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J Immunol. 2017 Oct 15;199(8):2613-2617. doi: 10.4049/jimmunol.1700385. Epub 2017 Sep 11.

Cutting Edge: Genetic Association between IFI16 Single Nucleotide Polymorphisms and Resistance to Genital Herpes Correlates with IFI16 Expression Levels and HSV-2-Induced IFN-β Expression.

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Department of Rheumatology and Inflammation Research, University of Gothenburg, 40530 Gothenburg, Sweden.
Department of Infectious Diseases, Aarhus University Hospital, 8200 Aarhus, Denmark.
Department of Dermatovenereology, Sahlgrenska University Hospital, 41345 Gothenburg, Sweden.
Rheumatology Unit, Department of Medicine, Karolinska University Hospital, Solna, 17176 Stockholm, Sweden.
Department of Infectious Diseases, University of Gothenburg, 41346 Gothenborg, Sweden; and.
Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark.
Department of Biomedicine, Aarhus University, 8000 Aarhus, Denmark


IFN-γ-inducible protein 16 (IFI16) is an immunological DNA sensor proposed to act in the cyclic GMP-AMP synthase-stimulator of IFN genes pathway. Because mice do not have a clear ortholog of IFI16, this system is not suitable for genetic studies of IFI16. In this study, we have compared the dependency on IFI16, cyclic GMP-AMP synthase, and stimulator of IFN genes for type I IFN induction by a panel of pathogenic bacteria and DNA viruses. The IFN response induced by HSV-2 was particularly dependent on IFI16. In a cohort of patients with genital herpes and healthy controls, the minor G allele of the IFI16 single nucleotide polymorphism rs2276404 was associated with resistance to infection. Furthermore, the combination of this allele with the C allele of rs1417806 was significantly overrepresented in uninfected individuals. Cells from individuals with the protective GC haplotype expressed higher levels of IFI16 and induced more IFN-β upon HSV-2 infection. These data provide genetic evidence for a role for IFI16 in protection against genital herpes.

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