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Biomedical subjects

F Deinhardt

Publications and source records attributed to F Deinhardt.

At least 199 records · Page 11Linked to original sources
PubMed1982

Viral hepatitis.

THREE FORMS OF VIRAL HEPATITIS CAN BE RECOGNIZED: hepatitis A, hepatitis B, and hepatitis non-A, non-B. Hepatitis A is caused by a picornavirus, is transmitted by the faceal-oral route, does not become chronic, and no chronic virus carriers exist. The virus can be grown in cell cultures, and killed as well as live attenuated virus vaccines are under development. Hepatitis B is caused by an enveloped virus containing a circular, double-stranded form of DNA. The disease is transmitted parenterally through inoculation of blood or blood products containing virus or through close personal contact with a virus-positive person. Hepatitis B becomes chronic in a certain number of cases and can lead to cirrhosis and primary liver cell carcinoma. The blood and certain body secretions of individuals with a persistent or chronic infection may remain infectious for many years. The hepatitis B virus cannot be grown in cell cultures but the entire genome has been sequenced and cloned in bacterial and eukaryotic cells. An inactivated virus vaccine has been prepared from hepatitis B surface antigen present in the plasma of hepatitis B virus carriers and further vaccines are under development. The agents of hepatitis non-A, non-B have not been identified. It is possible to distinguish between a predominantly parenterally transmitted and an orally transmitted form of hepatitis non-A, non-B. The latter is reported to be caused by a picornavirus that does not, however, have any antigenic relationship with hepatitis A virus.

Hepatitis A↗
PubMed1981

[Hepatitis B vaccine trial in healthy adults - an immunogenicity study (author's transl)].

The clinical and immunological response in healthy adults to active and passive - active immunization with a vaccine prepared from purified HBsAg (Merck Sharp and Dohme) in combination with a hepatitis B immune serum globulin (HBIG) were determined and compared with each other. The subjects were randomly assigned to one of three groups: group I received 3 doses of vaccine (20 micrograms per dose) at 0, 1 and 6 months, group II received in addition with the first dose of vaccine 3 ml of HBIG and group III received HBIG together with the first and the second doses of vaccine. No serious side effects were seen during the observation period. Antibody response was comparable in all three groups after 6 months, showing that the passive antibodies did not interfere with active antibody formation. Our results also prove the safety and efficacy of the hepatitis B vaccine and establish the feasibility of passive-active immunization.

Antibody Formation↗
PubMed1981

[Epidemiology of tick-borne encephalitis in Southern Germany (author's transl)].

A recently developed sensitive enzyme immunoassay for the detection of IgM antibodies to tick-borne encephalitis (TBE) virus was used to reinvestigate sera of patients with the clinical diagnosis of meningitis or encephalitis but without conclusive results in the complement fixation assay for TBE virus. 62 cases with sera positive for IgM antibodies to TBE virus collected from 1976 to 1980 were evaluated with regard to clinical and epidemiological aspects of the disease. Of the 62 cases, 37 had apparently been bitten by ticks. The mean age of the patients was 34 years. After a mean incubation period of 12 days (6-21 days) nearly all patients had severe headache and meningitis, in most cases connected with high fever. In 4 patients (6.4%) a serious clinical picture with incomplete recovery was observed. One patient died. Infection peaks occur in July and October. The place of infection or residence was predominantly in southeast Bavaria.

Adolescent↗
PubMed1981

Serological diagnosis of acute tick-borne encephalitis by demonstration of antibodies of the IgM class.

A sensitive enzyme immunoassay is described for demonstrating specific antibodies of the IgM class to tick-borne encephalitis virus (anti-TBEV IgM). Anti-mu-coated, flat-bottomed microtiter plates are incubated with diluted patients' serum (2 hr at 37 degrees C), then with purified TBEV, and later with peroxidase-coupled anti-TBEV immunoglobulin for a further 2 hr. After washing the plates, orthophenylenediamine is added and the optical density is measured at 510 nm. At an early stage after onset of illness anti-TBEV IgM could be demonstrated up to serum dilutions of 10(-4). The specificity of the test system was shown by total inhibition of the positive reaction by preincubation of patients' sera with anti-mu. Tick-borne encephalitis (TBE) could be diagnosed serologically in 54 patients by the described method, and anti-TBEV IgM could be demonstrated in sera drawn up to 9 months after onset of illness. A peak in the number of infections occurs in the age group of 31-40 years, and most infections occur from June to October with a small peak in July.

Adolescent↗
PubMed1981

Propagation of hepatitis A virus in human embryo fibroblasts.

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.

Antigens, Viral↗
PubMed1981

Cloning of hepatitis A virus genome.

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.

Base Sequence↗
PubMed1981

The physicochemical properties of infectious hepatitis A virions.

The propagation of hepatitis A virus (HAV) in the cell line PLC/PRF/5 made possible the radiolabelling in vivo of mature, infectious hepatitis A virions and the determination of their physicochemical properties. In contrast to poliovirus type 2 (160S, 1.340 g/ml), HAV had a sedimentation coefficient of 156 +/- 2S and a buoyant density of 1.332 g/ml in CsCl. The genome of HAV consisted of linear single-stranded RNA which sedimented at 32.5S under non-denaturing conditions. Compared to the size and sedimentation behaviour of poliovirus RNA (2.6 X 10(6) mol. wt., 35S) this corresponds to a mol. wt. of 2.3 X 10(6). Electrophoresis under fully denaturing conditions, however, revealed a mol. wt. of 2.8 X 10(6) and indicates the existence of relatively extended regions with secondary structure. The purified virus genome, containing a poly(A) sequence, served as a messenger for the synthesis of virus antigen in PLC/PRF/5 cells. Finally, in accordance with previous observations, the capsid of the virion was found to be constructed of three major polypeptides (VP1, 31 X 10(3); VP2, 26 X 10(3); VP3, 21 X 10(3) mol. wt.) and of two less readily demonstrable components probably corresponding to VP4 (8 X 10(3) to 10 X 10(3) mol. wt.) and the precursor polypeptide VP0 (40 X 10(3) mol. wt.).

Antigens, Viral↗