Biology subjects

Choumet, V.

Publications and source records attributed to Choumet, V..

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

Vector Competence of Temperate and Tropical Mosquito Species for Babanki virus

Babanki virus (BBKV), an alphavirus belonging to the Western Equine encephalitis complex, was isolated from Mansonia africana mosquitoes in 1969 but is not characterized yet. Transmitted to humans and animals through the bite of an infectious female arthropod, it is associated with febrile illness, rash, and arthritis similarly to Sindbis virus to which it is related. No specific treatment or vaccine is available. To investigate any risk of propagation, our study investigated the vector competence of several mosquito species towards BBKV. For this purpose, laboratory mosquito colonies from metropolitan France: Culex pipiens (Paris), Aedes albopictus (Nice) as well as tropical area: Aedes albopictus (Saint-Benoit, La Reunion) and Culex quinquefasciatus (Slab strain), Aedes aegypti (PAEA) were exposed to an artificial blood meal infected with BBKV molecular clone. Midguts, legs, salivary glands and saliva were collected from individual mosquitoes of different strains or species at various time points to assess the infection status, viral replication, and infectiousness. At 7 days post viral exposure, infection rates exceeded 70% in Aedes and 40% in Culex species. They remain above 50% except for Culex quinquefasciatus which decreases to 35% at 14 days post viral exposure. Using genome and protein detection, the dissemination rates are above 50% except for Aedes albopictus (Nice) at 7 days post viral exposure. Infection assays using VeroE6 cells indicated that BBKV replicative viral particles were found in the saliva of the different populations tested. Our data demonstrate that different mosquitoes species from both temperate and tropical areas are competent to transmit BBKV suggesting an emergence risk that could trigger an outbreak in humans. Author SummaryBabanki virus (BBKV) is a non-characterized arbovirus identified in 1969 in Cameroon. BBKV is closely related to Sindbis virus which causes symptoms like febrile illness, rash, and arthritis in humans and animals. Both are alphaviruses within the Western Equine Encephalitis complex. BBKV is identified only in the African continent so far. Despite its potential to cause disease, no effective treatments are available. This study investigates the vector competence of various mosquito species from temperate and tropical regions, to transmit BBKV. After mosquitoes were fed an infectious blood meal, various organs were collected at different time points to assess the infection status, viral replication, and infectiousness. The results showed that BBKV infection occurred in all tested mosquito species and persisted over time, with viral particles detected in mosquito or that can potentially be transmitted to vertebrate hosts via mosquito saliva. These findings highlight the broad vector competence of mosquitoes from diverse climatic regions for BBKV, indicating its potential risk for emergence and outbreaks in different regions of the world. The study emphasizes the need for enhanced surveillance and preventive measures to mitigate the potential threat posed by this emerging virus.

microbiology↗

bioRxiv2024

A recombinant CHIKV-NLuc virus identifies chondrocytes as target of Chikungunya virus in a immunocompetent mouse model

First isolated in 1953 in Tanzania, the arthritogenic Chikungunya virus (CHIKV) re-emerged globally in 2005, leading to widespread outbreaks. Unlike other arboviruses, CHIKV predominantly induces symptomatic infections (72-96%), marked by fever, myalgia, polyarthralgia, and rash. Although rarely fatal, atypical forms such as encephalopathies can occur. Notably, 75.4% of patients experience persistent arthralgias for up to three years after the acute phase. Understanding CHIKVs pathophysiology in the joints is challenging due to the difficulties to obtain biological samples. The study employs a mouse model infected with a reporter virus expressing a Nano Luciferase to investigate the diseases transition to chronic arthritis. The murine model reveals viral replication in metatarsi joints, particularly in chondrocytes, confirmed in primary human chondrocytes undergoing viral-induced apoptosis. Ex vivo analysis confirmed viral replication in leg bones and articular cartilages, with histological evidence of focal erosive lesions and periarticular inflammation. The study further utilizes an in vivo imaging mouse model to monitor viral replication over time. Human chondrocytes prove susceptible to CHIKV infection, exhibiting active viral replication, bioluminescence activity, and increased viral production. CHIKV induced apoptosis, the upregulation of markers associated with cartilage remodeling and altered the cytokine production. This comprehensive study, utilizing advanced techniques and models, provides insights into CHIKVs ability to infect articular cartilages, shedding light on the mechanisms of chronic arthritis following infection.

microbiology↗

bioRxiv2019

Midgut barriers prevent the replication and dissemination of the yellow fever vaccine in Aedes aegypti

BackgroundTo be transmitted to vertebrate hosts via the saliva of their vectors, arthropod-borne viruses have to cross several barriers in the mosquito body, including the midgut infection and escape barriers. Yellow fever virus (YFV) belongs to the genus Flavivirus, which includes human viruses transmitted by Aedes mosquitoes, such as Dengue and Zika viruses. The live-attenuated YFV-17D vaccine has been used safely and efficiently on a large scale since the end of World War II. Early studies have shown, using viral titration from salivary glands of infected mosquitoes, that YFV-17D can infect Aedes aegypti midgut, but does not disseminate to other tissues.\n\nMethodology/Principal FindingsHere, we re-visited this issue using a panel of techniques, such as RT-qPCR, Western blot, immunofluorescence and titration assays. We showed that YFV-17D replication was not efficient in Aedes aegypti midgut, as compared to the clinical isolate YFV-Dakar. Viruses that replicated in the midgut failed to disseminate to secondary organs. When injected into the thorax of mosquitoes, viruses succeeded in replicating into midgut-associated tissues, suggesting that, during natural infection, the block for YFV-17D replication occurs at the basal membrane of the midgut. Our NGS analysis revealed that YFV-Dakar genome exhibited a greater diversity than the vaccine strain; a trait that may contribute to its ability to infect and disseminate efficiently in Ae. aegypti.\n\nConclusions/SignificanceThe two barriers associated with Ae. aegypti midgut prevent YFV-17D replication. Our study contributes to our basic understanding of vector-pathogen interactions and may also aid in the development of non-transmissible live virus vaccines.\n\nAuthor summaryMost flaviviruses, including yellow fever virus (YFV), are transmitted between hosts by mosquito bites. The yellow fever vaccine (YFV-17D) is one of the safest and most effective live virus vaccine ever developed. It is also used as a platform for engineering vaccines against other health-threatening flaviviruses, such as Japanese encephalitis, West Nile, Dengue and Zika viruses. We studied here the replication and dissemination of YFV-17D in mosquitoes. Our data showed that YFV-17D replicates poorly in mosquito midgut and is unable to disseminate to secondary organs, as compare to a YFV clinical isolate. Our study contributes to our basic understanding of the interactions between viruses and their vectors, which is key for conceiving new approaches in inhibiting virus transmission and designing non-transmissible live virus vaccines.

microbiology↗