Browsing by Author "Florian Liegeois"

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    Differential susceptibility and innate immune response of aedes aegypti and aedes albopictus to the haitian strain of the mayaro virus
    (2019-10-09) Fodé Diop; Haoues Alout; Cheikh Tidiane Diagne; Michèle Bengue; Cécile Baronti; Rodolphe Hamel; Loïc Talignani; Florian Liegeois; Julien Pompon; Ronald E.Morales Vargas; Antoine Nougairède; Dorothée Missé; Animal, Santé, Territoires, Risques et Ecosystèmes (ASTRE); Maladies Infectieuses et Vecteurs : Écologie, Génétique, Évolution et Contrôle; Aix Marseille Université; Mahidol University
    © 2019 by the authors. Licensee MDPI, Basel, Switzerland. Mayaro (MAYV) is an emerging arthropod-borne virus belonging to the Alphavirus genus of the Togaviridae family. Although forest-dwelling Haemagogus mosquitoes have been considered as its main vector, the virus has also been detected in circulating Aedes ssp mosquitoes. Here we assess the susceptibility of Aedes aegypti and Aedes albopictus to infection with MAYV and their innate immune response at an early stage of infection. Aedes albopictus was more susceptible to infection with MAYV than Ae. aegypti. Analysis of transcript levels of twenty immunity-related genes by real-time PCR in the midgut of both mosquitoes infected with MAYV revealed increased expression of several immune genes, including CLIP-domain serine proteases, the anti-microbial peptides defensin A, E, cecropin E, and the virus inducible gene. The regulation of certain genes appeared to be Aedes species-dependent. Infection of Ae. aegypti with MAYV resulted in increased levels of myeloid differentiation2-related lipid recognition protein (ML26A) transcripts, as compared to Ae. albopictus. Increased expression levels of thio-ester-containing protein 22 (TEP22) and Niemann-Pick type C1 (NPC1) gene transcripts were observed in infected Ae. albopictus, but not Ae. aegypti. The differences in these gene expression levels during MAYV infection could explain the variation in susceptibility observed in both mosquito species.
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    Mayaro Virus Infects Human Chondrocytes and Induces the Expression of Arthritis-Related Genes Associated with Joint Degradation
    (2019-08-29) Michèle Bengue; Pauline Ferraris; Cécile Baronti; Cheikh Tidiane Diagne; Loïc Talignani; Sineewanlaya Wichit; Florian Liegeois; Catherine Bisbal; Antoine Nougairède; Dorothée Missé; Physiologie et Médecine Expérimentale du Cœur et des Muscles; Maladies Infectieuses et Vecteurs : Écologie, Génétique, Évolution et Contrôle; Mahidol University; Unité des virus émergents
    Mayaro virus (MAYV) is an emerging arthritogenic alphavirus belonging to the Togaviridae family. Infection leads to a dengue-like illness accompanied by severe polyarthralgia. However, the molecular and cellular mechanisms of arthritis as a result of MAYV infection remain poorly understood. In the present study, we assess the susceptibility of human chondrocytes (HC), fibroblast-like synoviocytes and osteoblasts that are the major cell types involved in osteoarthritis, to infection with MAYV. We show that these cells are highly permissive to MAYV infection and that viral RNA copy number and viral titers increase over time in infected cells. Knowing that HC are the primary cells in articular cartilage and are essential for maintaining the cartilaginous matrix, gene expression studies were conducted in MAYV-infected primary HC using polymerase chain reaction (PCR) arrays. The infection of the latter cells resulted in an induction in the expression of several matrix metalloproteinases (MMP) including MMP1, MMP7, MMP8, MMP10, MMP13, MMP14 and MMP15 which could be involved in the destruction of articular cartilage. Infected HC were also found to express significantly increased levels of various IFN-stimulated genes and arthritogenic mediators such as TNF-α and IL-6. In conclusion, MAYV-infected primary HC overexpress arthritis-related genes, which may contribute to joint degradation and pathogenesis.
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    Phylogenetic analysis revealed the co-circulation of four dengue virus serotypes in Southern Thailand
    (2019-01-01) Rodolphe Hamel; Pornapat Surasombatpattana; Sineewanlaya Wichit; Alexandra Dauvé; Celeste Donato; Julien Pompon; Dhanasekaran Vijaykrishna; Florian Liegeois; Ronald Morales Vargas; Natthanej Luplertlop; Dorothée Missé; Maladies Infectieuses et Vecteurs : Écologie, Génétique, Évolution et Contrôle; Duke-NUS Medical School Singapore; Monash University; Mahidol University; Prince of Songkla University
    © 2019 Hamel et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Dengue fever is caused by dengue viruses (DENV) from the Flavivirus genus and is the most prevalent arboviral disease. DENV exists in four immunogenically distinct and genetically-related serotypes (DENV-1 to 4), each subdivided in genotypes. Despite the endemicity of all four DENV serotypes in Thailand, no prior study has characterized the circulation of DENV in the southern provinces of the country. To determine the genetic diversity of DENV circulating in Southern Thailand in 2015 and 2016, we investigated 46 viruses from 182 patients’ sera confirmed positive for DENV by serological and Nested RT-PCR tests. Our dataset included 2 DENV-1, 20 DENV-2, 9 DENV-3 and 15 DENV-4. Phylogenetic analysis was performed on viral envelop sequences. This revealed that part of the identified genotypes from DENV-1 and DENV-4 had been predominant in Asia (genotype I for both serotypes), while genotype II for DENV-4 and the Cosmopolitan genotype DENV-2 were also circulating. Whereas DENV-3 genotype II had been predominantly detected in South East Asia during the previous decades, we found genotype III and genotype I in Southern Thailand. All DENV genotype identified in this study were closely related to contemporary strains circulating in Southeast Asian countries, emphasizing the regional circulation of DENV. These results provide new insights into the co-circulation of all four DENV serotypes in Southern Thailand, confirming the hyperendemicity of DENV in the region. These findings also suggest a new trend of dissemination for some DENV serotypes with a possible shift in genotype distribution; as recently observed in other Asian countries.
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    SAMHD1 enhances chikungunya and zika virus replication in human skin fibroblasts
    (2019-04-01) Sineewanlaya Wichit; Rodolphe Hamel; Andreas Zanzoni; Fodé Diop; Alexandra Cribier; Loïc Talignani; Abibatou Diack; Pauline Ferraris; Florian Liegeois; Serge Urbach; Peeraya Ekchariyawat; Andres Merits; Hans Yssel; Monsef Benkirane; Dorothée Missé; Géosciences Montpellier; Maladies Infectieuses et Vecteurs : Écologie, Génétique, Évolution et Contrôle; Technologie Avancée pour le Génome et la Clinique; University of Tartu; Mahidol University; Inserm; Institut de Génétique Fonctionnelle
    © 2019 by the authors. Licensee MDPI, Basel, Switzerland. Chikungunya virus (CHIKV) and Zika virus (ZIKV) are emerging arboviruses that pose a worldwide threat to human health. Currently, neither vaccine nor antiviral treatment to control their infections is available. As the skin is a major viral entry site for arboviruses in the human host, we determined the global proteomic profile of CHIKV and ZIKV infections in human skin fibroblasts using Stable Isotope Labelling by Amino acids in Cell culture (SILAC)-based mass-spectrometry analysis. We show that the expression of the interferon-stimulated proteins MX1, IFIT1, IFIT3 and ISG15, as well as expression of defense response proteins DDX58, STAT1, OAS3, EIF2AK2 and SAMHD1 was significantly up-regulated in these cells upon infection with either virus. Exogenous expression of IFITs proteins markedly inhibited CHIKV and ZIKV replication which, accordingly, was restored following the abrogation of IFIT1 or IFIT3. Overexpression of SAMHD1 in cutaneous cells, or pretreatment of cells with the virus-like particles containing SAMHD1 restriction factor Vpx, resulted in a strong increase or inhibition, respectively, of both CHIKV and ZIKV replication. Moreover, silencing of SAMHD1 by specific SAMHD1-siRNA resulted in a marked decrease of viral RNA levels. Together, these results suggest that IFITs are involved in the restriction of replication of CHIKV and ZIKV and provide, as yet unreported, evidence for a proviral role of SAMHD1 in arbovirus infection of human skin cells.
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    Zika virus infection modulates the metabolomic profile of microglial cells
    (2018-10-01) Fodé Diop; Thomas Vial; Pauline Ferraris; Sineewanlaya Wichit; Michèle Bengue; Rodolphe Hamel; Loïc Talignani; Florian Liegeois; Julien Pompon; Hans Yssel; Guillaume Marti; Dorothée Missé; Université de Toulouse; Mahidol University; CNRS Centre National de la Recherche Scientifique; Inserm
    Copyright: © 2018 Diop et al. Zika virus (ZIKV) is an emerging arbovirus of the Flaviviridae family. Although infection with ZIKV generally leads to mild disease, its recent emergence in the Americas has been associated with an increase in the development of the Guillain-Barré syndrome in adults, as well as with neurological complications, in particular congenital microcephaly, in new-borns. To date, little information is available on neuroinflammation induced by ZIKV, notably in microglial cells in the context of their metabolic activity, a series of chemical transformations that are essential for their growth, reproduction, structural maintenance and environmental responses. Therefore, in the present study we investigated the metabolomic profile of ZIKV-infected microglia. Microglial cells were exposed to ZIKV at different time points and were analyzed by a Liquid Chromatography-High Resolution mass spectrometry-based metabolomic approach. The results show that ZIKV infection in microglia leads to modulation of the expression of numerous metabolites, including lysophospholipids, particulary Lysophosphatidylcholine, and phospholipids such as Phosphatidylcholine, Phosphatidylserine, Ceramide and Sphingomyelin, and carboxylicic acids as Undecanedioic and Dodecanedioic acid. Some of these metabolites are involved in neuronal differentiation, regulation of apoptosis, virion architecture and viral replication. ZIKV infection was associated with concomitant secretion of inflammatory mediators linked with central nervous system inflammation such as IL-6, TNF-α, IL-1β, iNOS and NO. It also resulted in the upregulation of the expression of the gene encoding CX3CR1, a chemokine receptor known to regulate functional synapse plasticity and signaling between microglial cells. These findings highlight an important role for microglia and their metabolites in the process of neuroinflammation that occurs during ZIKV pathogenesis.