Abstract
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.
Highlights
Genital herpes is a common sexually transmitted disease (STD) caused mainly by herpes simplex virus type 2 (HSV2) and, with lower incidence, by herpes simplex virus type 1 (HSV-1) [1]
We have recently shown that secreted glycoprotein G from herpes simplex virus type 2 (HSV-2) (SgG2) binds nerve growth factor (NGF) and alters NGF-dependent Tyrosine kinase receptor for NFG (TrkA) activation
These results suggest that SgG2-NGF interaction alters thermal pain sensitivity, affecting the phosphorylation and spatio-temporal levels of TrkA and transient receptor potential vanilloid 1 (TRPV1) in a complex scenario
Summary
Genital herpes is a common sexually transmitted disease (STD) caused mainly by herpes simplex virus type 2 (HSV2) and, with lower incidence, by herpes simplex virus type 1 (HSV-1) [1]. Both viruses initially infect epithelial cells within the skin and the mucosa during primary infection. Each type of nociceptor expresses a subset of receptors that responds to tissue damage caused by chemical, mechanical, or thermal stimulation. These receptors are activated once the stimulus reaches a certain threshold that is considered harmful. Several factors are secreted by damaged tissue and/or by immune cells that regulate nociceptors, decreasing the threshold of pain receptors
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