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)

One hundred and thirty-four healthy subjects and 220 patients with liver diseases were studied for antibody to hepatitis A virus (anti-HAV) with radio-immunoassay. The frequency of anti-HAV related closely to the age of healthy subjects; the rate of positivity increased with age, being 5.9% in those under four years, 13.3% in the late first decade and over 90% after the third decade. Taking meals at stalls with poor sanitary standards is suspected to cause the prevailing infection in teenagers, although a cohort effect due to environmental and socio-economic improvement can not be excluded. Anti-HAV was present in most patients with frequencies comparable to healthy subjects of the same age. It is concluded that in Taiwan the prevalent chronic liver diseases and hepatocarcinoma are unrelated to HAV infection and the patients are infected to an extent similar to healthy people of the same age.
 ...
PMID:Hepatitis A virus infection in Taiwan. A hospital-based study. 625 86

Hepatitis A virus (HAV) was highly purified from faeces. The genomic RNA was transcribed to cDNA and this DNA was then cloned into plasmid pBR 322 at the Pst I site, and clones were selected in presence of tetracycline. Most clones contained inserts which hybridized to HAV-specific RNA isolated from HAV-infected cell cultures derived from a human hepatocellular carcinoma. Two clones expressed low amounts of viral antigens.
 ...
PMID:Cloning of hepatitis A virus genome. 626 95

human diploid fibroblasts and human primary liver cell carcinoma cells (PLC/PRF/5) were infected with hepatitis A virus (HAV) adapted to growth in cell culture or derived directly from human stool. Viral antigen was expressed in PLC/PRF/5 cells 28 days after infection with cell culture-adapted HAV, and 50 days after infection with virus from human stool. In human fibroblasts the periods until first expression of viral antigen were 90 and 210 days, respectively. During further passages of HAV in fibroblasts the time of first appearance of antigen decreased to about 28 days. Biophysical properties of HAV extracted from infected fibroblasts were comparable to those of HAV derived directly from human stool. Immunofluorescence studies showed that the antigen was located exclusively within the cytoplasm of the infected fibroblasts. Kinetics of antigen production indicated that an equilibrium between virus multiplication and cell metabolism was reached in persistently infected fibroblasts.
 ...
PMID:Propagation of hepatitis A virus in human embryo fibroblasts. 627 Feb 80

Replication of hepatitis A virus (HAV) in the human hepatoma-derived PLC/PRF/5 cell line was neither inhibited in the presence of various concentrations of guanidine or D-2-(alpha-hydroxybenzyl)benzimidazole (D-HBB), nor were the two chemicals effective in combination. Under identical conditions, however, replication of poliovirus type 1 was inhibited. Tracer experiments with radiolabelled guanidine and D-HBB also furnished no evidence that the two antiviral substances were metabolized gradually to inactive derivatives in PLC/PRF/5 cells. Therefore, it is concluded that resistance to the action of guanidine and D-HBB is an inherent characteristic of HAV. However, the insensitivity of HAV to these drugs does not exclude the virus from the family of picornaviruses.
 ...
PMID:Failure of guanidine and 2-(alpha-hydroxybenzyl)benzimidazole to inhibit replication of hepatitis A virus in vitro. 628 46

Dramatic advances in the understanding of the pathogenesis, pathophysiology, prevention, and treatment of the major viral diseases of the liver have been made. Hepatitis B and A viruses have been identified, with specific diagnostic serologic assays commercially available for these infections. The diagnosis of non-A, non-B hepatitis is currently made by exclusion. Morphological alterations in viral hepatitis are similar, regardless of the etiologic agent. Chronic viral hepatitis may be associated with hepatitis B and non-A, non-B, but not with hepatitis A. Persistent infection with hepatitis B virus is associated with an increased incidence of primary hepatocellular carcinoma. Viruses similar to the hepatitis B virus cause the same spectrum of liver disease in certain animals. With the development of a vaccine against hepatitis B virus infection, it may be possible to prevent a large proportion of worldwide chronic liver disease, as well as primary hepatocellular carcinoma.
 ...
PMID:The biology of viral hepatitis. 628 89

Hepatitis A virus (HAV) was propagated in a hepatoma cell line and complete viral particles with a density of 1.34 g/ml were purified from cell extracts. The topography of the viral proteins (VPs) was studied by surface labelling with 125I and a solid-phase oxidant. The order of labelling intensity in complete particles was VP1 much greater than VP3 greater than VP2; labelling of VP4 was undetectable. When the particles were denatured with sodium dodecyl sulfate at 100 degrees C before iodination, the labelling efficiency was 6 times higher and the order of labelling intensity was VP3 greater than VP2 greater than VP1. After denaturation, the viral proteins no longer reacted with human anti-HAV antibody. The results suggest that (i) as with other picornaviruses, HAV exposes an essential part of VP1 at its surface whereas VP3 and especially VP2 are more hidden; (ii) naturally immunized individuals do not form detectable amounts of antibodies against the denatured capsid proteins. The apparent molecular weights of the VPs were 33000, 29000 and 28000 daltons.
 ...
PMID:Topology and immunoreactivity of capsid proteins in hepatitis A virus. 631 Mar 55

The worldwide importance of human hepatitis B virus infection and the toll it takes in chronic liver disease, cirrhosis and hepatocarcinoma, make it imperative that a vaccine be developed for worldwide application. Human hepatitis B vaccines are presently prepared using hepatitis B surface antigen (HBsAg) that is purified from the plasma of human carriers of hepatitis B virus infection. The preparation of hepatitis B vaccine from a human source is restricted by the available supply of infected human plasma and by the need to apply stringent processes that purify the antigen and render it free of infectious hepatitis B virus and other possible living agents that might be present in the plasma. Joint efforts between our laboratories and those of Drs W. Rutter and B. Hall led to the preparation of vectors carrying the DNA sequence for HBsAg and antigen expression in the yeast Saccharomyces cerevisiae. Here we describe the development of hepatitis B vaccine of yeast cell origin. HBsAg of subtype adw was produced in recombinant yeast cell culture, and the purified antigen in alum formulation stimulated production of antibody in mice, grivet monkeys and chimpanzees. Vaccinated chimpanzees were totally protected when challenged intravenously with either homologous or heterologous subtype adr and ayw virus of human serum source. This is the first example of a vaccine produced from recombinant cells which is effective against a human viral infection.
 ...
PMID:Human hepatitis B vaccine from recombinant yeast. 631 24

Hepatitis A virus (HAV), obtained from human feces collected 3 days after the onset of jaundice, was propagated in human hepatocarcinoma cells (PLC/PRF/5). In the course of 5 passages, it was released into the supernatant without cytopathic effect. Released HAV was propagated after inoculation into PLC/PRF/5 cells. Its biophysical properties (buoyant density in CsCl: 1, 33 g/cm3; sedimentation coefficient: 155 S) were similar to those of the infectious particle present in the cells or in the stools of patients.
 ...
PMID:[Release of hepatitis A virus into the culture medium, during its replication in PLC/PRF/5 cells]. 631 25

Hepatitis A virus (HAV), when inoculated into cultures of the PLC/PRF/5 cell line which produces the surface antigen of hepatitis B virus (HBsAg), showed growth characteristics different from those of other picornaviruses. Antigen of HAV (HAAg) is expressed only about 10 days after infection. No major impact on the overall macromolecular biosynthesis of the host cells is observed. The growth rate of HAV-infected and uninfected cells was comparable, although the plating efficiency of infected cells was lower. Different hormonal factors were tested for their ability to stimulate viral antigen expression. Dexamethasone or prostaglandin E1 added to the culture medium increased HAAg expression; insulin reduced expression. Persistent infection of hepatoma cells by HAV never led to a cytolytic infection. In temperature-shift experiments, an adverse effect on the expression of HAAg and HBsAg was observed. In all experiments, the amounts of HBsAg in HAV-infected cells were reduced. On the whole, no major influence on host-cell metabolism is observed in cells persistently infected with HAV. Cell-mediated immunological response as a mechanism of pathological changes in HAV-infected liver is, therefore, more likely than a cytopathological effect.
 ...
PMID:Effect of hepatitis A virus infection on cell metabolism in vitro. 636 47

The term viral hepatitis refers to the diseases produced by at least three, and perhaps four or five aetiologic agents that differ in their virologic characteristics, ecologic mechanisms, epidemiologic patterns, and long term consequences. These divergences are now well-defined for hepatitis A virus (HAV) and hepatitis B virus (HBV). HAV is an RNA virus dependent upon consecutive transmission in childhood, and is not associated with long term sequelae. In contrast, HBV is a DNA virus capable of producing a reservoir of chronic human infection from which spread to adults as well as children can periodically occur by a variety of methods. Chronic HBV disease is not only a continuing source of potential viral transmission in the community, but also sometimes results years later in very serious consequences. Continuing destruction of the liver leads to cirrhosis and hepatic failure; in addition, integration of viral DNA into that of the hepatocyte is probably responsible for the high incidence of carcinoma of the liver associated with HBV infection in many areas of the world. The 'third' form of viral hepatitis is termed 'non-A, non-B' (NANB), because it is identified only by serologic exclusion of HAV and HBV infection. Its epidemiologic and clinical characterization are difficult because variations in behaviour in groups of cases suggest that more than one virus is responsible for this negatively defined entity. One or more of the agents leads to chronic infection, but the relative frequency with which it causes chronic active hepatitis or hepatocellular carcinoma cannot yet be stated.
 ...
PMID:Present knowledge of viral hepatitis. 642 53


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>