Anna Salvetti

Inserm

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David Durantel

Université Claude Bernard Lyon 1

Philippe Moullier

Gene Therapy Laboratory

Julie Lucifora

Université Claude Bernard Lyon 1

Michel Rivoire

Centre Léon Bérard

Gilliane Chadeuf

Institut du Thorax

Fabien Zoulim

Centre de Recherche en Cancérologie de Lyon

Maud Michelet

Centre de Recherche en Cancérologie de Lyon

Alberto L. Epstein

Université de Versailles Saint-Quentin-en-Yvelines

Hildegard Büning

Medizinische Hochschule Hannover

François‐Loïc Cosset

Inserm

Cooperative Institutions

Inserm

195

Centre National de la Recherche Scientifique

159

Université Claude Bernard Lyon 1

120

École Normale Supérieure de Lyon

European Foundation for the Study of Chronic Liver Failure

Centre de Recherche en Cancérologie de Lyon

Centre International de Recherche en Infectiologie

Université Paris Cité

Sorbonne Université

Centre Léon Bérard

Author Statistics

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Insights on the antiviral mechanisms of action of the TLR1/2 agonist Pam3CSK4 in hepatitis B virus (HBV)-infected hepatocytes

Antiviral Research (2022)

Manon Desmares Marion Delphin Brieux Chardès Caroline Pons Juliette Riedinger

cccDNA

TLR7

TLR3

10.1016/j.antiviral.2022.105386

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Citations (8)

Hepatitis D virus interferes with hepatitis B virus RNA production via interferon-dependent and -independent mechanisms

Journal of Hepatology (2023)

Julie Lucifora Dulce Alfaiate Caroline Pons Maud Michelet Ricardo Ramírez

Hepatitis D virus

Hepatitis D

Viral Interference

Hepatitis B

10.1016/j.jhep.2023.01.005

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Citations (16)

Efficiency of adeno-associated virus type-2 vectors in non-human primate Schwann cells

Neuroreport (2005)

Christelle Girard Liliane Tenenbaum A. Chtarto Bernard Attali Anna Salvetti

Adult macaque Schwann cells were infected using adeno-associated virus type-2-derived vectors expressing the green fluorescent protein reporter gene under the control of the cytomegalovirus, the hybrid cytomegalovirus-βactin, the myelin basic protein or the tetracycline-inducible promoters. On the basis of green fluorescent protein expression, gene transfer efficiency was compared in resting and dividing conditions following or not following hydroxyurea or etoposide treatment. Hydroxyurea allowed promoter-dependent expression of green fluorescent protein in infected Schwann cells. Etoposide treatment led to a high percentage of green fluorescent protein expressing cells (over 50%) with all promoters tested. When infected cells were grafted into demyelinated nude mice spinal cord, green fluorescent protein expression was only observed with the cytomegalovirus-βactin and tetracycline-inducible promoters. In addition, adeno-associated virus type-2 infection reduced the grafted cell survival but increased their differentiation.

Adeno-associated virus

10.1097/01.wnr.0000185960.11465.16

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Citations (3)

Analisi ultrasonografica videodensimetrica delle arterie di grosso calibro nei soggetti giovani normotesi con familiarità per ipertensione

The Cardiology (1999)

Carlo Palombo M. Kozàkovà G. Bigalli C. Morizzo Alessandra Magagna

Source

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AAV-mediated neuronal expression of a scFv antibody selective for Aβ oligomers protects synapses and rescues memory in Alzheimer models

bioRxiv (Cold Spring Harbor Laboratory) (2022)

María Clara Sellés Juliana T.S. Fortuna Magalí C. Cercato Luís E. Santos Luciana Domett Siqueira

Abstract Brain accumulation of soluble oligomers of the amyloid-β peptide (AβOs) has been implicated in synapse failure and memory impairment in Alzheimer’s disease. Here, we show that treatment with NUsc1, a single-chain variable fragment antibody (scFv) that selectively targets AβOs, prevents the inhibition of long-term potentiation in hippocampal slices and memory impairment induced by AβOs in mice. As a therapeutic approach for intracerebral antibody delivery, we developed an adeno-associated virus vector to drive neuronal expression of NUsc1 (AAV-NUsc1) within the brain. Transduction by AAV-NUsc1 induced NUsc1 expression and secretion in adult human brain slices, and inhibited AβO binding to neurons and AβO-induced loss of dendritic spine loss in primary rat hippocampal cultures. Treatment of mice with AAV-NUsc1 prevented memory impairment induced by AβOs and, importantly, reversed memory deficits in aged APPswe/PS1ΔE9 Alzheimer’s disease model mice. These results support the feasibility of gene-mediated immunotherapy using single-chain antibodies as a potential therapeutic approach in Alzheimer’s disease.

Memory Impairment

10.1101/2022.06.10.495369

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Citations (0)

Un monde de virus

médecine/sciences (2022)

Anna Salvetti Hélène Dutartre

10.1051/medsci/2022163

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Citations (0)

Les vecteurs AAV pour le transfert de gène in vivo ou comment un petit virus devient grand.

PubMed (2013)

Rachel Millet Axel Rossi Aurélie Ploquin Alberto L. Epstein Anna Greco

Among the variety of viral vectors, those derived from the human parvovirus Adeno-Associated Virus (AAV) have emerged as a very efficient tool for in vivo gene transfer into a variety of tissues and animal species during the two last decades. The relative simplicity of the organization of the AAV genome and the non-pathogenic property of the parental AAV has greatly contributed to the use of this viral vector among the gene transfer community. However, the limited knowledge of the wild type (wt) virus compared to other viral vectors has required considerable efforts to gain insight into wt AAV biology in order to improve the AAV vector system for therapy. This review will summarize the most important features of both wt and recombinant AAV to show how the increased understanding of the biology of the virus has enabled AAV vectors to lead the in vivo gene transfer field.

Gene transfer

Adeno-associated virus

10.1684/vir.2013.0534

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Loss of hepatitis D virus infectivity upon farnesyl transferase inhibitor treatment associates with increasing RNA editing rates revealed by a new RT-ddPCR method

Antiviral Research (2022)

Éloi R. Verrier Anna Salvetti Caroline Pons Maud Michelet Michel Rivoire

Chronic hepatitis D is the most severe form of chronic viral hepatitis and to date, efficient therapeutic approaches against hepatitis D virus (HDV) are limited. Among the antiviral molecules currently tested in clinical trials, the farnesyl transferase inhibitor (FTI) Lonafarnib inhibits the prenylation of the large delta antigen (L-HDAg), blocking virus assembly. Given the importance of L-HDAg in the virus life cycle, we hypothesized that Lonafarnib treatment may have side effects on virus replication. Here, we setup an innovative method for the quantification of HDV RNA allowing the independent quantification of edited and non-edited versions of the HDV genome upon infection. We demonstrated that FTI treatment of HBV/HDV co-infected dHepaRG or primary human hepatocytes leads to an accumulation of intracellular HDV RNAs and a marked increase in the levels of edited RNAs non only within the infected cells but also in the viral particles that are produced. Interestingly, these viral particles were less infectious, probably due to an enrichment in edited genomes that are packaged, leading to unproductive infection given the absence of S-HDAg synthesis after viral entry. Taken together, we setup an innovative quantification method allowing the investigation of RNA editing during HDV infection in a simple, fast, clinically-relevant assay and demonstrated for the first time the dual antiviral activity of FTI on HDV infection.

Hepatitis D virus

Infectivity

Hepatitis D

Viral life cycle

10.1016/j.antiviral.2022.105250

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Citations (13)

SCREENING MULTIPLE ENDOCRINE NEOPLASIA TYPE 2A FAMILIES USING DNA MARKERS

The Lancet (1988)

Hagay Sobol Anna Salvetti Colette Bonnardel GilbertM. Lenoir

10.1016/s0140-6736(88)91047-1

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Citations (26)

In VivoDelivery of Humanα-l-Iduronidase in Mice Implanted with Neo-Organs

Human Gene Therapy (1995)

Anna Salvetti Philippe Moullier Véronique Cornet Doug A. Brooks John J. Hopwood

Mucopolysaccharidose type I is a lysosomal storage disease caused by a deficiency in the enzyme α-l-iduronidase (IDUA). The existence of a secretory pathway for lysosomal enzymes and the capture of secreted molecules by distant cells through binding to mannose-6-phosphate receptors have provided a rationale for enzyme replacement therapy in lysosomal storage diseases. We have used genetically modified fibroblasts implanted into neo-organs as an in vivo delivery system for IDUA. The human IDUA cDNA was isolated and inserted into a retroviral vector where it was expressed from the phosphoglycerate kinase 1 gene promoter. MPS I fibroblasts transduced with this vector showed high levels of IDUA activity and secreted phosphory-lated molecules that could be internalized by naive deficient cells. Neo-organs containing 2 × 107 IDUA-secreting cells were implanted into nude mice. Human and murine IDUA activities were measured in the liver and spleen of animals sacrificed 35–77 days after implantation. Human IDUA activity corresponded to 0.6–2.3% of the murine enzyme activity in the liver and to 0.1–0.3% in the spleen. These data indicated that human IDUA was secreted from neo-organs and internalized in distant tissues. An approach for enzyme replacement in mucopolysaccharidose type I (MPS I) has been examined. Skin fibroblasts were transduced with a retroviral vector containing the human α-l-iduronidase cDNA and implanted as neo-organs in nude mice. The presence of the human enzyme in the liver and spleen was detected in treated animals. These data suggest that the implantation of engineered fibroblasts into neo-organs may be of a therapeutic benefit in MPS.

10.1089/hum.1995.6.9-1153

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Citations (18)