# Immunological Aspects of EBV and Oral Mucosa Interactions in Oral Lichen Planus
## 1 Introduction  
Lichen ruber planus (LP) is a chronic, autoimmune, inflammatory mucocutaneous disease that influences the hair, skin, and nails, as well as the genital, oesophageal, laryngeal, conjunctival, and oral mucosa [1, 2]. Mostly, it is isolated only in the oral cavity without involving the skin or other mucous membranes [3, 4]. According to the literature data, oral lichen planus (OLP) affects 0.2-4% of people [5], occurs more often in individuals between the ages of 30 and 70, and has a female predominance with a ratio of 1.4:1 [6, 7, 8]. Some cases of the disease have been described in children, but it is not common [9, 10]. The aetiology of OLP is unspecified, but an attempt has been made to identify and summarize the possible etiological factors [11]. Possible provocative factors are mentioned several systemic diseases, like hypertension, with chronic inflammation related to other cardiovascular risk factors: dyslipidemia, metabolic syndrome, thyroid and liver dysfunction, diabetes mellitus, kidney disease, celiac disease, and genetic susceptibility to cancer [12, 13, 14]. [PERSON] et al. [15] stated that the current data regarding autoimmune diseasessuch as Sjogren's syndrome, lupus erythematosus, and rheumatic conditions, dermatological diseases, fibromyalgiaalgia and gastrointestinal disorders do not allow conclude whether these diseases are really associated with OLP. Studies on the pathogenesis of OLP may be significantly influenced by Th17 cells and the IL17A polymorphism [15], but connections between 14 functional gene polymorphisms indicate that susceptibility to OLP might be linked to the TNFR2 +587 gene polymorphism [16]. There are studies on the role of vitamin and mineral (nutritional) deficiencies in the development of OLP, suggesting that the severity of OLP may be related to the presence of abnormally high blood homocysteine levels as well as deficiencies in Hb, iron, folic acid, and vitamin B12 [17]. Studies have shown that vitamin D receptor (VDR) variants could affect susceptibility to OLP, making VDR gene polymorphisms possible candidate susceptibility regions for the condition [18]. [PERSON] et al. [19] clarified through meta-analysis that the profile of oxidative stress and antioxidant state markers in OLP patients has been elucidated, revealing heterogeneity among the studies and underscoring the necessity for additional research on oxidative stress and antioxidant systems in both saliva and blood. In recent years, there have been several studies and review articles analyzing the pathogenesis of OLP from a microbiological standpoint, considering the potential for a microbial etiology of the disease [20; 21; 22]. Conflicting studies exist on _H. pylori_ involvement: no statistically significant correlation was found between the presence of the bacteria and OLP [23]. On the other hand, another study has shown a significant correlation between H. pylori infection and the pathogenesis of erosive OLP [24]. Many studies demonstrate that the influence of psychological factors (depression, anxiety, and stress) has not lost its relevance in OLP development, as proved by [25; 26; 27]. [PERSON] et al. [28] expressed the opinion that various external agents, particularly viruses, as well as internal agents such as stress and heat shock protein (HSP) antigen expression, may contribute to the pathogenesis of the condition, whether associated or not, and can trigger OLP. Over the past 10 years, researchers have re-engaged in studies on the potential involvement of viruses in the pathogenesis of OLP [29; 30; 31; 32]. Until now, the hepatitis-C virus (HCV) has been the most studied virus that is connected with the aetiology of OLP. There are a lot of studies devoted to the question of the hepatitis C virus link with LP [33; 34; 35]. It is established that in different geographical locations, the influence of environmental and genetic factors is also different.