Viral causes of Vitiligo: A New Perspective for Vitiligo Pathogenesis

Abstract

Vitiligo is an acquired skin depigmenting disorder due to loss of functional melanocytes in the epidermis. Several hypotheses have been proposed to explain its etiopathogenesis; however autoimmune pathomechanisms have been suggested to play an important role in the disease development. Previously, the viral causes of vitiligo have been suggested to be involved in vitiligo pathogenesis, however at present there are no such studies available to elucidate the role of viruses in inducing autoimmune mechanisms in vitiligo. The current article briefly summarizes all previous and currently available such studies involving viruses in vitiligo pathogenesis. The vitiligo being a complex autoimmune disorder and an important disease of research opens a new way to look at the virus based autoimmune mechanisms to cause vitiligo. Short Communication Vitiligo is an acquired, progressive, multifactorial, depigmenting disorder characterized by the appearance of circumscribed white macules in the skin due to chronic, progressive loss of functional melanocytes in the epidermis [1] (Figure 1). The selective destruction of melanocytes results in the development of depigmented patches. As such vitiligo is hardly a disease of medical significance but there is more of a social stigma attached to it because of cosmetic reasons. Although it might be viewed as minor disorder, these patches gradually increase in size and cause lot of psychological stress in the patient, self esteem and social interactions, particularly in patients with deeply pigmented skin [2]. The prevalence studies revealed that the worldwide prevalence of vitiligo ranges between 0.5 and 2% [3]. Based on a few dermatological outpatient records the prevalence of vitiligo in India is found to be 0.46% to 8.8% [4].

Targeting Innate Immunity to Combat Cutaneous Stress: The Vitiligo Perspective

“…Virus infection could thus activate the innate response and potentially trigger a vitiligo flare. There is some evidence that viral infections in a genetically predisposed host may induce excessive ROS production by recruited lymphocytes leading to destruction of epidermal melanocytes (29). Furthermore, IFIH1, encoding intracellular virus sensor MDA5, has been identified as a vitiligo susceptibility gene capable of inducing secretion of CXCL10 and CXCL16 from keratinocytes and inducing infiltration of CD8 + T cells in vitiligo (30).…”

Varicella‐zoster virus in actively spreading segmental vitiligo skin: Pathological, immunochemical, and ultrastructural findings (a first and preliminary study)

“…Few conflicting but not incompatible theories (van Geel et al, 2011 ) were mainly proposed for SV pathogenesis, such as neural mechanism (Arnozan & Lenoir, 1922 ; Gauthier & Benzekri, 2010 ; Koga, 1997 ), somatic mosaicism (Attili & Attili, 2015 ; Ezzedine et al, 2011 ; Taïeb et al, 2008 ; van Geel et al, 2013 ), adhesivity impairment (Grill et al, 2018 ), autoimmunity (Speeckaert et al, 2020 ), and microvascular skin homing (Ogg et al, 1998 ). A viral origin was previously evoked mainly in non‐segmental vitiligo (NSV), but was not histologically demonstrated (Dwiwedi et al, 2018 ; Grimes et al, 1996 ; Iverson, 2000 ). However, a possible role of VZV in SV pathogenesis could be suspected, taking into account its possible tropism for pigment cells (Harson & Grose, 1995 ) and numerous clinical and physio‐pathological similarities with herpes zoster (HZ).…”