New Viral Facets in Oral Diseases: The EBV Paradox

Abstract

The oral cavity contributes to overall health, psychosocial well-being and quality of human life. Oral inflammatory diseases represent a major global health problem with significant social and economic impact. The development of effective therapies, therefore, requires deeper insights into the etiopathogenesis of oral diseases. Epstein–Barr virus (EBV) infection results in a life-long persistence of the virus in the host and has been associated with numerous oral inflammatory diseases including oral lichen planus (OLP), periodontal disease and Sjogren’s syndrome (SS). There is considerable evidence that the EBV infection is a strong risk factor for the development and progression of these conditions, but is EBV a true pathogen? This long-standing EBV paradox yet needs to be solved. This review discusses novel viral aspects of the etiopathogenesis of non-tumorigenic diseases in the oral cavity, in particular, the contribution of EBV in OLP, periodontitis and SS, the tropism of EBV infection, the major players involved in the etiopathogenic mechanisms and emerging contribution of EBV-pathogenic bacteria bidirectional interaction. It also proposes the involvement of EBV-infected plasma cells in the development and progression of oral inflammatory diseases. A new direction for preventing and treating these conditions may focus on controlling pathogenic EBV with anti-herpetic drugs.

COVID-19: A Recommendation to Examine the Effect of Mouthrinses with β-Cyclodextrin Combined with Citrox in Preventing Infection and Progression

“…Moreover, in biofilms, bacteria can escape the immune system producing so-called superantigens [17]. In addition to host-microbe interactions, the interfaces of periodontal pathogens with other non-host pathogens, such as herpesviruses like Epstein-Barr virus and cytomegalovirus, can contribute to the pathogenesis of the periodontal disease [18], or can affect the outcome of viral infection and dissemination [19]. These risks are often significantly underestimated.…”

The association between Epstein‐Barr virus and oral lichen planus: A systematic review and meta‐analysis

“…Given the ubiquitous nature of EBV (with 50‐90% of population being seropositive), detection of EBV dictates the use of highly sensitive laboratory techniques to avoid false‐positive results 19 . In the present review, methods applied to identify EBV were highly variable across the studies: in situ hybridization method in one study, 23 PCR methods in six studies, 15,16,20‐22,29 immunohistochemistry in one study, 14 and serum EBV antibodies (using ELIZA) in two studies 13,28 .…”

“…EBV is a very common pathogen of the oral cavity, with a high salivary and gingival occurrence 19 . It has been shown that EBV preferentially infects B lymphocytes, but it can also infect other cells such as epithelial cells, natural killers cells (NK cells), monocytes, and T‐lymphocytes 19 . EBV has been implicated in pathogenesis of several oral and systemic inflammatory diseases.…”

“…EBV (also known as human herpesvirus 4) belongs to herpesvirus family, and the current evidence indicates that over 90% of the word’s adult population are infected with EBV 17 . EBV has been associated with several benign and malignant head and neck disorders, including infectious mononucleosis, hairy leukoplakia, Sjogren’s syndrome, Burkitt’s lymphoma, Hodgkin’s Lymphoma, and nasopharyngeal carcinoma 17‐19 . Recently, several observational studies have investigated the possible role of EBV in pathogenesis of OLP, and conflicting results were reported 5,13‐15,20,21 .…”

Detection of Epstein–Barr Virus in Periodontitis: A Review of Methodological Approaches

“…Periodontitis was thought to be (i) an infection caused by bacteria; (ii) a specific bacterial infection; (iii) a biofilm infection; (iv) a specific plaque; (v) result from dysbiosis; (vi) caused by complex interactions among bacteria–host–environmental factors and (vii) a viral-bacterial infection (reviewed in [ 5 , 6 ]). One specific recent hypothesis of interest is based on the herpesvirus–pathogenic bacteria–host response axis in which herpesviral–bacterial interactions assume a major etiopathogenic role [ 5 , 7 , 8 , 9 ]. This infectious disease model for periodontitis development proposes that bacteria initiate the gingival inflammation triggering further influx and propagation of herpesviruses.…”