Home Acta Virologica 2018 Acta Virologica Vol.62, No.3, p.287-293, 2018

Journal info

Founded: 1957
ISSN 0001-723X
E-ISSN 1336-2305

Published in English

Impact Factor = 1.82

Aims and Scope
Editorial Info

Abstracted and Indexed
Submission Guidelines

Select Journal

Webshop Cart

Your Cart is currently empty.

Info: Your browser does not accept cookies. To put products into your cart and purchase them you need to enable cookies.

Acta Virologica Vol.62, No.3, p.287-293, 2018

Title: Induction and antiviral activity of human β-defensin 3 in intestinal cells with picornavirus infection
Author: W. CHEN, Z. LIU, Q. ZHANG, Q. YAN, S. JING

Abstract: Antimicrobial peptides produced by epithelial and immune cells protect tissues from various infections. Whether enterovirus infection leads to stimulation of antimicrobial peptide expression is unknown. We examined antimicrobial peptide mRNA and protein production in HT-29 colon adenocarcinoma cells infected with picornaviruses. The antiviral activity of increased antimicrobial peptide production was evaluated by using a recombinant peptide and corresponding gene overexpression. Enterovirus infection enhanced both the mRNA expression and secretion of human β-defensin (hBD) 3 in intestinal epithelial cells but did not increase expression of human neutrophil peptide 1–3 (HNP 1–3), HNP4, human defensin 5 (HD5), HD6, hBD1, hBD2, and hBD5. The recombinant but not the intracellularly overexpressed hBD3 inhibited enterovirus (EV) 71, coxsackievirus A16 (CVA16), CVB5 and poliovirus 1 (PV1) infecting HT-29 cells. Our results suggest that enterovirus infection induces hBD3 production in human intestinal epithelial cells and that hBD3 can exert extracellular anti-enterovirus activity.

Keywords: enterovirus; human β-defensin 3; intestinal epithelial cells; antiviral activity
Published online: 30-Aug-2018
Year: 2018, Volume: 62, Issue: 3 Page From: 287, Page To: 293

download file

© AEPress s.r.o
Copyright notice: For any permission to reproduce, archive or otherwise use the documents in the ELiS, please contact AEP.