ArticleScientific reports2017
Access to a main alphaherpesvirus receptor, located basolaterally in the respiratory epithelium, is masked by intercellular junctions.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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20 citing papers in PubMed, 38 citations in OpenAlex.
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- Primary cell culture systems to investigate host-pathogen interactions in bacterial respiratory tract infections of livestock.Frontiers in cellular and infection microbiology · 2025Review
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- Pseudorabies virus infection increases the permeability of the mammalian respiratory barrier to facilitatemSphere · 2024Article
- Aspergillus Fumigatus Spore Proteases Alter the Respiratory Mucosa Architecture and Facilitate Equine Herpesvirus 1 Infection.Viruses · 2024Article
- Update on human herpesvirus 7 pathogenesis and clinical aspects as a roadmap for future research.Journal of virology · 2024Review
- Differential infection behavior of African swine fever virus (ASFV) genotype I and II in the upper respiratory tract.Veterinary research · 2023Article
- Bacterial Toxins fromViruses · 2022Article
- A Live-Attenuated Equine Influenza Vaccine Stimulates Innate Immunity in Equine Respiratory Epithelial Cell Cultures That Could Provide Protection From Equine Herpesvirus 1.Frontiers in veterinary science · 2021Article
- The Pathogenesis and Immune Evasive Mechanisms of Equine Herpesvirus Type 1.Frontiers in microbiology · 2021Review
- Pseudorabies Virus Infection of Epithelial Cells Leads to Persistent but Aberrant Activation of the NF-κB Pathway, Inhibiting Hallmark NF-κB-Induced Proinflammatory Gene Expression.Journal of virology · 2020Article
- An Alphaherpesvirus Exploits Antimicrobial β-Defensins To Initiate Respiratory Tract Infection.Journal of virology · 2020Article
- Porcine rotavirus mainly infects primary porcine enterocytes at the basolateral surface.Veterinary research · 2019Article
- Pollens destroy respiratory epithelial cell anchors and drive alphaherpesvirus infection.Scientific reports · 2019Article
- Unravelling the first key steps in equine herpesvirus type 5 (EHV5) pathogenesis using ex vivo and in vitro equine models.Veterinary research · 2019Article
- Gammaherpesvirus BoHV-4 infects bovine respiratory epithelial cells mainly at the basolateral side.Veterinary research · 2019Article
- EHV-1 Pathogenesis: CurrentFrontiers in veterinary science · 2019Article
- Abortigenic but Not Neurotropic Equine Herpes Virus 1 Modulates the Interferon Antiviral Defense.Frontiers in cellular and infection microbiology · 2018Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The respiratory epithelium of humans and animals is frequently exposed to alphaherpesviruses, originating from either external exposure or reactivation from latency. To date, the polarity of alphaherpesvirus infection in the respiratory epithelium and the role of respiratory epithelial integrity herein has not been studied. Equine herpesvirus type 1 (EHV1), a well-known member of the alphaherpesvirus family, was used to infect equine respiratory mucosal explants and primary equine respiratory epithelial cells (EREC), grown at the air-liquid interface. EHV1 binding to and infection of mucosal explants was greatly enhanced upon destruction of the respiratory epithelium integrity with EGTA or N-acetylcysteine. EHV1 preferentially bound to and entered EREC at basolateral cell surfaces. Restriction of infection via apical inoculation was overcome by disruption of intercellular junctions. Finally, basolateral but not apical EHV1 infection of EREC was dependent on cellular N-linked glycans. Overall, our findings demonstrate that integrity of the respiratory epithelium is crucial in the host's innate defence against primary alphaherpesvirus infections. In addition, by targeting a basolaterally located receptor in the respiratory epithelium, alphaherpesviruses have generated a strategy to efficiently escape from host defence mechanisms during reactivation from latency.
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