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Neurokinin 1 Receptor Signaling Affects the Local Innate Immune Defense against Genital Herpes Virus Infection¹

Alexandra Svensson^2,*, Joanna Kaim^2,, Carina Mallard, Annika Olsson, Ernst Brodin, Tomas Hökfelt^¶ and Kristina Eriksson^3,*

^* Department of Rheumatology and Inflammation Research, Department of Medical Microbiology and Immunology, and Department of Physiology, Göteborg University, Göteborg, Sweden; and Department of Physiology and Pharmacology and ^¶ Department of Neuroscience, Karoliska Institutet, Stockholm, Sweden

We show that genital infection with neurotropic HSV type 2 (HSV-2) induced a significant increase of the neuropeptide substance P (SP) within the genital tract of mice. SP was shown to weakly interfere with the HSV-2 replication. Furthermore, lack of SP signaling through the use of mice deficient in the SP receptor, neurokinin 1 receptor (NK1R), revealed an important role for SP in the innate defense against HSV-2. NK1R-deficient mice had significantly enhanced levels of HSV-2 in the genital tract and in the CNS following infection and a significantly accelerated disease progression, which was associated with an impaired NK cell activity locally in the vagina. Lack of NK1R signaling did, however, not impair the animals’ ability to mount a protective immune response to HSV-2 following vaccination with an attenuated virus. Both NK1R^+/+ and NK1R^–/– mice developed strong HSV-2-specific Th1 T cell responses following vaccination. No genital viral replication was observed in either vaccinated NK1R-deficient or NK1R^+/+ control animals following a genital HSV-2 challenge, and all of these animals survived without any symptoms of disease. In conclusion, the present results indicate that SP and NK1R signaling contributes to the innate resistance against HSV-2 infection in mice.

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