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Open Access Research

HSV-1-induced chemokine expression via IFI16-dependent and IFI16-independent pathways in human monocyte-derived macrophages

Stine Søby, Rune R Laursen, Lars Østergaard and Jesper Melchjorsen*

Author Affiliations

Department of Infectious Diseases, Aarhus University Hospital, Brendstrupgaardsvej 100, Aarhus N, DK-8200, Denmark

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Herpesviridae 2012, 3:6  doi:10.1186/2042-4280-3-6

Published: 14 October 2012

Abstract

Background

Innate recognition is essential in the antiviral response against infection by herpes simplex virus (HSV). Chemokines are important for control of HSV via recruitment of natural killer cells, T lymphocytes, and antigen-presenting cells. We previously found that early HSV-1-mediated chemokine responses are not dependent on TLR2 and TLR9 in human macrophages. Here, we investigated the role of the recently identified innate IFN-inducible DNA receptor IFI16 during HSV-1 infection in human macrophages.

Methods

Peripheral blood mononuclear cells were purified from buffy coats and monocytes were differentiated to macrophages. Macrophages infected with HSV-1 were analyzed using siRNA-mediated knock-down of IFI16 by real-time PCR, ELISA, and Western blotting.

Results

We determined that both CXCL10 and CCL3 are induced independent of HSV-1 replication. IFI16 mediates CCL3 mRNA accumulation during early HSV-1 infection. In contrast, CXCL10 was induced independently of IFI16.

Conclusions

Our data provide the first evidence of HSV-1-induced innate immune responses via IFI16 in human primary macrophages. In addition, the data suggest that at least one additional unidentified receptor or innate sensing mechanism is involved in recognizing HSV-1 prior to viral replication.

Keywords:
Herpes simplex virus; Innate; IFI16; Chemokine; PRR; DNA; Macrophages; Human