Biology subjects

Jeannin, P.

Publications and source records attributed to Jeannin, P..

4 recordsLinked to original sources

bioRxiv2026

Characterization of emerging Oropouche virus tropism and pathogenicity.

BackgroundOropouche virus is an emerging arbovirus increasingly associated with neurological complications, but its human cellular tropism and potential routes to the central nervous system remain poorly defined. This study aimed to characterize infection across clinically relevant human cell types and to investigate interactions with a human blood-brain barrier model and human neuronal/glial cells. MethodsA panel of human cell lines and primary human cells relevant to systemic and neurological disease was infected with Oropouche virus. Viral replication and production of infectious particles were quantified using molecular assays and infectivity titrations, and viral protein expression was assessed by immunoblotting and immunofluorescence. Barrier crossing was evaluated using a Transwell brain endothelial model with permeability monitoring, and infection dynamics in neuronal/glial cultures derived from human neural progenitors were quantified by imaging-based analyses. Group comparisons used non-parametric tests with Dunn-Bonferroni correction and Mann-Whitney tests; neuronal/glial cell counts were analysed using linear models with Fisher tests for interaction terms and multiplicity-adjusted post hoc comparisons. ResultsOropouche virus productively infected hepatocyte-like and intestinal epithelial cells, with high viral RNA output and release of infectious progeny. Primary synoviocytes, chondrocytes and skeletal muscle cells were permissive but produced lower infectious titers. Brain endothelial cells were inoculated and virus was progressively detected in the basolateral compartment, while endothelial permeability remained unchanged, indicating barrier crossing without disruption. In neuronal/glial cultures, both neurons and astrocytes were susceptible; infection was associated with marked cytopathic changes and a preferential, accelerated decline in neuron abundance over time. ConclusionsThese findings demonstrate broad human cell tropism and support blood-brain barrier crossing without major loss of barrier integrity, alongside pronounced neuronal vulnerability. The described models provide a platform to dissect mechanisms of neuroinvasion and to evaluate targeted antiviral strategies.

microbiology↗

bioRxiv2025

In vivo risk assessment of yellow fever virus transmission through breastfeeding, and mechanistic insights

Yellow fever virus (YFV), a mosquito-borne flavivirus, remains a significant public health threat, especially in areas with low vaccine coverage. Since 2010, yellowfevervaccination is not recommended for breastfeeding women due to reported cases of vaccine strain transmission through breast milk, leading to neonatal meningoencephalitis. However, the efficiency of YFV vaccine strain transmission via breastfeeding remains unknown, and wild-type strains transmission may be suspected based on viral RNA detection in breast milk. Direct evidence of breastfeeding-related transmission in humans is challenging to obtain given the confounding presence of vector-borne transmission, making animal models crucial for evaluating this risk. In this study, the A129 mouse model was used to investigate YFV transmission via breastfeeding for both wild-type and vaccine strains. Results show that both strains can spread to mammary glands, leading to viral detection in breast milk as free viral particles and cell-associated virus, with similar viral loads for all strains. Mammary stromal and immune cells are primary targets of YFV in vivo, while mammary epithelial cells also support infection, suggesting two possible mechanisms of mammary epithelial crossing. Neonates are found to be susceptible to oral infection, with higher infection rates for the wild-type strain but evidence of neuroinvasion for both strains. Both strains can infect and cross an in vitro human intestinal barrier model, indicating this epithelium as a potential viral entry site for neonates. Finally, this study confirms the existence of YFV transmission through breastfeeding in an animal model, highlighting the need to consider it among transmission risks.

microbiology↗

bioRxiv2022

Transcriptomic landscapes of SARS-CoV-2-infected and bystander lung cells reveal a selective upregulation of NF-κB-dependent coding and non-coding proviral transcripts

Investigations of cellular responses to viral infection are commonly performed on mixed populations of infected and uninfected cells or using single-cell RNA sequencing, leading to inaccurate and low-resolution gene expression interpretations. Here, we performed deep polyA+ transcriptome analyses and novel RNA profiling of SARS-CoV-2 infected lung epithelial cells, sorted based on the expression of the viral spike (S) protein. Infection caused a massive reduction in mRNAs and lncRNAs, including transcripts coding for antiviral factors, such as interferons (IFN). This absence of IFN signaling probably explained the poor transcriptomic response of bystander cells co-cultured with S+ ones. NF-{kappa}B pathway and the inflammatory response escaped the global shutoff in S+ cells. Functional investigations revealed the proviral function of the NF-{kappa}B pathway and the antiviral activity of CYLD, a negative regulator of the pathway. Thus, our transcriptomic analysis on sorted cells revealed additional genes that modulate SARS-CoV-2 replication in lung cells.

microbiology↗

bioRxiv2019

Comparative analysis of neuroinvasion by Japanese encephalitis virulent and vaccine strains in an in cellulo model of human blood-brain barrier

Japanese encephalitis virus (JEV) is the major cause of viral encephalitis in South East Asia. It has been suggested that JEV gets access to the central nervous system (CNS) as a consequence of a preceding inflammatory process which leads to the blood-brain barrier (BBB) disruption and viral neuroinvasion. However, what happens at early times of JEV contact with the BBB is poorly understood. In the present work, we evaluated the ability of both a virulent and a vaccine strain of JEV (JEV RP9 and SA14-14-2, respectively) to cross an in cellulo human BBB model consisting of hCMEC/D3 human endothelial cells cultivated on permeable inserts above SK-N-SH human neuroblastoma cells. Using this system, we demonstrated that both JEV RP9 and SA14-14-2 are able to cross the BBB without disrupting it at early times post-addition. Furthermore, this BBB model was able to discriminate between the virulent RP9 and the vaccine SA14-14-2 strains, as demonstrated by the presence of almost 10 times more RP9 infectious particles that crossed the BBB than SA14-14 particles at a high MOI. Besides contributing to the understanding of early events in JEV neuroinvasion, this in cellulo BBB model represents a suitable and useful system to study the viral determinants of JEV neuroinvasiveness and the molecular mechanisms by which this flavivirus crosses the BBB at early times of neuroinvasion.

microbiology↗