This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Shabman, R. S.
Right arrow Articles by Heise, M. T.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Shabman, R. S.
Right arrow Articles by Heise, M. T.

 Previous Article  |  Next Article 

Journal of Virology, December 2008, p. 12374-12383, Vol. 82, No. 24
0022-538X/08/$08.00+0     doi:10.1128/JVI.00985-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.

Ross River Virus Envelope Glycans Contribute to Type I Interferon Production in Myeloid Dendritic Cells{triangledown}

Reed S. Shabman, Kristin M. Rogers, and Mark T. Heise*

Department of Genetics, Department of Microbiology and Immunology, and Carolina Vaccine Institute, University of North Carolina—Chapel Hill, Chapel Hill, North Carolina 27599

Received 12 May 2008/ Accepted 25 September 2008

Alphaviruses are mosquito-transmitted viruses that cause significant human disease, and understanding how these pathogens successfully transition from the mosquito vector to the vertebrate host is an important area of research. Previous studies demonstrated that mosquito and mammalian-cell-derived alphaviruses differentially induce type I interferons (alpha/beta interferon [IFN-{alpha}/β]) in myeloid dendritic cells (mDCs), where the mosquito cell-derived virus is a poor inducer of IFN-{alpha}/β compared to the mammalian-cell-derived virus. Furthermore, the reduced IFN-{alpha}/β induction by the mosquito cell-derived virus is attributed to differential N-linked glycosylation (29). To further evaluate the role of viral envelope glycans in regulating the IFN-{alpha}/β response, studies were performed to assess whether the mosquito cell-derived virus actively inhibits IFN-{alpha}/β induction or is simply a poor inducer of IFN-{alpha}/β. Coinfection studies using mammalian- and mosquito cell-derived Ross River virus (mam-RRV and mos-RRV, respectively) indicated that mos-RRV was unable to suppress IFN-{alpha}/β induction by mam-RRV in mDC cultures. Additionally, a panel of mutant viruses lacking either individual or multiple N-linked glycosylation sites was used to demonstrate that N-linked glycans were essential for high-level IFN-{alpha}/β induction by the mammalian-cell-derived virus. These results suggest that the failure of the mosquito cell-derived virus to induce IFN-{alpha} is due to a lack of complex carbohydrates on the virion rather than the active suppression of the DC antiviral response.


* Corresponding author. Mailing address: Carolina Vaccine Institute, University of North Carolina, Chapel Hill, NC 27599. Phone: (919) 843-1492. Fax: (919) 843-6924. E-mail: heisem{at}med.unc.edu

{triangledown} Published ahead of print on 15 October 2008.


Journal of Virology, December 2008, p. 12374-12383, Vol. 82, No. 24
0022-538X/08/$08.00+0     doi:10.1128/JVI.00985-08
Copyright © 2008, American Society for Microbiology. All Rights Reserved.