Next Article in Journal
Heterologous Humoral Response against H5N1, H7N3, and H9N2 Avian Influenza Viruses after Seasonal Vaccination in a European Elderly Population
Next Article in Special Issue
The TRIMendous Role of TRIMs in Virus–Host Interactions
Previous Article in Journal
Reemergence of Measles in the Americas: The Genotype B3 2011–2012 Outbreak in Ecuador
Article Menu

Export Article

Open AccessArticle
Vaccines 2017, 5(3), 16; doi:10.3390/vaccines5030016

The Central Conserved Region (CCR) of Respiratory Syncytial Virus (RSV) G Protein Modulates Host miRNA Expression and Alters the Cellular Response to Infection

1
Department of Infectious Diseases, College of Veterinary Medicine, University of Georgia, Athens, GA 30602, USA
2
National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention (CDC), Atlanta, GA 30333, USA
3
Division of Pediatric Infectious Diseases, Emory University Atlanta, Atlanta, GA 30322, USA
*
Author to whom correspondence should be addressed.
Received: 30 March 2017 / Revised: 23 June 2017 / Accepted: 28 June 2017 / Published: 3 July 2017
(This article belongs to the Special Issue Host Responses to Viral Infection)
View Full-Text   |   Download PDF [2128 KB, uploaded 3 July 2017]   |  

Abstract

Respiratory Syncytial Virus (RSV) infects respiratory epithelial cells and deregulates host gene expression by many mechanisms including expression of RSV G protein (RSV G). RSV G protein encodes a central conserved region (CCR) containing a CX3C motif that functions as a fractalkine mimic. Disruption of the CX3C motif (a.a. 182–186) located in the CCR of the G protein has been shown to affect G protein function in vitro and the severity of RSV disease pathogenesis in vivo. We show that infection of polarized Calu3 respiratory cells with recombinant RSV having point mutations in Cys173 and 176 (C173/176S) (rA2-GC12), or Cys186 (C186S) (rA2-GC4) is associated with a decline in the integrity of polarized Calu-3 cultures and decreased virus production. This is accompanied with downregulation of miRNAs let-7f and miR-24 and upregulation of interferon lambda (IFNλ), a primary antiviral cytokine for RSV in rA2-GC12/rA2-GC4 infected cells. These results suggest that residues in the cysteine noose region of RSV G protein can modulate IFN λ expression accompanied by downregulation of miRNAs, and are important for RSV G protein function and targeting. View Full-Text
Keywords: respiratory syncytial virus; RSV; microRNAs; CX3CR1; IFNλ respiratory syncytial virus; RSV; microRNAs; CX3CR1; IFNλ
Figures

Figure 1

This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. (CC BY 4.0).

Supplementary material

Scifeed alert for new publications

Never miss any articles matching your research from any publisher
  • Get alerts for new papers matching your research
  • Find out the new papers from selected authors
  • Updated daily for 49'000+ journals and 6000+ publishers
  • Define your Scifeed now

SciFeed Share & Cite This Article

MDPI and ACS Style

Bakre, A.A.; Harcourt, J.L.; Haynes, L.M.; Anderson, L.J.; Tripp, R.A. The Central Conserved Region (CCR) of Respiratory Syncytial Virus (RSV) G Protein Modulates Host miRNA Expression and Alters the Cellular Response to Infection. Vaccines 2017, 5, 16.

Show more citation formats Show less citations formats

Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Related Articles

Article Metrics

Article Access Statistics

1

Comments

[Return to top]
Vaccines EISSN 2076-393X Published by MDPI AG, Basel, Switzerland RSS E-Mail Table of Contents Alert
Back to Top