Publisher Summary This chapter explores and compares different possible mechanisms by which hepadnaviruses maytrigger liver cell proliferation and transformation, and considers the factors that may influence the primacy of some oncogenic pathways over others in tumors induced by different viruses of the same family. Primary hepatocellular carcinoma (HCC) is one of the most common cancers in many parts of the world and is also one of the rare human cancers showing seroepidemiologic association with a viral infection. The role of hepatitis B virus (HBV) as a causal agent of HCC is established and the increased risks of developing HCC are estimated. Productive HBV infections potentiate the action of exogenous carcinogenic factors like aflatoxins and alcohol. The clinical and immunological aspects of HBV infections and their modes of transmission are also discussed as are genetic organization of the HBV genome, genome structure and replication, and regulated expression of viral genes. HBV DNA integration patterns into host-cell DNA have led to a different hypothesis on the contribution of HBV to hepatocarcinogenesis. Hepatitis B is rendered highly contagious by the unusual stability of infectious HBV virions present in the blood and other body fluids like saliva, urine, and semen.

Hepatitis B viruses and hepatocellular carcinoma.

Background The clinical impact and relevance of human herpesvirus-6 (HHV-6) infection in liver transplant recipients, has not been fully discerned. Methods A prospective study of 80 consecutive liver transplant recipients was performed using surveillance cultures for HHV-6 at weeks 2, 3, 4, and 6 after transplantation. Viral isolation was used for the detection of HHV-6. Results HHV-6 infection occurred in 39% (31 of 80) of the patients. Patients with HHV-6 infection were more likely to have hepatocellular carcinoma as underlying liver disease (P=.09). Mental status changes of unidentifiable etiology were significantly more likely to occur in patients with HHV-6 compared with those without (26%, 9 of 31 vs. 6%, 3 of 49, P=.008). HHV-6 infection was an independent predictor of invasive fungal infections (odds ratio 8.3, 95% confidence interval, 1.2-58.0, P=.03). A significant association between HHV-6 infection and CMV infection after transplantation, CMV recipient and donor serostatus, rejection, or fever of unknown origin, could not be documented. Mortality at last follow-up in patients with HHV-6 infection (29%, 9 of 31) was significantly greater than those without HHV-6 (6%, 3 of 49, P=.008). Conclusions Central nervous system complications of unknown etiology after liver transplantation may be related to HHV-6 infection. HHV-6 viremia was an independently significant predictor of invasive fungal infections and was associated with late mortality in liver transplantation recipients.

Human herpesvirus-6 in liver transplant recipients: role in pathogenesis of fungal infections, neurologic complications, and outcome.

Hepatitis B virus (HBV) has been reported to exist in peripheral blood mononuclear cells (PBMC), but it is not clear whether it replicates there. A precondition for replication should be the formation of covalently closed viral DNA and transcription of all essential viral mRNAs. The mRNAs of HBV form a nested box with common 3' ends. In order to detect even low levels of potential replication, we developed a quantitative reverse transcription-PCR method for detection of a smaller HBV mRNA species in the presence of the larger ones. All three highly viremic patients tested so far had mRNAs for the large and the small surface proteins and the X protein of the virus within PBMC but not in the virus from their sera. Furthermore, we detected by PCR covalently closed viral DNA in their PBMC. These data suggest that HBV may be not only taken up but also replicated by mononuclear blood cells and that these cells may be an extrahepatic site of viral persistence. X mRNA was detected in the largest amount. Possibly, X protein interferes with functions of the mononuclear cells during the immune response against the virus.

Transcription of hepatitis B virus in peripheral blood mononuclear cells from persistently infected patients.

Current information on the immunologic status of occult hepatitis B infection.

Death and the retrovirus

. Hepatitis B virus (HBV) DNA sequences have been detected in leucocytes from HBV-infected individuals. The aim of this study was to assess the specificity of HBV for a special leucocyte subset in nine healthy chronic HBV carriers, nine HBs antigen-positive patients with chronic active hepatitis, 16 HBs antigen-negative haemophiliacs with HBc and/or HBs antibodies, and 10 patients with HBV-related systemic necrotizing vasculitis. HBV-DNA sequences were found by Southern blot hybridization in the leucocytes of 15 out of the 44 (34%) patients. The prevalence was not significantly different between the four groups. HBV-DNA was found in the CD4+ cells (9/11) as well as in the CD8+ cells (4/11), B cells (4/12) and monocytes (2/12). In conclusion, leucocytes, and particularly CD4+ lymphocytes, are frequently infected by HBV in patients with HBV serum markers.

Distribution of hepatitis B virus DNA sequences in different peripheral blood mononuclear cell subsets in HBs antigen-positive and negative patients.

Summary. We have tested the different mononuclear blood cell populations of seven patients with severe haemophilia and one patient with F VII deficiency for the presence of HBV DNA. These subjects were all polytransfused with non-heated coagulation factors; three were HBsAg positive, five HBsAg negative but anti-HBc and anti-HBs positive; HBV DNA sequences were detected in six subjects including three without detectable serum HBsAg. Furthermore the viral DNA sequences were identified in the T lymphocyte subpopulations (OKT4+ and/or OKT8+ cells). This observation suggests that HBV infection of lymphocytes might be related to the immunological disorders observed in these patients.

Frequent lymphocytes infection by hepatitis B virus in haemophiliacs.

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Distribution of hepatitis B virus DNA sequences in different peripheral blood mononuclear cell subsets in HBs antigen-positive and negative patients.

Frequent lymphocytes infection by hepatitis B virus in haemophiliacs.