Enterovirus infection and activation of human umbilical vein endothelial cells

✍ Scribed by Salla Saijets; Petri Ylipaasto; Outi Vaarala; Tapani Hovi; Merja Roivainen

• Publisher: John Wiley and Sons
• Year: 2003
• Tongue: English
• Weight: 354 KB
• Volume: 70
• Category: Article
• ISSN: 0146-6615
• DOI: 10.1002/jmv.10413

✦ Synopsis

Abstract

Gastrointestinal tract associated lymphoid tissue is considered to be the main replication site for enteroviruses. In order to invade tissues to reach pancreatic islets, cardiac muscles, and other secondary replication sites, the virus has to survive circulation in the blood and find a way to get through endothelial cells. In the present study, the susceptibility of human endothelial cells to infections caused by human parechovirus 1 and several prototype strains of enteroviruses, representing different species (human poliovirus, human enterovirus B and C), and acting through different receptor families was examined. Primary endothelial cells isolated from human umbilical vein by collagenase perfusion and also an established human endothelial cell line, HUVEC, were used. Primary endothelial cells were highly susceptible to several serotypes of enteroviruses (coxsackievirus A13, echoviruses 6, 7, 11, 30, and poliovirus 1). However, coxsackievirus A 9 and echovirus 1 infected only a few individual cells while human parechovirus 1 and coxsackie B viruses did not show evidence of replication in primary endothelial cells. In general, primary endothelial cells were more sensitive to infection‐induced cytolytic effect than HUVEC. Activation of endothelial cells by interleukin‐1β did not change the pattern of enterovirus infection. Immunofluorescence stainings of infected primary endothelial cells showed that expression of activation markers, E‐selectin, and intercellular adhesion molecule‐1, was clearly increased by several virus infections and the former molecule also by exposing cells to UV‐light inactivated coxsackieviruses. In contrast, human leukocyte antigen‐DR expression was not increased by virus infection. J. Med. Virol. 70:430–439, 2003. © 2003 Wiley‐Liss, Inc.