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Dying to Replicate: The Orchestration of the Viral Life Cycle, Cell Death Pathways, and Immunity

Authors :
Matthew L. Albert
Nader Yatim
Immunobiologie des Cellules Dendritiques
Institut Pasteur [Paris] (IP)-Institut National de la Santé et de la Recherche Médicale (INSERM)
Funding support is from the Agence National de Recherche (ANR) and the Immuno-Oncology LabEx Project
We would like to dedicate this review to the memory of R. Steinman, the consummate mentor and a leader in the field of dendritic cell biology and host response to infection. Far ahead of his time, he informed the dendritic cell community in 2000 that we must always consider the microbes agenda if we are going to understand how to vaccinate the host. His insights and support will be sorely missed. We would like to thank A. Oberst, O. Schwartz, and M. Laird for their careful read of the manuscript. We also acknowledge helpful discussions with L. Quintana-Murci, D. Green and members of his lab, and the Laboratory of Dendritic Cell Biology
ANR-11-IDEX-0005,USPC,Université Sorbonne Paris Cité(2011)
Institut Pasteur [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)
Source :
Immunity, Immunity, 2011, 35 (4), pp.478-490. ⟨10.1016/j.immuni.2011.10.010⟩, Immunity, Elsevier, 2011, 35 (4), pp.478-490. ⟨10.1016/j.immuni.2011.10.010⟩
Publication Year :
2011
Publisher :
HAL CCSD, 2011.

Abstract

International audience; Manipulation of cell death pathways has been identified as a common feature of host-microbe interactions. We examine two examples: influenza A as a representative acute infection and cytomegalovirus as an example of chronic infection. From the perspective of viral entry, replication, and transmission, we identify points of interconnection with the host response to infection, namely the induction of host cell death, inflammation, and immunity. Following from this analysis, we argue that the evolution and fine-tuned regulation of death-associated genes may result from constant microbial pressure--past and present--that helped to support and coordinate cell death programs within the host. Interestingly, the delay in host cell death allows time for the virus to replicate while perturbations in cell death allow the host cell to initiate an immune response. This may represent a genetically encoded trade-off ensuring survival of both host and virus, or it may be a part of the complex agenda of infectious microbes

Details

Language :
English
ISSN :
10747613
Database :
OpenAIRE
Journal :
Immunity, Immunity, 2011, 35 (4), pp.478-490. ⟨10.1016/j.immuni.2011.10.010⟩, Immunity, Elsevier, 2011, 35 (4), pp.478-490. ⟨10.1016/j.immuni.2011.10.010⟩
Accession number :
edsair.doi.dedup.....c2372eea415649a54780a8f0a551cde1