Florica Stăniceanu *, Sabina Zurac *, A. Streinu Cercel **
* Conf. dr: Fiorica Stăniceanu, dr. Sabina Zurac, Laboratorul de Anatomie Patologică, Spitalul Clinic Colentina, București
** Dr. Adrian Streinu-Cercel, medic primar șef de secție Institutul de Boli Infecțioase Prof. dr. Matei Balș, șef de lucrări UMF Carol Davila, București
Abstract
The capacity of the viruses to induce autoimmunity is well known; this is accomplished by autoreactive T cell activation either by cytokine release stimulation, by antigen mimicry or by superantigen activity with autoreactive lymphocytes stimulation. Autoimmune hepatitis is characterized by the seric presence of high levels of autoantibodies (antinuclear ANA, smooth muscle SMA, liver kidney microsomal antibody, soluble liver antigen, anti GOR (GOR – a host fusion protein expressed by a cDNA derived from HCV infected chimpanzee)); the histopathologic picture is that of a chronic hepatitis with severe necroin flammatory activity and mild fibrosis 1’n the initial stages. The autoimmune disorders documented 1’n HBV infection are less important as those 1’n HCV infection. 5% of the patients with essential mixed cryoglobulinemia have HBV infection. The association with the primary membranoproliferative glomerulonephritis, previously reported1’n large series, proved to be a false positive result. The occurrence of arthritis, artralgia, polyarteritis nodosa, papulous acrodermitis was correlated with HBV infection. The presence of the autoantibodies (ANA, SMA) 1’n chronic hepatitis B is the consequence of the existence of common aminoacidic sequences between the HBV DNA polymerase and nuclear proteins (MHC II transactivator, nuclear pore core protein, nuclear mitotic apparatus, polymyositis sclerosis antigen) and muscular proteins (caldesmon, myosin); 1’n this process is implicated the CD4 positive Th type cellular response (presence of lgG antibodies). Molecular mimicry phenomena are also implicated 1’n the production of cross/reactive antibodies with myelin basic protein (the autoantigen 1’n multiple sclerosis) via 66-75 epitope of HBV-DNA polymerase.