolar nature: they are ubiquitous pathogens that occasionally cause life-threatening diseases or they can be engineered into powerful gene transfer vectors. The goal of this article is to summarize the most recent advances in adenovirus receptor engagement, internalization, endosomal maturation, endosomal escape and trafficking to the nuclear pore. A better understanding of this initial part of the adenovirus lifecycle may identify new mechanistic-based treatments for adenovirus-induced diseases and help in the engineering of more efficient vectors.

Keywords:

• adenovirus
• CAR
• CD46
• endosomolysis
• MTOC
• receptor
• trafficking

Financial & competing interests disclosure

The authors thank the members of our laboratory for constructive comments. Work in the Kremer laboratory is supported by the Motor Neurone Disease Association, the European Community‘s 7th Framework Programme (FP7/2007–2013; grant 222992, BrainCAV), the French Agence National de la Recherche (program Blanc, E-RARE and MNP), the Region Languedoc Roussillon, the Fondation de France and the Association Française contre les Myopathies. EJ Kremer and S Salinas are Institut National de la Santé et de la Recherche Médicale (Inserm) fellows. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.

No writing assistance was utilized in the production of this manuscript.

Additional information

Funding

The authors thank the members of our laboratory for constructive comments. Work in the Kremer laboratory is supported by the Motor Neurone Disease Association, the European Community‘s 7th Framework Programme (FP7/2007–2013; grant 222992, BrainCAV), the French Agence National de la Recherche (program Blanc, E-RARE and MNP), the Region Languedoc Roussillon, the Fondation de France and the Association Française contre les Myopathies. EJ Kremer and S Salinas are Institut National de la Santé et de la Recherche Médicale (Inserm) fellows. The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed.