Journal
VIROLOGY
Volume 390, Issue 2, Pages 330-337Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.virol.2009.05.013
Keywords
Human cytomegalovirus; Interleukin 10; Type I interferons; Plasmacytoid dendritic cells
Categories
Funding
- National Institutes of Health [P01 DE016839, R01 A1055881, R01 AI049342, P51 RR000169]
Ask authors/readers for more resources
Type I interferons (IFNs) are innate cytokines with potent antiviral and immunoregulatory activities. It remains unclear how human cytomegalovirus (HCMV) can establish persistence in the face of these strongly antagonistic cytokines. In this study, we confirm that IFN-alpha efficiently suppresses the penetration of HCMV into susceptible cells, including monocytes, the major cell population in peripheral blood that is highly susceptible to HCMV infection. We further demonstrate that the HCMV-derived interleukin 10 (IL-10) homolog functions similar to cellular IL-10 and broadly inhibits TLR-induced transcriptional activation of IFN-alpha/beta genes in plasmacytoid dendritic cells (PDCs), a major type I IFN-producer in vivo that is highly resistant to HCMV infection in vitro. These results suggest that HCMV subverts innate immunity by suppressing type I IFN production of PDCs during primary viral infection via its IL-10 homolog. (C) 2009 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available