A5031119799- HIV Research and Treatment
- HIV/AIDS drug development and treatment
- Immune Cell Function and Interaction
- Hepatitis C virus research
- Single-cell and spatial transcriptomics
- CRISPR and Genetic Engineering
- Cytomegalovirus and herpesvirus research
- T-cell and B-cell Immunology
- Biochemical and Molecular Research
- HIV/AIDS Research and Interventions
- interferon and immune responses
- Bacteriophages and microbial interactions
- Animal Disease Management and Epidemiology
- Fungal Infections and Studies
- Plant Pathogens and Fungal Diseases
- Nail Diseases and Treatments
- T-cell and Retrovirus Studies
- Monoclonal and Polyclonal Antibodies Research
- Bioinformatics and Genomic Networks
- Virology and Viral Diseases
University of Lausanne
2015-2019
Inserm
2013-2016
University of Lisbon
2006-2015
Université Paris Cité
2013
Délégation Paris 7
2013
Instituto de Medicina Molecular João Lobo Antunes
2012
Universidade Nova de Lisboa
2006
Despite effective treatment, HIV can persist in latent reservoirs, which represent a major obstacle toward eradication. Targeting and reactivating cells is challenging due to the heterogeneous nature of HIV-infected cells. Here, we used primary model latency single-cell RNA sequencing characterize transcriptional heterogeneity during reactivation. Our analysis identified programs leading successful reactivation expression.
Cellular permissiveness to HIV infection is highly heterogeneous across individuals. Heterogeneity also found CD4+ T cells from the same individual, where only a fraction of gets infected. To explore basis permissiveness, we performed single-cell RNA-seq analysis non-infected high and low permissive Transcriptional heterogeneity translated in continuum cell states, driven by T-cell receptor-mediated activation was strongly linked permissiveness. Proteins expressed at surface displaying...
Oral presentations Session 1: Entry & uncoating O1 Host cell polo-like kinases (PLKs) promote early prototype foamy virus (PFV) replication Irena Zurnic, Sylvia Hütter, Ute Lehmann, Nicole Stanke, Juliane Reh, Tobias Kern, Fabian Lindel, Gesche Gerresheim, Martin Hamann, Erik Müllers, Paul Lesbats, Peter Cherepanov, Serrao, Alan Engelman, Dirk Lindemann O2 A novel entry/uncoating assay reveals the presence of at least two species viral capsids during synchronized HIV-1 infection Claire Da...
Throughout the HIV-1 replication cycle, complex host-pathogen interactions take place in infected cell, leading to production of new virions. The virus modulates host cellular machinery order support its life while counteracting intracellular defense mechanisms. We investigated dynamic response infection by systematically measuring transcriptomic, proteomic, and phosphoproteomic expression changes uninfected SupT1 CD4+ T cells at five time points viral process. By means a Gaussian...
HIV-1 is a complex retrovirus that uses host machinery to promote its replication. Understanding cellular proteins involved in the multistep process of infection may result discovery more adapted and effective therapeutic targets. Kinases phosphatases are druggable class critically regulation signal pathways eukaryotic cells. Here, we focused on kinases essential for replication but dispensable cell viability. We performed an iterative screen Jurkat T-cells with short-hairpin-RNA (shRNA)...
This report describes application of PCR fingerprinting to identify common species dermatophytes using the microsatellite primers M13, (GACA)4, and (GTG)5. The initial analysis rendered a specific DNA fragment for Microsporum audouinii, which was cloned sequenced. Based on sequencing data this fragment, forward (MA_1F) reverse (MA_1R) were designed verified by establish their reliability in diagnosis M. audouinii. These produced singular band 431 bp only strains isolates based global test...
HIV resistance to the integrase inhibitor raltegravir in treated patients is characterized by distinct pathways. We hypothesize that differences vivo dynamics of are due genetic context present at baseline.We studied four whose viruses evolved towards different The baseline sequences were inserted into a reference clone. Primary mutations then introduced and their impact on viral replication capacity (RC) was measured.Patients A B experienced emergence persistence mutation N155H under...
Abstract Type-I interferons (IFNs) induce the expression of hundreds cellular genes, some which have direct antiviral activities. Although IFNs restrict different steps HIV replication cycle, their dominant effect remains unclear. We first quantified inhibition by IFN in tissue culture, using viruses with tropism and growth kinetics. By combining experimental mathematical analyses, we determined quantitative estimates for key parameters demonstrate that mainly inhibits de novo infection (33%...
The human immunodeficiency virus type 1 (HIV-1) integrase (IN) protein plays an important role during the early stages of retroviral life cycle and therefore is attractive target for therapeutic intervention. We immunized rabbits with HIV-1 IN developed a combinatorial single-chain variable fragment (scFv) library against IN. Five different scFv antibodies high binding activity specificity were identified. These scFvs recognize catalytic C-terminal domains block strand-transfer process....
Background Type-I interferons (IFN) inhibit HIV replication by inducing the expression of several cellular genes, some which have direct antiviral activity. Forcing to replicate in culture presence IFN is expected lead selection variants with decreased susceptibility. The characterization emerging viral may help identifying nature activities induced capable affecting replication.
Background HIV resistance to the integrase inhibitor raltegravir (RAL) in treated patients is characterized by three main distinct pathways, for which primary mutations are: N155H, Q148H/K/R, or Y143R/H/C. These genotypes may emerge sequentially, always carried viral genomes. The mechanism explaining sequential emergence and vivo dynamics along with escape from RAL treatment are poorly understood. We hypothesize that differences of RAL, must be a direct consequence phenotypic expression...