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François-Loïc Cosset
CIRI – Centre International de Recherche en Infectiologie, Univ Lyon, Université Claude Bernard Lyon 1, Inserm, U1111, CNRS, UMR5308, ENS Lyon, Lyon, France

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Short communication
Published: 07 July 2021 in JHEP Reports
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Background & aims HBV persists in the nucleus of infected hepatocytes as a dsDNA episome (cccDNA) that constitutes the template for viral RNA and protein syntheses. Both HBx and HBc (Core) viral proteins associate to cccDNA but, while HBx is required for viral transcription, the role of HBc is still unclear in particular during the early steps of infection following entry, when this structural protein is transported to the nucleus together with the genome. The aim of this study was to determine if HBc derived from incoming nucleocapsid can associate to cccDNA before the onset of viral transcription and protein production. Methods ChIP assays were performed in native conditions. In addition, differentiated HepaRG (dHepaRG) cells infected with HBx-deficient HBV were used to investigate if HBc delivered by incoming virions can associate to cccDNA. Conclusions Our results indicate that HBc can associate to cccDNA in the absence of viral transcription and de novo protein synthesis. In dHepaRG cells, this association is stable for at least 6 weeks. These results suggest that virion-delivered HBc may participate at an early step of cccDNA formation and/or transcription. Lay summary The HBV genome is released into the nucleoplasm after disassembly of the viral nucleocapsids at the nuclear membrane. Using a sensitive ChIP assay, we show for the first time that virion-delivered HBc, the component of the viral capsid, can stably associate to cccDNA independently of viral transcription and de novo protein production.

ACS Style

Julie Lucifora; Florentin Pastor; Émilie Charles; Caroline Pons; Héloïse Auclair; Floriane Fusil; Michel Rivoire; François-Loïc Cosset; David Durantel; Anna Salvetti. Evidence for long-term association of virion-delivered HBV core protein with cccDNA independently of viral protein production. JHEP Reports 2021, 3, 1 .

AMA Style

Julie Lucifora, Florentin Pastor, Émilie Charles, Caroline Pons, Héloïse Auclair, Floriane Fusil, Michel Rivoire, François-Loïc Cosset, David Durantel, Anna Salvetti. Evidence for long-term association of virion-delivered HBV core protein with cccDNA independently of viral protein production. JHEP Reports. 2021; 3 (5):1.

Chicago/Turabian Style

Julie Lucifora; Florentin Pastor; Émilie Charles; Caroline Pons; Héloïse Auclair; Floriane Fusil; Michel Rivoire; François-Loïc Cosset; David Durantel; Anna Salvetti. 2021. "Evidence for long-term association of virion-delivered HBV core protein with cccDNA independently of viral protein production." JHEP Reports 3, no. 5: 1.

Journal article
Published: 30 June 2021 in eLife
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Cell entry of enveloped viruses relies on the fusion between the viral and plasma or endosomal membranes, through a mechanism that is triggered by a cellular signal. Here we used a combination of computational and experimental approaches to unravel the main determinants of hepatitis B virus (HBV) membrane fusion process. We discovered that ERp57 is a host factor critically involved in triggering HBV fusion and infection. Then, through modelling approaches, we uncovered a putative allosteric cross-strand disulfide (CSD) bond in the HBV S glycoprotein and we demonstrate that its stabilization could prevent membrane fusion. Finally, we identified and characterized a potential fusion peptide in the preS1 domain of the HBV L glycoprotein. These results underscore a membrane fusion mechanism that could be triggered by ERp57, allowing a thiol/disulfide exchange reaction to occur and regulate isomerization of a critical CSD, which ultimately leads to the exposition of the fusion peptide.

ACS Style

Jimena Pérez-Vargas; Elin Teppa; Fouzia Amirache; Bertrand Boson; Rémi Pereira de Oliveira; Christophe Combet; Anja Böckmann; Floriane Fusil; Natalia Freitas; Alessandra Carbone; François-Loïc Cosset. A fusion peptide in preS1 and the human protein-disulfide isomerase ERp57 are involved in HBV membrane fusion process. eLife 2021, 10, 1 .

AMA Style

Jimena Pérez-Vargas, Elin Teppa, Fouzia Amirache, Bertrand Boson, Rémi Pereira de Oliveira, Christophe Combet, Anja Böckmann, Floriane Fusil, Natalia Freitas, Alessandra Carbone, François-Loïc Cosset. A fusion peptide in preS1 and the human protein-disulfide isomerase ERp57 are involved in HBV membrane fusion process. eLife. 2021; 10 ():1.

Chicago/Turabian Style

Jimena Pérez-Vargas; Elin Teppa; Fouzia Amirache; Bertrand Boson; Rémi Pereira de Oliveira; Christophe Combet; Anja Böckmann; Floriane Fusil; Natalia Freitas; Alessandra Carbone; François-Loïc Cosset. 2021. "A fusion peptide in preS1 and the human protein-disulfide isomerase ERp57 are involved in HBV membrane fusion process." eLife 10, no. : 1.

Review
Published: 23 June 2021 in Viruses
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Hepatitis delta virus (HDV) is a defective human virus that lacks the ability to produce its own envelope proteins and is thus dependent on the presence of a helper virus, which provides its surface proteins to produce infectious particles. Hepatitis B virus (HBV) was so far thought to be the only helper virus described to be associated with HDV. However, recent studies showed that divergent HDV-like viruses could be detected in fishes, birds, amphibians, and invertebrates, without evidence of any HBV-like agent supporting infection. Another recent study demonstrated that HDV can be transmitted and propagated in experimental infections ex vivo and in vivo by different enveloped viruses unrelated to HBV, including hepatitis C virus (HCV) and flaviviruses such as Dengue and West Nile virus. All this new evidence, in addition to the identification of novel virus species within a large range of hosts in absence of HBV, suggests that deltaviruses may take advantage of a large spectrum of helper viruses and raises questions about HDV origins and evolution.

ACS Style

Jimena Pérez-Vargas; Rémi Pereira de Oliveira; Stéphanie Jacquet; Dominique Pontier; François-Loïc Cosset; Natalia Freitas. HDV-Like Viruses. Viruses 2021, 13, 1207 .

AMA Style

Jimena Pérez-Vargas, Rémi Pereira de Oliveira, Stéphanie Jacquet, Dominique Pontier, François-Loïc Cosset, Natalia Freitas. HDV-Like Viruses. Viruses. 2021; 13 (7):1207.

Chicago/Turabian Style

Jimena Pérez-Vargas; Rémi Pereira de Oliveira; Stéphanie Jacquet; Dominique Pontier; François-Loïc Cosset; Natalia Freitas. 2021. "HDV-Like Viruses." Viruses 13, no. 7: 1207.

Review
Published: 28 April 2021 in Viruses
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The Bunyavirales order comprises more than 500 viruses (generally defined as bunyaviruses) classified into 12 families. Some of these are highly pathogenic viruses infecting different hosts, including humans, mammals, reptiles, arthropods, birds, and/or plants. Host cell sensing of infection activates the innate immune system that aims at inhibiting viral replication and propagation. Upon recognition of pathogen-associated molecular patterns (PAMPs) by cellular pattern recognition receptors (PRRs), numerous signaling cascades are activated, leading to the production of interferons (IFNs). IFNs act in an autocrine and paracrine manner to establish an antiviral state by inducing the expression of hundreds of IFN-stimulated genes (ISGs). Some of these ISGs are known to restrict bunyavirus infection. Along with other constitutively expressed host cellular factors with antiviral activity, these proteins (hereafter referred to as “restriction factors”) target different steps of the viral cycle, including viral entry, genome transcription and replication, and virion egress. In reaction to this, bunyaviruses have developed strategies to circumvent this antiviral response, by avoiding cellular recognition of PAMPs, inhibiting IFN production or interfering with the IFN-mediated response. Herein, we review the current knowledge on host cellular factors that were shown to restrict infections by bunyaviruses. Moreover, we focus on the strategies developed by bunyaviruses in order to escape the antiviral state developed by the infected cells.

ACS Style

Solène Lerolle; Natalia Freitas; François-Loïc Cosset; Vincent Legros. Host Cell Restriction Factors of Bunyaviruses and Viral Countermeasures. Viruses 2021, 13, 784 .

AMA Style

Solène Lerolle, Natalia Freitas, François-Loïc Cosset, Vincent Legros. Host Cell Restriction Factors of Bunyaviruses and Viral Countermeasures. Viruses. 2021; 13 (5):784.

Chicago/Turabian Style

Solène Lerolle; Natalia Freitas; François-Loïc Cosset; Vincent Legros. 2021. "Host Cell Restriction Factors of Bunyaviruses and Viral Countermeasures." Viruses 13, no. 5: 784.

Short review
Published: 19 February 2021 in Joint Bone Spine
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Rheumatoid arthritis is a chronic systemic autoimmune disease, affecting mainly the joints. It is caused by an adaptive immune reaction against self-antigens, leading to the over production of inflammatory cytokines and autoantibodies, mainly mediated by autoreactive CD4+ T cells and pathological B cell clones. The treatment options currently available rely on palliative global immunosuppression and do not restore tolerance to self-components. Here, we review antigen-specific tolerance approaches that have been developed to inhibit or delete autoreactive clones, while maintaining a potent immune system for rheumatoid arthritis. The first attempts relied on the oral ingestion of self-reactive peptides, with lukewarm results in human clinical trials. To enhance treatment efficacy, self-peptides have been engineered and combined with immunosuppressive molecules. In addition, several routes of delivery have been tested, in particular, nanoparticles carrying self-antigens and immunomodulatory molecules. More recently, transfer of immune cells, such as tolerogenic dendritic cells or regulatory T cells, has been considered to restore tolerance. Although promising results have been obtained in mouse models, the translation to humans remains highly challenging, mainly because the disease is already well developed when treatments start and because patient's specific self-antigens are often unknown. Nevertheless, these approaches hold great promises for long-term RA treatment.

ACS Style

Audrey Page; Floriane Fusil; François-Loïc Cosset. Antigen-specific tolerance approach for rheumatoid arthritis: Past, present and future. Joint Bone Spine 2021, 88, 105164 .

AMA Style

Audrey Page, Floriane Fusil, François-Loïc Cosset. Antigen-specific tolerance approach for rheumatoid arthritis: Past, present and future. Joint Bone Spine. 2021; 88 (4):105164.

Chicago/Turabian Style

Audrey Page; Floriane Fusil; François-Loïc Cosset. 2021. "Antigen-specific tolerance approach for rheumatoid arthritis: Past, present and future." Joint Bone Spine 88, no. 4: 105164.

Journal article
Published: 06 January 2021 in Cellular & Molecular Immunology
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Understanding the immune responses elicited by SARS-CoV-2 infection is critical in terms of protection against reinfection and, thus, for public health policy and vaccine development for COVID-19. In this study, using either live SARS-CoV-2 particles or retroviruses pseudotyped with the SARS-CoV-2 S viral surface protein (Spike), we studied the neutralizing antibody (nAb) response in serum samples from a cohort of 140 SARS-CoV-2 qPCR-confirmed infections, including patients with mild symptoms and also more severe forms, including those that required intensive care. We show that nAb titers correlated strongly with disease severity and with anti-spike IgG levels. Indeed, patients from intensive care units exhibited high nAb titers; conversely, patients with milder disease symptoms had heterogeneous nAb titers, and asymptomatic or exclusive outpatient-care patients had no or low nAbs. We found that nAb activity in SARS-CoV-2-infected patients displayed a relatively rapid decline after recovery compared to individuals infected with other coronaviruses. Moreover, we found an absence of cross-neutralization between endemic coronaviruses and SARS-CoV-2, indicating that previous infection by human coronaviruses may not generate protective nAbs against SARS-CoV-2. Finally, we found that the D614G mutation in the spike protein, which has recently been identified as the current major variant in Europe, does not allow neutralization escape. Altogether, our results contribute to our understanding of the immune correlates of SARS-CoV-2-induced disease, and rapid evaluation of the role of the humoral response in the pathogenesis of SARS-CoV-2 is warranted.

ACS Style

Vincent Legros; Solène Denolly; Manon Vogrig; Bertrand Boson; Eglantine Siret; Josselin Rigaill; Sylvie Pillet; Florence Grattard; Sylvie Gonzalo; Paul Verhoeven; Omran Allatif; Philippe Berthelot; Carole Pélissier; Guillaume Thiery; Elisabeth Botelho-Nevers; Guillaume Millet; Jérôme Morel; Stéphane Paul; Thierry Walzer; François-Loïc Cosset; Thomas Bourlet; Bruno Pozzetto. A longitudinal study of SARS-CoV-2-infected patients reveals a high correlation between neutralizing antibodies and COVID-19 severity. Cellular & Molecular Immunology 2021, 18, 318 -327.

AMA Style

Vincent Legros, Solène Denolly, Manon Vogrig, Bertrand Boson, Eglantine Siret, Josselin Rigaill, Sylvie Pillet, Florence Grattard, Sylvie Gonzalo, Paul Verhoeven, Omran Allatif, Philippe Berthelot, Carole Pélissier, Guillaume Thiery, Elisabeth Botelho-Nevers, Guillaume Millet, Jérôme Morel, Stéphane Paul, Thierry Walzer, François-Loïc Cosset, Thomas Bourlet, Bruno Pozzetto. A longitudinal study of SARS-CoV-2-infected patients reveals a high correlation between neutralizing antibodies and COVID-19 severity. Cellular & Molecular Immunology. 2021; 18 (2):318-327.

Chicago/Turabian Style

Vincent Legros; Solène Denolly; Manon Vogrig; Bertrand Boson; Eglantine Siret; Josselin Rigaill; Sylvie Pillet; Florence Grattard; Sylvie Gonzalo; Paul Verhoeven; Omran Allatif; Philippe Berthelot; Carole Pélissier; Guillaume Thiery; Elisabeth Botelho-Nevers; Guillaume Millet; Jérôme Morel; Stéphane Paul; Thierry Walzer; François-Loïc Cosset; Thomas Bourlet; Bruno Pozzetto. 2021. "A longitudinal study of SARS-CoV-2-infected patients reveals a high correlation between neutralizing antibodies and COVID-19 severity." Cellular & Molecular Immunology 18, no. 2: 318-327.

Journal article
Published: 01 January 2021 in Journal of Biological Chemistry
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The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), a β-coronavirus, is the causative agent of the COVID-19 pandemic. Like for other coronaviruses, its particles are composed of four structural proteins: Spike (S), Envelope (E), Membrane (M) and Nucleoprotein (N) proteins. The involvement of each of these proteins and their interactions are critical for assembly and production of β-coronavirus particles. Here, we sought to characterize the interplay of SARS-CoV-2 structural proteins during the viral assembly process. By combining biochemical and imaging assays in infected vs. transfected cells, we show that E and M regulate intracellular trafficking of S as well as its intracellular processing. Indeed, the imaging data reveal that S is re-localized at endoplasmic reticulum (ER)-Golgi intermediate compartment (ERGIC) or Golgi compartments upon co-expression of E or M, as observed in SARS-CoV-2-infected cells, which prevents syncytia formation. We show that a C-terminal retrieval motif in the cytoplasmic tail of S is required for its M-mediated retention in the ERGIC, whereas E induces S retention by modulating the cell secretory pathway. We also highlight that E and M induce a specific maturation of N-glycosylation of S, independently of the regulation of its localization, with a profile that is observed both in infected cells and in purified viral particles. Finally, we show that E, M and N are required for optimal production of virus- like-particles. Altogether, these results highlight how E and M proteins may influence the properties of S proteins and promote the assembly of SARS-CoV-2 viral particles.

ACS Style

Bertrand Boson; Vincent Legros; Bingjie Zhou; Eglantine Siret; Cyrille Mathieu; François-Loïc Cosset; Dimitri Lavillette; Solène Denolly. The SARS-CoV-2 envelope and membrane proteins modulate maturation and retention of the spike protein, allowing assembly of virus-like particles. Journal of Biological Chemistry 2021, 296, 100111 -100111.

AMA Style

Bertrand Boson, Vincent Legros, Bingjie Zhou, Eglantine Siret, Cyrille Mathieu, François-Loïc Cosset, Dimitri Lavillette, Solène Denolly. The SARS-CoV-2 envelope and membrane proteins modulate maturation and retention of the spike protein, allowing assembly of virus-like particles. Journal of Biological Chemistry. 2021; 296 ():100111-100111.

Chicago/Turabian Style

Bertrand Boson; Vincent Legros; Bingjie Zhou; Eglantine Siret; Cyrille Mathieu; François-Loïc Cosset; Dimitri Lavillette; Solène Denolly. 2021. "The SARS-CoV-2 envelope and membrane proteins modulate maturation and retention of the spike protein, allowing assembly of virus-like particles." Journal of Biological Chemistry 296, no. : 100111-100111.

Review
Published: 11 December 2020 in Viruses
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Lentiviral vectors are versatile tools for gene delivery purposes. While in the earlier versions of retroviral vectors, transgene expression was controlled by the long terminal repeats (LTRs), the latter generations of vectors, including those derived from lentiviruses, incorporate internal constitutive or regulated promoters in order to regulate transgene expression. This allows to temporally and/or quantitatively control transgene expression, which is required for many applications such as for clinical applications, when transgene expression is required in specific tissues and at a specific timing. Here we review the main systems that have been developed for transgene regulated expression following lentiviral gene transfer. First, the induction of gene expression can be triggered either by external or by internal cues. Indeed, these regulated vector systems may harbor promoters inducible by exogenous stimuli, such as small molecules (e.g., antibiotics) or temperature variations, offering the possibility to tune rapidly transgene expression in case of adverse events. Second, expression can be indirectly adjusted by playing on inserted sequence copies, for instance by gene excision. Finally, synthetic networks can be developed to sense specific endogenous signals and trigger defined responses after information processing. Regulatable lentiviral vectors (LV)-mediated transgene expression systems have been widely used in basic research to uncover gene functions or to temporally reprogram cells. Clinical applications are also under development to induce therapeutic molecule secretion or to implement safety switches. Such regulatable approaches are currently focusing much attention and will benefit from the development of other technologies in order to launch autonomously controlled systems.

ACS Style

Audrey Page; Floriane Fusil; François-Loïc Cosset. Toward Tightly Tuned Gene Expression Following Lentiviral Vector Transduction. Viruses 2020, 12, 1427 .

AMA Style

Audrey Page, Floriane Fusil, François-Loïc Cosset. Toward Tightly Tuned Gene Expression Following Lentiviral Vector Transduction. Viruses. 2020; 12 (12):1427.

Chicago/Turabian Style

Audrey Page; Floriane Fusil; François-Loïc Cosset. 2020. "Toward Tightly Tuned Gene Expression Following Lentiviral Vector Transduction." Viruses 12, no. 12: 1427.

Research article
Published: 12 November 2020 in PLOS Pathogens
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Despite the existence of a preventive vaccine, chronic infection with Hepatitis B virus (HBV) affects more than 250 million people and represents a major global cause of hepatocellular carcinoma (HCC) worldwide. Current clinical treatments, in most of cases, do not eliminate viral genome that persists as a DNA episome in the nucleus of hepatocytes and constitutes a stable template for the continuous expression of viral genes. Several studies suggest that, among viral factors, the HBV core protein (HBc), well-known for its structural role in the cytoplasm, could have critical regulatory functions in the nucleus of infected hepatocytes. To elucidate these functions, we performed a proteomic analysis of HBc-interacting host-factors in the nucleus of differentiated HepaRG, a surrogate model of human hepatocytes. The HBc interactome was found to consist primarily of RNA-binding proteins (RBPs), which are involved in various aspects of mRNA metabolism. Among them, we focused our studies on SRSF10, a RBP that was previously shown to regulate alternative splicing (AS) in a phosphorylation-dependent manner and to control stress and DNA damage responses, as well as viral replication. Functional studies combining SRSF10 knockdown and a pharmacological inhibitor of SRSF10 phosphorylation (1C8) showed that SRSF10 behaves as a restriction factor that regulates HBV RNAs levels and that its dephosphorylated form is likely responsible for the anti-viral effect. Surprisingly, neither SRSF10 knock-down nor 1C8 treatment modified the splicing of HBV RNAs but rather modulated the level of nascent HBV RNA. Altogether, our work suggests that in the nucleus of infected cells HBc interacts with multiple RBPs that regulate viral RNA metabolism. Our identification of SRSF10 as a new anti-HBV restriction factor offers new perspectives for the development of new host-targeted antiviral strategies.

ACS Style

Hélène Chabrolles; Héloïse Auclair; Serena Vegna; Thomas Lahlali; Caroline Pons; Maud Michelet; Yohann Couté; Lucid Belmudes; Gilliane Chadeuf; Yujin Kim; Ariel Di Bernardo; Pascal Jalaguier; François-Loïc Cosset; Floriane Fusil; Michel Rivoire; Lee D. Arnold; Uri Lopatin; Christophe Combet; Fabien Zoulim; David Grierson; Benoit Chabot; Julie Lucifora; David Durantel; Anna Salvetti. Hepatitis B virus Core protein nuclear interactome identifies SRSF10 as a host RNA-binding protein restricting HBV RNA production. PLOS Pathogens 2020, 16, e1008593 .

AMA Style

Hélène Chabrolles, Héloïse Auclair, Serena Vegna, Thomas Lahlali, Caroline Pons, Maud Michelet, Yohann Couté, Lucid Belmudes, Gilliane Chadeuf, Yujin Kim, Ariel Di Bernardo, Pascal Jalaguier, François-Loïc Cosset, Floriane Fusil, Michel Rivoire, Lee D. Arnold, Uri Lopatin, Christophe Combet, Fabien Zoulim, David Grierson, Benoit Chabot, Julie Lucifora, David Durantel, Anna Salvetti. Hepatitis B virus Core protein nuclear interactome identifies SRSF10 as a host RNA-binding protein restricting HBV RNA production. PLOS Pathogens. 2020; 16 (11):e1008593.

Chicago/Turabian Style

Hélène Chabrolles; Héloïse Auclair; Serena Vegna; Thomas Lahlali; Caroline Pons; Maud Michelet; Yohann Couté; Lucid Belmudes; Gilliane Chadeuf; Yujin Kim; Ariel Di Bernardo; Pascal Jalaguier; François-Loïc Cosset; Floriane Fusil; Michel Rivoire; Lee D. Arnold; Uri Lopatin; Christophe Combet; Fabien Zoulim; David Grierson; Benoit Chabot; Julie Lucifora; David Durantel; Anna Salvetti. 2020. "Hepatitis B virus Core protein nuclear interactome identifies SRSF10 as a host RNA-binding protein restricting HBV RNA production." PLOS Pathogens 16, no. 11: e1008593.

Journal article
Published: 01 November 2020 in Journal of Biological Chemistry
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The penetration of enveloped viruses into target cells requires the fusion of the lipid envelope of their virions with the host lipid membrane though a stepwise and highly sophisticated process. However, the intermediate steps in this process have seldom been visualized due to their rarity and rapidity. Here, using cryo-electron tomography, TIRF microscopy, and cell membrane–derived vesicles called blebs, Ward et al. visualize intermediates of the HIV-cell membrane fusion process and demonstrate how Serinc proteins prevent full fusion by interfering with this process.

ACS Style

Solène Denolly; François-Loïc Cosset. HIV fusion: Catch me if you can. Journal of Biological Chemistry 2020, 295, 15196 -15197.

AMA Style

Solène Denolly, François-Loïc Cosset. HIV fusion: Catch me if you can. Journal of Biological Chemistry. 2020; 295 (45):15196-15197.

Chicago/Turabian Style

Solène Denolly; François-Loïc Cosset. 2020. "HIV fusion: Catch me if you can." Journal of Biological Chemistry 295, no. 45: 15196-15197.

Microbiology
Published: 21 September 2020 in PLOS Pathogens
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Crimean-Congo hemorrhagic fever virus (CCHFV) is a tick-borne orthonairovirus that has become a serious threat to the public health. CCHFV has a single-stranded, tripartite RNA genome composed of L, M, and S segments. Cleavage of the M polyprotein precursor generates the two envelope glycoproteins (GPs) as well as three secreted nonstructural proteins GP38 and GP85 or GP160, representing GP38 only or GP38 linked to a mucin-like protein (MLD), and a double-membrane-spanning protein called NSm. Here, we examined the relevance of each M-segment non-structural proteins in virus assembly, egress and infectivity using a well-established CCHFV virus-like-particle system (tc-VLP). Deletion of MLD protein had no impact on infectivity although it reduced by 60% incorporation of GPs into particles. Additional deletion of GP38 abolished production of infectious tc-VLPs. The loss of infectivity was associated with impaired Gc maturation and exclusion from the Golgi, showing that Gn is not sufficient to target CCHFV GPs to the site of assembly. Consistent with this, efficient complementation was achieved in cells expressing MLD-GP38 in trans with increased levels of preGc to Gc conversion, co-targeting to the Golgi, resulting in particle incorporation and restored infectivity. Contrastingly, a MLD-GP38 variant retained in the ER allowed preGc cleavage but failed to rescue miss-localization or infectivity. NSm deletion, conversely, did not affect trafficking of Gc but interfered with Gc processing, particle formation and secretion. NSm expression affected N-glycosylation of different viral proteins most likely due to increased speed of trafficking through the secretory pathway. This highlights a potential role of NSm in overcoming Golgi retention and facilitating CCHFV egress. Thus, deletions of GP38 or NSm demonstrate their important role on CCHFV particle production and infectivity. GP85 is an essential viral factor for preGc cleavage, trafficking and Gc incorporation into particles, whereas NSm protein is involved in CCHFV assembly and virion secretion. Orthonairoviruses, like the lethal Crimean-Congo hemorrhagic fever virus (CCHFV), encode secreted glycoproteins, such as GP38, in addition to virion envelope glycoproteins (Gn and Gc) that are processed by internal cleavage of the viral M segment encoded polyprotein. CCHFV MLD-GP38 proteins (GP160/GP85) also include an N-terminal domain encompassing a mucin-like protein that is released from GP38 by Furin. The protective effect of non-neutralizing monoclonal antibodies targeting GP38 against lethal CCHFV challenge previously highlighted the importance of GP38 in CCHFV replication. CCHFV also encodes a double-membrane-spanning protein (NSm) of unknown function, located between the Gn and Gc on the polyprotein. To investigate the roles of these so-called accessory proteins encoded by the CCHFV M-segment in virus formation and infectivity, we generated several M-segment deletion mutants and tested them in a CCHFV transcription-entry-competent virus-like particle (tc-VLP) system. Here, we demonstrate that GP38 is crucial for Gc biogenesis, interaction with Gn and trafficking to the Golgi, and that its deletion abrogates formation of infectious particles. We also show that NSm increases the rate of protein trafficking through the secretory pathway with altered N-glycosylation profiles that are advantageous for efficient virus release. These data advanced our understanding of GP38 and NSm roles and CCHFV-host interactions.

ACS Style

Natalia Freitas; Margot Enguehard; Solène Denolly; Camille Levy; Gregory Neveu; Solène Lerolle; Stephanie Devignot; Friedemann Weber; Eric Bergeron; Vincent Legros; François-Loïc Cosset. The interplays between Crimean-Congo hemorrhagic fever virus (CCHFV) M segment-encoded accessory proteins and structural proteins promote virus assembly and infectivity. PLOS Pathogens 2020, 16, e1008850 .

AMA Style

Natalia Freitas, Margot Enguehard, Solène Denolly, Camille Levy, Gregory Neveu, Solène Lerolle, Stephanie Devignot, Friedemann Weber, Eric Bergeron, Vincent Legros, François-Loïc Cosset. The interplays between Crimean-Congo hemorrhagic fever virus (CCHFV) M segment-encoded accessory proteins and structural proteins promote virus assembly and infectivity. PLOS Pathogens. 2020; 16 (9):e1008850.

Chicago/Turabian Style

Natalia Freitas; Margot Enguehard; Solène Denolly; Camille Levy; Gregory Neveu; Solène Lerolle; Stephanie Devignot; Friedemann Weber; Eric Bergeron; Vincent Legros; François-Loïc Cosset. 2020. "The interplays between Crimean-Congo hemorrhagic fever virus (CCHFV) M segment-encoded accessory proteins and structural proteins promote virus assembly and infectivity." PLOS Pathogens 16, no. 9: e1008850.

Review
Published: 11 September 2020 in Viruses
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: Viruses have been repurposed into tools for gene delivery by transforming them into viral vectors. The most frequently used vectors are lentiviral vectors (LVs), derived from the human immune deficiency virus allowing efficient gene transfer in mammalian cells. They represent one of the safest and most efficient treatments for monogenic diseases affecting the hematopoietic system. LVs are modified with different viral envelopes (pseudotyping) to alter and improve their tropism for different primary cell types. The vesicular stomatitis virus glycoprotein (VSV-G) is commonly used for pseudotyping as it enhances gene transfer into multiple hematopoietic cell types. However, VSV-G pseudotyped LVs are not able to confer efficient transduction in quiescent blood cells, such as hematopoietic stem cells (HSC), B and T cells. To solve this problem, VSV-G can be exchanged for other heterologous viral envelopes glycoproteins, such as those from the Measles virus, Baboon endogenous retrovirus, Cocal virus, Nipah virus or Sendai virus. Here, we provide an overview of how these LV pseudotypes improved transduction efficiency of HSC, B, T and natural killer (NK) cells, underlined by multiple in vitro and in vivo studies demonstrating how pseudotyped LVs deliver therapeutic genes or gene editing tools to treat different genetic diseases and efficiently generate CAR T cells for cancer treatment.

ACS Style

Alejandra Gutierrez-Guerrero; François-Loïc Cosset; Els Verhoeyen. Lentiviral Vector Pseudotypes: Precious Tools to Improve Gene Modification of Hematopoietic Cells for Research and Gene Therapy. Viruses 2020, 12, 1016 .

AMA Style

Alejandra Gutierrez-Guerrero, François-Loïc Cosset, Els Verhoeyen. Lentiviral Vector Pseudotypes: Precious Tools to Improve Gene Modification of Hematopoietic Cells for Research and Gene Therapy. Viruses. 2020; 12 (9):1016.

Chicago/Turabian Style

Alejandra Gutierrez-Guerrero; François-Loïc Cosset; Els Verhoeyen. 2020. "Lentiviral Vector Pseudotypes: Precious Tools to Improve Gene Modification of Hematopoietic Cells for Research and Gene Therapy." Viruses 12, no. 9: 1016.

Other
Published: 01 September 2020
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Understanding the immune responses elicited by SARS-CoV-2 infection is critical in terms of protection from re-infection and, thus, for public health policy and for vaccine development against the COVID-19. Here, using either live SARS-CoV-2 particles or retroviruses pseudotyped with the SARS-CoV-2 S viral surface protein (Spike), we studied the neutralizing antibody (nAb) response in serum specimens from a cohort of 140 SARS-CoV-2 qPCR-confirmed patients, including patient with mild symptoms but also more severe form including those that require intensive care. We show that nAb titers were strongly correlated with disease severity and with anti-Spike IgG levels. Indeed, patients from intensive care units exhibited high nAb titers, whereas patients with milder disease symptoms displayed heterogenous nAb titers and asymptomatic or exclusive outpatient care patients had no or poor nAb levels. We found that the nAb activity in SARS-CoV-2-infected patients displayed a relatively rapid decline after recovery, as compared to individuals infected with alternative coronaviruses. We show the absence of cross-neutralization between endemic coronaviruses and SARS-CoV-2, indicating that previous infection by human coronaviruses may not generate protective nAb against SARS-CoV-2 infection. Finally, we found that the D614G mutation in the Spike protein, which has recently been identified as the major variant now found in Europe, does not allow neutralization escape. Altogether, our results contribute to the understanding of the immune correlate of SARS-CoV-2 induced disease and claim for a rapid evaluation of the role of the humoral response in the pathogenesis of SARS-CoV-2.

ACS Style

Vincent Legros; Solène Denolly; Manon Vogrig; Bertrand Boson; Josselin Rigaill; Sylvie Pillet; Florence Grattard; Sylvie Gonzalo; Paul Verhoeven; Omran Allatif; Philippe Berthelot; Carole Pélissier; Guillaume Thierry; Elisabeth Botelho-Nevers; Stéphane Paul; Thierry Walzer; François-Loïc Cosset; Thomas Bourlet; Bruno Pozzetto. A longitudinal study of SARS-CoV-2 infected patients shows high correlation between neutralizing antibodies and COVID-19 severity. 2020, 1 .

AMA Style

Vincent Legros, Solène Denolly, Manon Vogrig, Bertrand Boson, Josselin Rigaill, Sylvie Pillet, Florence Grattard, Sylvie Gonzalo, Paul Verhoeven, Omran Allatif, Philippe Berthelot, Carole Pélissier, Guillaume Thierry, Elisabeth Botelho-Nevers, Stéphane Paul, Thierry Walzer, François-Loïc Cosset, Thomas Bourlet, Bruno Pozzetto. A longitudinal study of SARS-CoV-2 infected patients shows high correlation between neutralizing antibodies and COVID-19 severity. . 2020; ():1.

Chicago/Turabian Style

Vincent Legros; Solène Denolly; Manon Vogrig; Bertrand Boson; Josselin Rigaill; Sylvie Pillet; Florence Grattard; Sylvie Gonzalo; Paul Verhoeven; Omran Allatif; Philippe Berthelot; Carole Pélissier; Guillaume Thierry; Elisabeth Botelho-Nevers; Stéphane Paul; Thierry Walzer; François-Loïc Cosset; Thomas Bourlet; Bruno Pozzetto. 2020. "A longitudinal study of SARS-CoV-2 infected patients shows high correlation between neutralizing antibodies and COVID-19 severity." , no. : 1.

Clinical observations in hepatology
Published: 06 July 2020 in Hepatology
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Hepatitis delta virus (HDV) is a defective human virus that lacks the ability to produce its own envelope proteins and is thus dependent on the presence of a helper virus, which provides its surface proteins to produce infectious particles. Hepatitis B virus (HBV) was so far thought to be the only helper virus described to be associated to HDV. However, recent studies showed that divergent HDV‐like viruses can be detected in fishes, birds, amphibians, and invertebrates, without evidence of any HBV‐like agent supporting infection.

ACS Style

Isabelle Chemin; Flor H. Pujol; Caroline Scholtès; Carmen L. Loureiro; Fouzia Amirache; Massimo Levrero; Fabien Zoulim; Jimena Pérez‐Vargas; François‐Loïc Cosset. Preliminary Evidence for Hepatitis Delta Virus Exposure in Patients Who Are Apparently Not Infected With Hepatitis B Virus. Hepatology 2020, 73, 861 -864.

AMA Style

Isabelle Chemin, Flor H. Pujol, Caroline Scholtès, Carmen L. Loureiro, Fouzia Amirache, Massimo Levrero, Fabien Zoulim, Jimena Pérez‐Vargas, François‐Loïc Cosset. Preliminary Evidence for Hepatitis Delta Virus Exposure in Patients Who Are Apparently Not Infected With Hepatitis B Virus. Hepatology. 2020; 73 (2):861-864.

Chicago/Turabian Style

Isabelle Chemin; Flor H. Pujol; Caroline Scholtès; Carmen L. Loureiro; Fouzia Amirache; Massimo Levrero; Fabien Zoulim; Jimena Pérez‐Vargas; François‐Loïc Cosset. 2020. "Preliminary Evidence for Hepatitis Delta Virus Exposure in Patients Who Are Apparently Not Infected With Hepatitis B Virus." Hepatology 73, no. 2: 861-864.

Review
Published: 13 April 2020 in Cancers
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Cancers represent highly significant health issues and the options for their treatment are often not efficient to cure the disease. Immunotherapy strategies have been developed to modulate the patient’s immune system in order to eradicate cancerous cells. For instance, passive immunization consists in the administration at high doses of exogenously produced monoclonal antibodies directed either against tumor antigen or against immune checkpoint inhibitors. Its main advantage is that it provides immediate immunity, though during a relatively short period, which consequently requires frequent injections. To circumvent this limitation, several approaches, reviewed here, have emerged to induce in vivo antibody secretion at physiological doses. Gene delivery vectors, such as adenoviral vectors or adeno-associated vectors, have been designed to induce antibody secretion in vivo after in situ cell modification, and have driven significant improvements in several cancer models. However, anti-idiotypic antibodies and escape mutants have been detected, probably because of both the continuous expression of antibodies and their expression by unspecialized cell types. To overcome these hurdles, adoptive transfer of genetically modified B cells that secrete antibodies either constitutively or in a regulated manner have been developed by ex vivo transgene insertion with viral vectors. Recently, with the emergence of gene editing technologies, the endogenous B cell receptor loci of B cells have been modified with the clustered regularly interspaced short palindromic repeats (CRISPR)/CRISPR-associated endonuclease (Cas-9) system to change their specificity in order to target a given antigen. The expression of the modified BCR gene hence follows the endogenous regulation mechanisms, which may prevent or at least reduce side effects. Although these approaches seem promising for cancer treatments, major questions, such as the persistence and the re-activation potential of these engineered cells, remain to be addressed in clinically relevant animal models before translation to humans.

ACS Style

Audrey Page; Floriane Fusil; François-Loïc Cosset. Towards Physiologically and Tightly Regulated Vectored Antibody Therapies. Cancers 2020, 12, 962 .

AMA Style

Audrey Page, Floriane Fusil, François-Loïc Cosset. Towards Physiologically and Tightly Regulated Vectored Antibody Therapies. Cancers. 2020; 12 (4):962.

Chicago/Turabian Style

Audrey Page; Floriane Fusil; François-Loïc Cosset. 2020. "Towards Physiologically and Tightly Regulated Vectored Antibody Therapies." Cancers 12, no. 4: 962.

Review
Published: 12 April 2020 in Viruses
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Hepatitis C virus (HCV) infection is a major public health issue leading to chronic liver diseases. HCV particles are unique owing to their particular lipid composition, namely the incorporation of neutral lipids and apolipoproteins. The mechanism of association between HCV virion components and these lipoproteins factors remains poorly understood as well as its impact in subsequent steps of the viral life cycle, such as entry into cells. It was proposed that the lipoprotein biogenesis pathway is involved in HCV morphogenesis; yet, recent evidence indicated that HCV particles can mature and evolve biochemically in the extracellular medium after egress. In addition, several viral, cellular and blood components have been shown to influence and regulate this specific association. Finally, this specific structure and composition of HCV particles was found to influence entry into cells as well as their stability and sensitivity to neutralizing antibodies. Due to its specific particle composition, studying the association of HCV particles with lipoproteins remains an important goal towards the rational design of a protective vaccine.

ACS Style

François-Loïc Cosset; Chloé Mialon; Bertrand Boson; Christelle Granier; Solène Denolly. HCV Interplay with Lipoproteins: Inside or Outside the Cells? Viruses 2020, 12, 434 .

AMA Style

François-Loïc Cosset, Chloé Mialon, Bertrand Boson, Christelle Granier, Solène Denolly. HCV Interplay with Lipoproteins: Inside or Outside the Cells? Viruses. 2020; 12 (4):434.

Chicago/Turabian Style

François-Loïc Cosset; Chloé Mialon; Bertrand Boson; Christelle Granier; Solène Denolly. 2020. "HCV Interplay with Lipoproteins: Inside or Outside the Cells?" Viruses 12, no. 4: 434.

Preprint content
Published: 18 March 2020
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Sporozoite forms of the malaria parasite Plasmodium are transmitted by mosquitoes and first infect the liver for an initial round of replication before parasite proliferation in the blood. The molecular mechanisms involved during sporozoite invasion of hepatocytes remain poorly understood. Two receptors of the Hepatitis C virus (HCV), the tetraspanin CD81 and the scavenger receptor class B type 1 (SR-B1), play an important role during the entry of Plasmodium sporozoites into hepatocytic cells. In contrast to HCV entry, which requires both CD81 and SR-B1 together with additional host factors, CD81 and SR-B1 operate independently during malaria liver infection. Sporozoites from human-infecting P. falciparum and P. vivax rely respectively on CD81 or SR-B1. Rodent-infecting P. berghei can use SR-B1 to infect host cells as an alternative pathway to CD81, providing a tractable model to investigate the role of SR-B1 during Plasmodium liver infection. Here we show that mouse SR-B1 is less functional as compared to human SR-B1 during P. berghei infection. We took advantage of this functional difference to investigate the structural determinants of SR-B1 required for infection. Using a structure-guided strategy and chimeric mouse/human SR-B1 constructs, we could map the functional region of human SR-B1 within apical loops, suggesting that this region of the protein may play a crucial role for interaction of sporozoite ligands with host cells and thus the very first step of Plasmodium infection.IMPORTANCEMalaria is caused by Plasmodium parasites and remains one of the deadliest parasitic diseases worldwide. The parasite is transmitted by a blood feeding mosquito and first invades the liver for an initial, obligatory and silent round of replication. The liver infection is an attractive target for antimalarial vaccine strategies, however the molecular mechanisms of parasite invasion of hepatocytes remain to be fully elucidated. Two hepatocyte surface proteins are known to be important for parasite entry into hepatocytes, the tetraspanin CD81 and the scavenger receptor class B type 1 (SR-B1). These receptors constitute independent gateways depending on the Plasmodium species. Here, we identified the structural determinants of SR-B1, an important hepatocyte entry factor for human-infecting P. vivax. This study paves the way toward a better characterization of the molecular interactions underlying the crucial early stages of infection, a pre-requisite for the development of novel malaria vaccine strategies.

ACS Style

Anne-Claire Langlois; Giulia Manzoni; Laetitia Vincensini; Romain Coppée; Carine Marinach; Maryse Guérin; Thierry Huby; Véronique Carrière; François-Loïc Cosset; Marlene Dreux; Eric Rubinstein; Olivier Silvie. Molecular determinants of SR-B1-dependent Plasmodium sporozoite entry into hepatocytic cells. 2020, 1 .

AMA Style

Anne-Claire Langlois, Giulia Manzoni, Laetitia Vincensini, Romain Coppée, Carine Marinach, Maryse Guérin, Thierry Huby, Véronique Carrière, François-Loïc Cosset, Marlene Dreux, Eric Rubinstein, Olivier Silvie. Molecular determinants of SR-B1-dependent Plasmodium sporozoite entry into hepatocytic cells. . 2020; ():1.

Chicago/Turabian Style

Anne-Claire Langlois; Giulia Manzoni; Laetitia Vincensini; Romain Coppée; Carine Marinach; Maryse Guérin; Thierry Huby; Véronique Carrière; François-Loïc Cosset; Marlene Dreux; Eric Rubinstein; Olivier Silvie. 2020. "Molecular determinants of SR-B1-dependent Plasmodium sporozoite entry into hepatocytic cells." , no. : 1.

Rna microbiology
Published: 01 February 2020 in Journal of Biological Chemistry
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Viruses depend on the host cell translation machinery for their replication, and one common strategy is the presence of internal ribosome entry sites (IRESs) in the viral RNAs, using different sets of host translation initiation factors. The hepatitis C virus (HCV) IRES binds eukaryotic translation initiation factor 3 (eIF3), but the exact functional role of the eIF3 complex and of its subunits remains to be precisely defined. Toward this goal, here we focused on eIF3 subunit e. We used an in vitro assay combining a ribosome-depleted rabbit reticulocyte lysate and ribosomes prepared from HeLa or Huh-7.5 cells transfected with either control or eIF3e siRNAs. eIF3e silencing reduced translation mediated by the 5′UTR of various cellular genes and HCV-like IRESs. However, this effect was not observed with the bona fide HCV IRES. Silencing of eIF3e reduced the intracellular levels of the c, d, and l subunits of eIF3 and their association with the eIF3 core subunit a. A pulldown analysis of eIF3 subunits associated with the HCV IRES disclosed similar effects and that the a subunit is critical for binding to the HCV IRES. Carrying out HCV infections of control and eIF3e-silenced Huh-7.5 cells, we found that in agreement with the in vitro findings, eIF3e silencing does not reduce HCV replication and viral protein expression. We conclude that unlike for host cellular mRNAs, the entire eIF3 is not required for HCV RNA translation, favoring viral expression under conditions of low eIF3e levels.

ACS Style

Baptiste Panthu; Solene Denolly; Cendrine Faivre-Moskalenko; Theophile Ohlmann; François-Loïc Cosset; Pierre Jalinot. Unlike for cellular mRNAs and other viral internal ribosome entry sites (IRESs), the eIF3 subunit e is not required for the translational activity of the HCV IRES. Journal of Biological Chemistry 2020, 295, 1843 -1856.

AMA Style

Baptiste Panthu, Solene Denolly, Cendrine Faivre-Moskalenko, Theophile Ohlmann, François-Loïc Cosset, Pierre Jalinot. Unlike for cellular mRNAs and other viral internal ribosome entry sites (IRESs), the eIF3 subunit e is not required for the translational activity of the HCV IRES. Journal of Biological Chemistry. 2020; 295 (7):1843-1856.

Chicago/Turabian Style

Baptiste Panthu; Solene Denolly; Cendrine Faivre-Moskalenko; Theophile Ohlmann; François-Loïc Cosset; Pierre Jalinot. 2020. "Unlike for cellular mRNAs and other viral internal ribosome entry sites (IRESs), the eIF3 subunit e is not required for the translational activity of the HCV IRES." Journal of Biological Chemistry 295, no. 7: 1843-1856.

Journal article
Published: 01 January 2020 in médecine/sciences
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Médecine/sciences (M/S), revue internationale dans le domaine de la recherche biologique, médicale et en santé

ACS Style

Anaïs Vignon; Solene Denolly; Jimena Perez-Vargas; François-Loïc Cosset. Le virus de l’hépatite Delta. médecine/sciences 2020, 36, 27 -29.

AMA Style

Anaïs Vignon, Solene Denolly, Jimena Perez-Vargas, François-Loïc Cosset. Le virus de l’hépatite Delta. médecine/sciences. 2020; 36 (1):27-29.

Chicago/Turabian Style

Anaïs Vignon; Solene Denolly; Jimena Perez-Vargas; François-Loïc Cosset. 2020. "Le virus de l’hépatite Delta." médecine/sciences 36, no. 1: 27-29.

Journal article
Published: 01 December 2019 in Human Gene Therapy
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Cell and gene therapies are finally becoming viable patient treatment options, with both T cell- and hematopoietic stem cell (HSC)-based therapies being approved to market in Europe. However, these therapies, which involve the use of viral vector to modify the target cells, are expensive and there is an urgent need to reduce manufacturing costs. One major cost factor is the viral vector production itself, therefore improving the gene modification efficiency could significantly reduce the amount of vector required per patient. This study describes the use of a transduction enhancing peptide, Vectofusin-1®, to improve the transduction efficiency of primary target cells using lentiviral and gammaretroviral vectors (LV and RV) pseudotyped with a variety of envelope proteins. Using Vectofusin-1 in combination with LV pseudotyped with viral glycoproteins derived from baboon endogenous retrovirus, feline endogenous virus (RD114), and measles virus (MV), a strongly improved transduction of HSCs, B cells and T cells, even when cultivated under low stimulation conditions, could be observed. The formation of Vectofusin-1 complexes with MV-LV retargeted to CD20 did not alter the selectivity in mixed cell culture populations, emphasizing the precision of this targeting technology. Functional, ErbB2-specific chimeric antigen receptor-expressing T cells could be generated using a gibbon ape leukemia virus (GALV)-pseudotyped RV. Using a variety of viral vectors and target cells, Vectofusin-1 performed in a comparable manner to the traditionally used surface-bound recombinant fibronectin. As Vectofusin-1 is a soluble peptide, it was possible to easily transfer the T cell transduction method to an automated closed manufacturing platform, where proof of concept studies demonstrated efficient genetic modification of T cells with GALV-RV and RD114-RV and the subsequent expansion of mainly central memory T cells to a clinically relevant dose.

ACS Style

Constanze Radek; Ornellie Bernadin; Katharina Drechsel; Nicole Cordes; Rita Pfeifer; Pia Sträßer; Mirella Mormin; Alejandra Gutierrez-Guerrero; François-Loïc Cosset; Andrew D. Kaiser; Thomas Schaser; Anne Galy; Els Verhoeyen; Ian C.D. Johnston. Vectofusin-1 Improves Transduction of Primary Human Cells with Diverse Retroviral and Lentiviral Pseudotypes, Enabling Robust, Automated Closed-System Manufacturing. Human Gene Therapy 2019, 30, 1477 -1493.

AMA Style

Constanze Radek, Ornellie Bernadin, Katharina Drechsel, Nicole Cordes, Rita Pfeifer, Pia Sträßer, Mirella Mormin, Alejandra Gutierrez-Guerrero, François-Loïc Cosset, Andrew D. Kaiser, Thomas Schaser, Anne Galy, Els Verhoeyen, Ian C.D. Johnston. Vectofusin-1 Improves Transduction of Primary Human Cells with Diverse Retroviral and Lentiviral Pseudotypes, Enabling Robust, Automated Closed-System Manufacturing. Human Gene Therapy. 2019; 30 (12):1477-1493.

Chicago/Turabian Style

Constanze Radek; Ornellie Bernadin; Katharina Drechsel; Nicole Cordes; Rita Pfeifer; Pia Sträßer; Mirella Mormin; Alejandra Gutierrez-Guerrero; François-Loïc Cosset; Andrew D. Kaiser; Thomas Schaser; Anne Galy; Els Verhoeyen; Ian C.D. Johnston. 2019. "Vectofusin-1 Improves Transduction of Primary Human Cells with Diverse Retroviral and Lentiviral Pseudotypes, Enabling Robust, Automated Closed-System Manufacturing." Human Gene Therapy 30, no. 12: 1477-1493.