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Dr. Olivier Terrier
Centre International de Recherche en Infectiologie, Lyon, France
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Academic Career Length
19Years (2008-Present)
(Calculated once Scilit publication data is synced: current year − year of first publication + 1)
Representative Publications
View All Publications22 July 2020 in Nature
Journal Article
PMPauline Maisonnasse
Pauline MaisonnasseJGJeremie Guedj
Jeremie GuedjVCVanessa Contreras
Vanessa ContrerasSBSylvie Behillil
Sylvie Behillil
CSCaroline Solas
Caroline Solas
RGRoger Le Grand
Roger Le Grand +18
7 August 2020 in CPT: Pharmacometrics & Systems Pharmacology
Journal Article
AGAntonio Gonçalves
Antonio GonçalvesJBJulie Bertrand
Julie BertrandRKRuian Ke
Ruian Ke
ECEmmanuelle Comets
Emmanuelle CometsXLXavier de Lamballerie
Xavier de Lamballerie
JGJeremie Guedj
Jeremie Guedj +7
We modeled the viral dynamics of 13 untreated patients infected with severe acute respiratory syndrome‐coronavirus 2 to infer viral growth parameters and predict the effects of antiviral treatments. In order to reduce peak viral load by more than two logs, drug efficacy needs to be > 90% if treatment is administered after symptom onset; an efficacy of 60% could be sufficient if treatment is initiated before symptom onset. Given their pharmacokinetic/pharmacodynamic properties, current investigated drugs may be in a range of 6–87% efficacy. They may help control virus if administered very early, but may not have a major effect in severely ill patients.
1 July 2020 in Cell Reports Medicine
Journal Article
MPMario Andrés Pizzorno
Mario Andrés PizzornoBPBlandine Padey
Blandine PadeyTJThomas Julien
Thomas JulienSTSophie Trouillet-Assant
Sophie Trouillet-Assant
ATAurélien Traversier
Aurélien Traversier
MRManuel Rosa-Calatrava
Manuel Rosa-Calatrava +12
In the current COVID-19 pandemic context, proposing and validating effective treatments represents a major challenge. However, the scarcity of biologically relevant pre-clinical models of SARS-CoV-2 infection imposes a significant barrier for scientific and medical progress, including the rapid transition of potentially effective treatments to the clinical setting. We use reconstituted human airway epithelia to isolate and then characterize the viral infection kinetics, tissue-level remodeling of the cellular ultrastructure, and transcriptional early immune signatures induced by SARS-CoV-2 in a physiologically relevant model. Our results emphasize distinctive transcriptional immune signatures between nasal and bronchial HAE, both in terms of kinetics and intensity, hence suggesting putative intrinsic differences in the early response to SARS-CoV-2 infection. Most important, we provide evidence in human-derived tissues on the antiviral efficacy of remdesivir monotherapy and explore the potential of the remdesivir-diltiazem combination as an option worthy of further investigation to respond to the still-unmet COVID-19 medical need.
1 July 2014 in mBio
Journal Article
JDJulia Dubois
Julia DuboisOTOlivier Terrier
Olivier TerrierMRManuel Rosa-Calatrava
Manuel Rosa-CalatravaDuring their nuclear replication stage, influenza viruses hijack the host splicing machinery to process some of their RNA segments, the M and NS segments. In this review, we provide an overview of the current knowledge gathered on this interplay between influenza viruses and the cellular spliceosome, with a particular focus on influenza A viruses (IAV). These viruses have developed accurate regulation mechanisms to reassign the host spliceosome to alter host cellular expression and enable an optimal expression of specific spliced viral products throughout infection. Moreover, IAV segments undergoing splicing display high levels of similarity with human consensus splice sites and their viral transcripts show noteworthy secondary structures. Sequence alignments and consensus analyses, along with recently published studies, suggest both conservation and evolution of viral splice site sequences and structure for improved adaptation to the host. Altogether, these results emphasize the ability of IAV to be well adapted to the host’s splicing machinery, and further investigations may contribute to a better understanding of splicing regulation with regard to viral replication, host range, and pathogenesis.
1 September 2020 in Antiviral Research
Journal Article
MPMario Andrés Pizzorno
Mario Andrés PizzornoBPBlandine Padey
Blandine PadeyJDJulia Dubois
Julia DuboisTJThomas Julien
Thomas JulienATAurélien Traversier
Aurélien Traversier
OTOlivier Terrier
Olivier Terrier +4
16 September 2013 in Proceedings of the National Academy of Sciences
Journal Article
BEBoris Essere
Boris Essere
MYMatthieu Yver
Matthieu Yver
CGCyrille Gavazzi
Cyrille Gavazzi
OTOlivier Terrier
Olivier TerrierCICatherine Isel
Catherine IselVMVincent Moules
Vincent Moules +8
The fragmented nature of the influenza A genome allows the exchange of gene segments when two or more influenza viruses infect the same cell, but little is known about the rules underlying this process. Here, we studied genetic reassortment between the A/Moscow/10/99 (H3N2, MO) virus originally isolated from human and the avian A/Finch/England/2051/91 (H5N2, EN) virus and found that this process is strongly biased. Importantly, the avian HA segment never entered the MO genetic background alone but always was accompanied by the avian PA and M fragments. Introduction of the 5′ and 3′ packaging sequences of HAMO into an otherwise HAEN backbone allowed efficient incorporation of the chimerical viral RNA (vRNA) into the MO genetic background. Furthermore, forcing the incorporation of the avian M segment or introducing five silent mutations into the human M segment was sufficient to drive coincorporation of the avian HA segment into the MO genetic background. These silent mutations also strongly affected the genotype of reassortant viruses. Taken together, our results indicate that packaging signals are crucial for genetic reassortment and that suboptimal compatibility between the vRNA packaging signals, which are detected only when vRNAs compete for packaging, limit this process.
About Me
Current position : Researcher - Assistant Professor (CR1 CNRS, HDR),
I was appointed in 2015 as permanent CNRS researcher in the VirPath Team (Pr Bruno Lina/Dr Manuel Rosa-Calatrava), which is part of the Centre International de Recherche en Infectiologie (CIRI, INSERM U1111, CNRS UMR5308, ENS Lyon & Université Claude Bernard Lyon 1), based in Lyon, France. My current research projects consist to study virus-host interactions at the level of human respiratory epithelium. Another part of my current work is dedicated to the development of innovative approaches to identify/repurpose small molecules of interest in the field of respiratory viruses based on their transcriptional signatures of infection. I am particularly interested in the study of co-infections/superinfections between viruses and bacteria, and I am developing new experimental models for this purpose.
Over the past 15 years, I have developed a strong expertise in the study of respiratory viruses, combining virology, molecular and cellular biology approaches, and developing experimental infection models in reconstituted human airway epithelium (HAE). In the context of the COVID-19 pandemic, our group set up and published the first model of SARS-CoV-2 infections in HAE, a model that enabled crucial steps to be taken to validate preclinical candidate molecules (Pizzorno et al. cell Rep Medicine 2020; Maissonasse et al. Nature 2020; Pizzorno et al. Antiviral Research 2020).