Abstract

Herpes simplex virus 1 (HSV-1) is wide-spread virus that triggers painful and recurrent infections, as herpes labialis, causing blister lesions on the lip. HSV-1 infection can be a lifelong condition starting from childhood due to the latency of the virus hidden in the trigeminal ganglia. Despite the use of antiviral treatments, there is not a resolutive cure for herpes. In our study, we tested blue light against HSV-1 in a neuronal cellular model, aimed at mimicking the neuronal tropism of HSV-1. Two laser protocols employing continuous wave and pulse modalities were delivered to infected cell cultures and to the virus alone. A significant reduction of viral replication was observed when the beam was directly applied to the virus, along with an increase in cell survival. Our findings, considering the limitation of the still-unknown mechanisms by which the blue light acts on the virus, suggested a potential use of photobiomodulation therapy for clinical applications against herpes labialis in pediatric patients.

Highlights

  • Herpes simplex virus type 1 (HSV-1), a double-strand DNA virus belonging to the Herpesviridae virus family, is a wide-spread viral pathogen that is able to establish life-long infections in humans [1].Generally, HSV-1 is mainly transmitted by mouth-to-mouth contact, through exposure to sores, saliva and surfaces in or around the mouth

  • We previously reported the antiviral effect of blue laser light on HSV-1 in an epithelial cellular model of infection [13]; in the present study blue Photobiomodulation therapy (PBMT) was tested against HSV-1 in vitro in a neuronal model of HSV-1 infection, with the aim of mimicking the neuronal tropism of HSV-1

  • The following protocols were tested to determine the doses tolerated by the cells: λ, 445; irradiance, 0.3, 0.2, 0.1 W/cm2; fluency, 10, 20 J/cm2 for each irradiance, both in continuous (CW)

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Summary

Introduction

Herpes simplex virus type 1 (HSV-1), a double-strand DNA virus belonging to the Herpesviridae virus family, is a wide-spread viral pathogen that is able to establish life-long infections in humans [1].Generally, HSV-1 is mainly transmitted by mouth-to-mouth contact, through exposure to sores, saliva and surfaces in or around the mouth. From the first site of infection, HSV-1 can assault peripheral sensory nerve endings and establish a latent infection in neuronal cell bodies of the trigeminal ganglia; from here HSV-1 reactivation can result in the spread of the virus towards the mucocutaneous region near the mouth. Gingivostomatitis and pharyngitis characterize the first infection, while virus reactivation provokes the recurrent herpes labialis, where cold sores, intraoral mucosal ulcerations/blisters on the mouth or on facial skin occur [1]. It has been estimated by the World Health Organization that immunoglobulin against

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