[Epstein-Barr, hepatitis B and hepatitis C virus infections and their oncogenic potentials]. / Infekcije Epstein barovim, hepatitis B i hepatitis C virusom i njihov onkogeni potencijal.

There are two ways of connecting Epstein-Barr virus (EBV) with the uncontrolled growth of EBV infected B lymphocytes: in case of evident immunosuppression when the control by cellular immunity is missing or in the case of pathological growth of malignant clone as a result of genetic translocations. Today, EBV is linked with the development of lymphomas in immunosuppressed patients, Hodgkin's and Burkitt's lymphoma and nasopharyngeal carcinoma. The presence of EBV genome in these patients can be confirmed in malignant cells, in lower or higher percent, as well as the high titers of antibodies against specific virus antigens. Hepatitis B viral infection (HBVI) of specific chronic course and associated with intensified inflammation and mitotic activity is of one of the most important factors in the appearance of hepatocellular carcinoma. Although the integration of viral DNA in DNA of hepatocytes has been one of the possible preconditions for carcinogenesis, recently a great attention has been paid to the inactivation of p53 suppressor gene, being a transcriptive transactivator. Other possible cofactors of carcinogenesis imply long-lasting viral replication, coinfection with HVB, HCV or HDV, interaction with other chemical carcinogens (hormones, aflatoxin, alcohol and similar). In distinction from other human DNA viruses, Hepatitis C virus (HCV) is a RNA virus which is not integrated in genome of hepatocyte and active replication of virus is maintained even when hepatocellular carcinoma is detected. It has been assumed that HCV inactivate or mutate the gene of tumor suppression p53 in an early stage of hepatocellular carcinoma development.

[Interferon alpha in the treatment of prolonged hepatitis A virus infection]. / Interferon alfa u lecenju protrahovane infekcije virusom hepatitisa A.

Hepatitis A viral infection usually lasts up to 12 weeks, but in 3-16% of patients relapses may occur and the course of the disease is protracted. The outcome of hepatitis A is always good, so that antiviral therapy is not necessary. However, from the aspect of patients with protracted course of the disease up to a year, it might be important to restore clinical recovery in a shorter period of time. Knowing about antiviral and immunomodulatory effects of endogenous interferon (virally activated) in treatment of protracted hepatitis A, we introduced interferon-alpha in the 12th week of the disease and followed-up its effects on the further course of the disease. The study comprised 80 patients with established diagnosis of acute protracted hepatitis A, excluding hepatitis B, Epstein-Barr, cytomegalovirus, adenovirus or toxic liver lesion. In 40 patients treated with interferon we followed up the activity of aminotransferases and persistence of IgM-anti-HAV in correlation with the same parameters in 40 patients treated symptomatically. The registered persistence of aminotransferases' pathological activity was 20:30 weeks (interferon: symptomatic therapy). In greater doses interferon affected the length of persistence IgM-anti-HAV, 20:34 weeks (interferon: symptomatic therapy).