Abstract
BackgroundInnate 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.MethodsPeripheral 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.ResultsWe 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.ConclusionsOur 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.
Highlights
Herpes simplex virus 1 (HSV-1) is a common human pathogen that primarily gives rise to orofacial and anogenital infections, which are controlled by the immune system in most cases
To evaluate whether early CC chemokine ligand 3 (CCL3) and CXCL10 chemokine production is dependent on viral replication, we infected cells with replication-impaired UV-inactivated virus
We found that IFI16 is present in human primary macrophages and that type I IFN induced IFI16 protein accumulation (Figure 2A)
Summary
Herpes simplex virus 1 (HSV-1) is a common human pathogen that primarily gives rise to orofacial and anogenital infections, which are controlled by the immune system in most cases. Production of CXC chemokine ligand 9 (CXCL9) and CXCL10 is important for controlling genital infection with HSV. These chemokines mediate recruitment of T lymphocytes and natural killer (NK) cells [6], which are essential for Macrophages are sentinel cells in the innate immune response [10], and human primary macrophages are potent chemokine-producing cells important for controlling HSV infection [5,11,12]. 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 investigated the role of the recently identified innate IFN-inducible DNA receptor IFI16 during HSV-1 infection in human macrophages
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