@article{saito_innate_2008,
	title = {Innate immunity induced by composition-dependent {RIG}-{I} recognition of hepatitis {C} virus {RNA}},
	volume = {454},
	issn = {1476-4687},
	doi = {10.1038/nature07106},
	abstract = {Innate immune defences are essential for the control of virus infection and are triggered through host recognition of viral macromolecular motifs known as pathogen-associated molecular patterns (PAMPs). Hepatitis C virus (HCV) is an RNA virus that replicates in the liver, and infects 200 million people worldwide. Infection is regulated by hepatic immune defences triggered by the cellular RIG-I helicase. RIG-I binds PAMP RNA and signals interferon regulatory factor 3 activation to induce the expression of interferon-alpha/beta and antiviral/interferon-stimulated genes (ISGs) that limit infection. Here we identify the polyuridine motif of the HCV genome 3' non-translated region and its replication intermediate as the PAMP substrate of RIG-I, and show that this and similar homopolyuridine or homopolyriboadenine motifs present in the genomes of RNA viruses are the chief feature of RIG-I recognition and immune triggering in human and murine cells. 5' terminal triphosphate on the PAMP RNA was necessary but not sufficient for RIG-I binding, which was primarily dependent on homopolymeric ribonucleotide composition, linear structure and length. The HCV PAMP RNA stimulated RIG-I-dependent signalling to induce a hepatic innate immune response in vivo, and triggered interferon and ISG expression to suppress HCV infection in vitro. These results provide a conceptual advance by defining specific homopolymeric RNA motifs within the genome of HCV and other RNA viruses as the PAMP substrate of RIG-I, and demonstrate immunogenic features of the PAMP-RIG-I interaction that could be used as an immune adjuvant for vaccine and immunotherapy approaches.},
	language = {eng},
	number = {7203},
	journal = {Nature},
	author = {Saito, Takeshi and Owen, David M. and Jiang, Fuguo and Marcotrigiano, Joseph and Gale, Michael},
	month = jul,
	year = {2008},
	pmid = {18548002},
	pmcid = {PMC2856441},
	keywords = {Humans, Adenine, Animals, Cell Line, DEAD Box Protein 58, DEAD-box RNA Helicases, Genome, Viral, Hepacivirus, Immunity, Innate, Interferon-beta, Ligands, Liver, Mice, RNA, Viral, Uridine, Virus Replication},
	pages = {523--527},
	file = {Version acceptée:/home/virginie/snap/zotero-snap/common/Zotero/storage/K9CLJT9Q/Saito et al. - 2008 - Innate immunity induced by composition-dependent R.pdf:application/pdf},
}

@article{chigbu_hepatitis_2019,
	title = {Hepatitis {C} {Virus} {Infection}: {Host}⁻{Virus} {Interaction} and {Mechanisms} of {Viral} {Persistence}},
	volume = {8},
	issn = {2073-4409},
	shorttitle = {Hepatitis {C} {Virus} {Infection}},
	doi = {10.3390/cells8040376},
	abstract = {Hepatitis C (HCV) is a major cause of liver disease, in which a third of individuals with chronic HCV infections may develop liver cirrhosis. In a chronic HCV infection, host immune factors along with the actions of HCV proteins that promote viral persistence and dysregulation of the immune system have an impact on immunopathogenesis of HCV-induced hepatitis. The genome of HCV encodes a single polyprotein, which is translated and processed into structural and nonstructural proteins. These HCV proteins are the target of the innate and adaptive immune system of the host. Retinoic acid-inducible gene-I (RIG-I)-like receptors and Toll-like receptors are the main pattern recognition receptors that recognize HCV pathogen-associated molecular patterns. This interaction results in a downstream cascade that generates antiviral cytokines including interferons. The cytolysis of HCV-infected hepatocytes is mediated by perforin and granzyme B secreted by cytotoxic T lymphocyte (CTL) and natural killer (NK) cells, whereas noncytolytic HCV clearance is mediated by interferon gamma (IFN-γ) secreted by CTL and NK cells. A host-HCV interaction determines whether the acute phase of an HCV infection will undergo complete resolution or progress to the development of viral persistence with a consequential progression to chronic HCV infection. Furthermore, these host-HCV interactions could pose a challenge to developing an HCV vaccine. This review will focus on the role of the innate and adaptive immunity in HCV infection, the failure of the immune response to clear an HCV infection, and the factors that promote viral persistence.},
	language = {eng},
	number = {4},
	journal = {Cells},
	author = {Chigbu, DeGaulle I. and Loonawat, Ronak and Sehgal, Mohit and Patel, Dip and Jain, Pooja},
	month = apr,
	year = {2019},
	pmid = {31027278},
	pmcid = {PMC6523734},
	keywords = {Humans, Hepacivirus, Immunity, Innate, Adaptive Immunity, Antiviral Agents, Cytokines, dendritic cells, HCV, Hepatitis C, Hepatocytes, Host Microbial Interactions, immune dysregulation, interferons, Interferons, Killer Cells, Natural, Liver Cirrhosis, NK cells, T cells, Toll-Like Receptors, viral persistence},
	pages = {376},
	file = {Texte intégral:/home/virginie/snap/zotero-snap/common/Zotero/storage/7DV4MBT8/Chigbu et al. - 2019 - Hepatitis C Virus Infection Host⁻Virus Interactio.pdf:application/pdf},
}

@book{willey_prescott_2008,
	address = {New York},
	edition = {7th ed},
	title = {Prescott, {Harley}, and {Klein}'s microbiology},
	isbn = {978-0-07-299291-5 978-0-07-330208-9},
	publisher = {McGraw-Hill Higher Education},
	author = {Willey, Joanne M. and Sherwood, Linda and Woolverton, Christopher J. and Prescott, Lansing M.},
	year = {2008},
	note = {OCLC: ocm71044581},
	keywords = {Microbiology},
	file = {Willey et al. - 2008 - Prescott, Harley, and Klein's microbiology.pdf:/home/virginie/snap/zotero-snap/common/Zotero/storage/VAMPNWBX/Willey et al. - 2008 - Prescott, Harley, and Klein's microbiology.pdf:application/pdf},
}