Journal
JOURNAL OF NEUROINFLAMMATION
Volume 13, Issue -, Pages -Publisher
BIOMED CENTRAL LTD
DOI: 10.1186/s12974-016-0677-5
Keywords
Herpes infection; Pain sensitivity; Inflammation; Signaling
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Funding
- Spanish Ministry of Science and Innovation [SAF2009-07857, SAF2012-38957, SAF2012-39148-C03-01]
- Instituto de Salud Carlos III (CIBERNED)
- Instituto de Salud Carlos III (Red Espanola de Esclerosis Multiple) [RD12/0032/0014]
- Fundacion Areces
- CIBERNED
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Genital herpes is a painful disease frequently caused by the neurotropic pathogen herpes simplex virus type 2 (HSV-2). We have recently shown that HSV-2-secreted glycoprotein G (SgG2) interacts with and modulates the activity of the neurotrophin nerve growth factor (NGF). This interaction modifies the response of the NGF receptor TrkA, increasing NGF-dependent axonal growth. NGF is not only an axonal growth modulator but also an important mediator of pain and inflammation regulating the amount, localization, and activation of the thermal pain receptor transient receptor potential vanilloid 1 (TRPV1). In this work, we addressed whether SgG2 could contribute to HSV-2-induced pain. Injection of SgG2 in the mouse hindpaw produced a rapid and transient increase in thermal pain sensitivity. At the molecular level, this acute increase in thermal pain induced by SgG2 injection was dependent on differential NGF-induced phosphorylation and in changes in the amount of TrkA and TRPV1 in the dermis. These results suggest that SgG2 alters thermal pain sensitivity by modulating TRPV1 receptor.
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