Potential pathogenic mechanisms involved in the association between lichen planus and hepatitis C virus infection

• Published in: Experimental and therapeutic medicine Vol. 17; no. 2; pp. 1045 - 1051
• Main Authors: Georgescu, Simona Roxana, Tampa, Mircea, Mitran, Madalina Irina, Mitran, Cristina Iulia, Sarbu, Maria Isabela, Nicolae, Ilinca, Matei, Clara, Caruntu, Constantin, Neagu, Monica, Popa, Mircea Ioan
• Format: Journal Article
• Language: English
• Published: Greece Spandidos Publications 01.02.2019; Spandidos Publications UK Ltd; D.A. Spandidos
• Subjects: Antibodies; Antigens; Apoptosis; Autoantibodies; Autoimmunity; B cells; Cancer therapies; Care and treatment; Complications and side effects; Cytotoxicity; Development and progression; Etiology (Medicine); Genotype & phenotype; Geography; Health risk assessment; Hepatitis; Hepatitis C; Hepatitis C virus; Hypotheses; Immune response; Immunoglobulins; Infection; Infections; Inflammation; Interferon; Lichen planus; Liver; Lymphocytes; Medical research; Meta-analysis; Oral cancer; Review; RNA; Skin; Skin diseases; Studies; Viral infections; Virus diseases; Virus replication; Italy; Japan; viral replication; pathogenesis; immune response; lichen planus; hepatitis C
• ISSN: 1792-0981; 1792-1015
• DOI: 10.3892/etm.2018.6987

Lichen planus (LP) is an immune-mediated inflammatory disease that particularly affects the skin and mucous membranes. Its etiology remains elusive, however some trigger factors, including viral or bacterial antigens, drugs and metals, have been postulated. There is a higher prevalence of hepatitis C virus (HCV) infection among patients with LP, with some geographical variations. HCV is an enveloped RNA virus that belongs to the Flaviviridae family and in most instances causes chronic liver infections. It has been hypothesized that HCV may contribute to LP development, but the link between the two disorders is not fully understood. It is still debatable whether HCV leads to the occurrence of LP lesions directly by replication inside the infected cells or indirectly by activating immunological pathways. Molecular studies have revealed HCV RNA in specimens collected from patients with LP. The autoimmune theory was also suggested given that several studies have revealed viral replication and immune response activation associated with autoantibody synthesis. The aim of this review is to summarize the main potential mechanisms involved in the association between LP and HCV infection. Understanding the link between the two disorders may shed some light on the pathogenesis of LP, which is a challenging issue.