Tick-borne encephalitis virus infects human brain microvascular endothelial cells without compromising blood-brain barrier integrity
Jazyk angličtina Země Spojené státy americké Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
28432926
DOI
10.1016/j.virol.2017.04.012
PII: S0042-6822(17)30120-4
Knihovny.cz E-zdroje
- Klíčová slova
- Blood-brain barrier, Neuroinfection, Tick-borne encephalitis, Tick-borne encephalitis virus,
- MeSH
- endoteliální buňky virologie MeSH
- hematoencefalická bariéra virologie MeSH
- internalizace viru MeSH
- klíšťová encefalitida virologie MeSH
- lidé MeSH
- mozek krevní zásobení virologie MeSH
- viry klíšťové encefalitidy genetika fyziologie MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Alteration of the blood-brain barrier (BBB) is a hallmark of tick-borne encephalitis (TBE), a life-threating human viral neuroinfection. However, the mechanism of BBB breakdown during TBE, as well as TBE virus (TBEV) entry into the brain is unclear. Here, primary human microvascular endothelial cells (HBMECs) were infected with TBEV to study interactions with the BBB. Although the number of infected cells was relatively low in culture (<5%), the infection was persistent with high TBEV yields (>106pfu/ml). Infection did not induce any significant changes in the expression of key tight junction proteins or upregulate the expression of cell adhesion molecules, and did not alter the highly organized intercellular junctions between HBMECs. In an in vitro BBB model, the virus crossed the BBB via a transcellular pathway without compromising the integrity of the cell monolayer. The results indicate that HBMECs may support TBEV entry into the brain without altering BBB integrity.
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