Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019204 (hepatocellular carcinoma)
 71,386 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Chronic infection with hepatitis B viruses (hepadnaviruses) is a major cause of hepatocellular carcinoma (HCC), but the incubation time varies from 1 to 2 years to several decades in different host species infected with indigenous viruses. To discern the influence of viral and host factors on the kinetics of induction of HCC, we exploited the recent observation that ground squirrel hepatitis virus (GSHV) is infectious in woodchucks (C. Seeger, P. L. Marion, D. Ganem, and H. E. Varmus, J. Virol. 61:3241-3247, 1987) to compare the pathogenic potential of GSHV and woodchuck hepatitis virus (WHV) in chronically infected woodchucks. Chronic GSHV infection in woodchucks produces mild to moderate portal hepatitis, similar to that observed in woodchucks chronically infected with WHV. However, HCC developed in GSHV carriers about 18 months later than in WHV carriers. Thus, although both viruses are oncogenic in woodchucks, GSHV and WHV differ in oncogenic determinants that can affect the kinetics of appearance of HCC in chronically infected animals.
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PMID:Woodchuck hepatitis virus is a more efficient oncogenic agent than ground squirrel hepatitis virus in a common host. 200 38

Recent studies suggest that hepatitis B virus (HBV), despite being a DNA virus, replicates via an RNA intermediate (R. H. Miller, P. L. Marion, and S. W. Robinson, Virology 139:64-72, 1984; J. Summers and W. S. Mason, Cell 29:403-415, 1982). The HBV life cycle is therefore a permuted version of the RNA retroviral life cycle. Sequence homology between retroviral reverse transcriptase and the putative HBV polymerase gene product suggests the presence of an HBV reverse transcriptase (H. Toh, H. Hajashida, and T. Miyata, Nature (London) 305:827-829, 1983). As yet, there has been no direct evidence that reverse transcriptase activity is present in the viral particle. We used activity gel analysis to detect the in situ catalytic activities of DNA polymerases after sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Our studies demonstrated that HBV-like particles secreted by a differentiated human hepatoma cell line transfected with genomic HBV DNA contain two major polymerase activities which migrate as approximately 90- and approximately 70-kilodalton (kDa) proteins. This demonstrated, for the first time, that HBV-like particles contain a novel DNA polymerase-reverse transcriptase activity. Furthermore, we propose that the 70-kDa reverse transcriptase may be produced by proteolytic self-cleavage of the 90-kDa precursor protein.
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PMID:Two proteins with reverse transcriptase activities associated with hepatitis B virus-like particles. 244 93

HIV and hepatitis B virus (HBV) coinfection increases HIV and HBV replication, hepatitis flares, and risk of progression to chronic HBV infection, cirrhosis, and hepatocellular carcinoma. HIV and HBV coinfection decreases frequency of hepatitis Be antibody (anti-HBe) and hepatitis B surface antibody (anti-HBs) seroconversion, increases risk of antiretroviral therapy-related hepatotoxicity, and reduces efficacy of HBV therapy. All newly diagnosed HIV patients should be screened for hepatitis A, B, and C viruses and vaccinated if not immune to hepatitis A or B viruses. HBV serology often is atypical in coinfection. Diagnosis of HBV coinfection in HIV infection is made on the basis of hepatitis B surface antigen (HBsAg)-positive, hepatitis B core antibody (anti-HBc total)-positive, anti-HBs-positive status. Alanine aminotransferase levels in coinfected patients often are not reliable markers of liver inflammation. HBV infection should always be treated if coinfected patients are receiving antiretroviral therapy, since immune reconstitution under antiretroviral therapy poses risk for immune-associated liver damage in these patients. This article summarizes a presentation on HIV and HBV coinfection made by Marion G. Peters, MD, at an International AIDS Society-USA Continuing Medical Education course in San Francisco in May 2007.
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PMID:Diagnosis and management of hepatitis B virus and HIV coinfection. 1807 52

Hepatitis B virus (HBV) infection is a lifelong dynamic disease that can be controlled with treatment but cannot yet be cured. Risk of end-stage liver disease and hepatocellular carcinoma (HCC) increases with ongoing inflammation and HBV viremia. Initial treatments consist of tenofovir or entecavir. Patients who require treatment include those with chronic hepatitis, cirrhosis, HCC, or HIV coinfection; patients receiving immunosuppressive treatments; and women in the third trimester of pregnancy who have elevated HBV DNA level. A number of virologic and host immune approaches are being investigated with the aim of achieving HBV eradication. This article summarizes an IAS-USA webinar given by Marion G. Peters, MD, on June 14, 2018.
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PMID:Hepatitis B Virus Infection: What Is Current and New. 3064 84