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The role of the Transient Receptor Potencial vanilloid-1 in the induction and maintenance of herpetic- and post-herpetic neuralgia.

Grant number: 15/22182-9
Support type:Scholarships in Brazil - Scientific Initiation
Effective date (Start): February 01, 2016
Effective date (End): January 31, 2017
Field of knowledge:Health Sciences - Pharmacy
Principal Investigator:Thiago Mattar Cunha
Grantee:Janaina de Andrade Pereira
Home Institution: Faculdade de Medicina de Ribeirão Preto (FMRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil
Associated research grant:11/19670-0 - Mechanisms involved in the pathophysiology of rheumatoid arthritis, pain and sepsis, AP.TEM

Abstract

Herpetic neuralgia (HN) is characterized by a painful vesicular rash resulting from Varicella Zoster virus (VZV) reactivation in dorsal root ganglia (DRGs) or the cranial nerves, decades after the primary infection. However, even after the rash resolution, pain may persist for months or even years, characterizing the post-herpetic neuralgia (PHN). Infection with herpes simplex virus type-1 (HSV-1) is used as the animal model of HN and PHN. The virus equally infects humans and rodents and is from the same family as VZV. It is described that innate and adaptive immunity are both involved in controlling HSV-1 infection. Furthermore, HSV-1 (and VZV) is able to reach the sensory neurons cell body, which also appears to have an important role during the infection. Interestingly, a subpopulation of these sensory neurons, responsible for pain transmission, express the transient receptor potential V1 (TRPV1). TRPV1 activation is involved in the modulation of inflammatory and neuropathic pain resulting from peripheral nerves injury, and TRPV1 antagonism shows as a promise analgesic tool against different forms of acute and chronic pain. Additionally, this receptor is expressed by non-neuronal cells that act on the immune system, such as glial cells, macrophages and dendritic cells, representing another possible site of HN and PH modulation. Although some studies suggest a possible involvement of TRPV1 receptors in herpetic and post-herpetic neuralgia, little progress has been achieved in order to determine the mechanisms involved in the induction and maintenance of these painful conditions. Thus, the aim of this study was to evaluate the role of TRPV1 receptors in the development of herpetic and post-herpetic hipersensitivity, in order to point the receptor antagonism as a potential new therapeutic target for the treatment of these difficult to treat conditions.