Tick-borne encephalitis virus infects human brain microvascular endothelial cells without compromising blood-brain barrier integrity

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00027162%3A_____%2F17%3AN0000103" target="_blank" >RIV/00027162:_____/17:N0000103 - isvavai.cz</a>

Nalezeny alternativní kódy

RIV/60077344:_____/17:00479207 RIV/60076658:12310/17:43895485

Výsledek na webu

<a href="http://www.sciencedirect.com/science/article/pii/S0042682217301204?via%3Dihub" target="_blank" >http://www.sciencedirect.com/science/article/pii/S0042682217301204?via%3Dihub</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.viro1.2017.04.012" target="_blank" >10.1016/j.viro1.2017.04.012</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Tick-borne encephalitis virus infects human brain microvascular endothelial cells without compromising blood-brain barrier integrity

Popis výsledku v původním jazyce

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 (> 10(6) pfu/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.

Název v anglickém jazyce

Tick-borne encephalitis virus infects human brain microvascular endothelial cells without compromising blood-brain barrier integrity

Popis výsledku anglicky

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 (> 10(6) pfu/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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

10607 - Virology

Projekt

Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

Návaznosti

P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)<br>I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2017

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Virology

ISSN

0042-6822

e-ISSN

—

Svazek periodika

—

Číslo periodika v rámci svazku

507

Stát vydavatele periodika

US - Spojené státy americké

Počet stran výsledku

13

Strana od-do

110-122

Kód UT WoS článku

000402218500013

EID výsledku v databázi Scopus

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