A role for the JAK-STAT1 pathway in blocking replication of HSV-1 in dendritic cells and macrophages

doi:10.1186/1743-422X-6-56

Virology Journal

Volume 6

Viewing options:

Abstract
Full text
PDF (2MB)

Associated material:

Related literature:

Articles citing this article
on Google Scholar
on ISI Web of Science
on PubMed Central
Other articles by authors
on Google Scholar

Mott KR
UnderHill D
Wechsler SL
Town T
Ghiasi H

on PubMed

Mott KR
UnderHill D
Wechsler SL
Town T
Ghiasi H
Related articles/pages
on Google

on Google Scholar

on PubMed

Tools:

Post to:

Research

A role for the JAK-STAT1 pathway in blocking replication of HSV-1 in dendritic cells and macrophages

Kevin R Mott¹ , David UnderHill² , Steven L Wechsler³^,4^,5 , Terrence Town⁶^,7 and Homayon Ghiasi¹

¹Center for Neurobiology & Vaccine Development, Ophthalmology Research, Department of Surgery, Cedars-Sinai Medical Center, Los Angeles, CA, USA

²Immunobiology Research Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA

³The Gavin Herbert Eye Institute, University of California, Irvine, CA, USA

⁴The Department of Microbiology and Molecular Genetics, University of California, Irvine, School of Medicine, Irvine, CA, USA

⁵Center for Virus Research, University of California, Irvine, USA

⁶Departments of Neurosurgery and Biomedical Sciences, Maxine Dunitz Neurosurgical Institute, Cedars-Sinai Medical Center, Los Angeles, CA, USA

⁷Department of Medicine, David Geffen School of Medicine at UCLA, Los Angeles, CA, USA

author email corresponding author email

Virology Journal 2009, 6:56doi:10.1186/1743-422X-6-56


Published:	13 May 2009

Abstract

Background

Macrophages and dendritic cells (DCs) play key roles in host defense against HSV-1 infection. Although macrophages and DCs can be infected by herpes simplex virus type 1 (HSV-1), both cell types are resistant to HSV-1 replication. The aim of our study was to determine factor (s) that are involved in the resistance of DCs and macrophages to productive HSV-1 infection.

Results

We report here that, in contrast to bone marrow-derived DCs and macrophages from wild type mice, DCs and macrophages isolated from signal transducers and activators of transcription-1 deficient (STAT1^-/-) mice were susceptible to HSV-1 replication and the production of viral mRNAs and DNA. There were differences in expression of immediate early, early, and late gene transcripts between STAT1^+/+and STAT1^-/-infected APCs.

Conclusion

These results suggest for the first time that the JAK-STAT1 pathway is involved in blocking replication of HSV-1 in DCs and macrophages.