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Herpesvirus Infections of the Skin
Published in Marie Studahl, Paola Cinque, Tomas Bergström, Herpes Simplex Viruses, 2017
Karan K. Sra, Gisela Torres, Stephen K. Tyring
Herpes gladiatorum, another cutaneous manifestation of HSV-1, is seen in athletes involved in close contact sports, such as wrestling. The infection commonly affects the head or eye but involvement of the extremities and trunk can occur (6). Because the virus is acquired through skin-to-skin contact, it is recommended that infected wrestlers be diagnosed and excluded during an acute outbreak in order to prevent transmission (6). In addition, antiviral therapy (i.e., valacyclovir 500mg every day) may be used to prevent recurrences in those with frequent outbreaks (7).
Aciclovir and Valaciclovir
Published in M. Lindsay Grayson, Sara E. Cosgrove, Suzanne M. Crowe, M. Lindsay Grayson, William Hope, James S. McCarthy, John Mills, Johan W. Mouton, David L. Paterson, Kucers’ The Use of Antibiotics, 2017
Renee-Claude Mercier, Gregory Mertz
Herpetic whitlow responds to aciclovir suppressive therapy and treatment (Laskin, 1985; Schwandt et al., 1987). It is safe to presume that recurrent HSV in other locations (e.g. herpes gladiatorum) would also respond to aciclovir treatment and/or chemosuppression.
Current vaccine approaches and emerging strategies against herpes simplex virus (HSV)
Published in Expert Review of Vaccines, 2021
Vindya Nilakshi Wijesinghe, Isra Ahmad Farouk, Nur Zawanah Zabidi, Ashwini Puniyamurti, Wee Sim Choo, Sunil Kumar Lal
Herpes simplex virus (HSV) is a neurotropic virus [1] belonging to the Herpesviridae family which houses eight different types of viruses for which humans are the primary host [2]. Within this family, the viruses are divided into three different groups – alpha-, beta- and gamma-herpesvirinae [3]. HSV belongs to the subgroup of alphaherpesvirinae and is found in two forms, HSV type 1 (HSV-1) and HSV type 2 (HSV-2) [4], with biological distinctions in where they establish latent infections [5]. HSV-1 and HSV-2 mostly cause mucocutaneous disease as they affect mucous membranes and the skin, particularly, the oral cavity and genital area, respectively. Most HSV-1 infections lead to oral herpes (also referred to as cold sores) though the virus can also be transmitted to the genital area via contact with the oral cavity, causing genital herpes [6], which is more commonly derived from HSV-2 infections [7]. In 2016 alone, approximately two-thirds of people below 50 years of age were infected with HSV-1, amounting to ~3.7 billion affected individuals worldwide, while ~13% of the population suffered from HSV-2 infections [6]. However, most individuals are asymptomatic for both oral and genital forms of the disease, leaving a comparatively small fraction of people who actually display clinical symptoms [6]; i.e. development of febrile vesicular lesions associated with redness and a burning sensation, gradually forming a painful fluid-containing blister around the mouth or genitalia, in the case of both oral and genital herpes [8]. Unfortunately, genital herpes and cold sores are not the only forms of HSV-related diseases. Others include ocular herpes, herpes gladiatorum, herpetic whitlow, neonatal herpes and so on [9].
The intestinal microbial metabolite nicotinamide n-oxide prevents herpes simplex encephalitis via activating mitophagy in microglia
Published in Gut Microbes, 2022
Feng Li, Yiliang Wang, Xiaowei Song, Zhaoyang Wang, Jiaoyan Jia, Shurong Qing, Lianzhou Huang, Yuan Wang, Shuai Wang, Zhe Ren, Kai Zheng, Yifei Wang
Herpes simplex virus type I (HSV-1) is a neurotropic virus that causes several diseases, including herpes simplex encephalitis (HSE), keratitis, oral or facial lesions (Herpes labialis), and skin lesions (Herpes gladiatorum)1. Neuronal infection of HSV-1 also implicates in the pathological development of neurodegenerative diseases, such as Alzheimer’s disease and Parkinson’s disease.1,2 Despite improvements in antiviral treatment, HSE is still associated with neurological disorders and high mortality, especially in immunocompromised adults and newborns. Fatal HSE mainly results from immune pathology rather than virus replication-induced damage and different outcomes in HSE tropism following HSV-1 infection depend on the innate immune response controlling HSV-1 early dissemination in the central nervous system (CNS).3,4 It has recently emerged that different cell types adapt different antiviral innate signals to restrict HSV-1 replication and prevent HSE, among which microglia plays a central role.5–11 For instance, neurons and astrocytes utilized RNA-sensing TLR3 pathway,6–10 whereas microglia stimulated type I IFN-mediated antiviral action and enabled innate sensing pathway of other cell types in DNA-sensing cGAG-STING-dependent manner.11 Importantly, microglia induced antiviral response when challenged with lower HSV-1 doses, whereas underwent cGAS-dependent apoptosis at high virus loads to limit excessive type I IFN production and the augment of HSE pathology.12 Besides, microglia proliferation at early stage of HSE requires the activation of the macrophage colony-stimulating factor (MCSF)/macrophage colony-stimulating factor 1 receptor (CSF1R) axis.13 However, the regulatory mechanisms limiting microglia over-activation are unclear, and the acquired environmental or genetic factors that balance the beneficial or detrimental immune responses in microglia and how this response restricts HSV-1 level and HSE progression remain poorly explored.