Evaluation of immune response in dorsal root ganglion of mice infected with Herpes Simplex Virus type 1 (HSV-1) (76.8)

Abstract

Abstract Herpes Zoster (HZ) is a disease caused by reactivation of latent herpesvirus Varicella Zoster in the sensory ganglion, characterized by dermal rash and severe pain. A model of mice infected with HSV-1 on the skin of the hind paw has been used to study the pathophysiology of HZ, since they develop HZ-like skin lesions and pain-related responses. There are no data available about the immune response in dorsal root ganglion (DRG) of these mice. Thus, the aim of this study was to evaluate cells and inflammatory mediators present in DRGs and its relationship with hypernociception during HSV-1 cutaneous infection. Mice developed hypernociception from day 3 to 7 post inoculation in the ipsilateral (Ips) paws, but not in the contralateral (Cl) paws. A higher viral load, measured by qPCR, was detected in DRGs L3, L4 and L5 of infected mice, when compared to control mice or naïve mice. By flow citometry analysis, we observed an inflammatory infiltrate composed by CD4+, CD8+, CD11b and Gr1+ cells in DRGs L3, L4 and L5, but not in spinal cord, that correlated with virus presence previously found. A higher expression of COX-2, IFN-γ, GFAP and IL-22 was detected in the same DRGs of Ips paws from infected mice, when compared to the same ganglion of Cl paws or ganglion from naïve mice. Our results show the presence of an inflammatory infiltrate in DRGs of infected mice and the expression of inflammatory mediators which might contribute for the development of hypernociception.