Lichen planus (RP) is an immune-mediated inflammatory disease affecting skin, nails, and mucous membranes. Its etiology is unknown, but there are widely recognized trigger factors, including viral and bacterial antigens, drugs, and metals. Patients with RP have the highest prevalence of hepatitis C virus (HCV) infection. HCV is an RNA virus that belongs to the family Flaviviridae and, in most cases, causes chronic liver infections. It is suggested that HCV may contribute to the development of RP, but the relationship between these two diseases is not fully understood. It is debatable whether HCV causes RP directly by replication in infected cells or indirectly by activation of immunological mechanisms. Molecular studies have identified HCV RNA in samples taken from patients with RP. An autoimmune theory is proposed based on reported viral replication and activation of the immune response associated with the synthesis of autoantibodies. This literature review aims to summarize the scientific evidence on potential mechanisms involved in the association of RP and HCV infection. Studying the relationship between these diseases is necessary for understanding the pathogenesis of RP since this dermatosis is an urgent problem of modern dermatovenerology. A clinical case of a rare morphological form of RP in a patient with HCV is presented, clearly illustrating the association between these diseases. New data, concepts, and possible etiopathogenetic associations between CPL and HCV are discussed. Apparently, skin lesions result from an immune response to viral components, not from a direct action of HCV.