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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.

Journal article
Authors Kristina Eriksson
Alexandra Svensson
Alon S Hait
Kerstin Schlüter
Petra Tunbäck
Inger Nordström
Leonid Padyukov
Jan-Åke Liljeqvist
Trine H Mogensen
Søren R Paludan
Published in Journal of immunology (Baltimore, Md. : 1950)
Volume 199
Issue 8
Pages 2613-2617
ISSN 1550-6606
Publication year 2017
Published at Institute of Medicine, Department of Rheumatology and Inflammation Research
Institute of Biomedicine, Department of Infectious Medicine
Pages 2613-2617
Language en
Keywords Adult, Aged, Animals, Cell Line, Cohort Studies, DNA, Viral, immunology, Gene Frequency, Genetic Association Studies, Genotype, Herpes Genitalis, immunology, Herpesvirus 2, Human, immunology, Humans, Interferon-beta, metabolism, Male, Mice, Middle Aged, Nuclear Proteins, genetics, metabolism, Phosphoproteins, genetics, metabolism, Polymorphism, Single Nucleotide, Up-Regulation, Young Adult
Subject categories Other Medical Sciences


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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