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Biomedical subjects

M Roggendorf

Publications and source records attributed to M Roggendorf.

At least 199 records · Page 11Linked to original sources

Demonstration of a transient rheumatoid factor in the acute phase of hepatitis non A, non B.

The evaluation of an enzyme-linked immunosorbent assay (ELISA) test designed to detect antigens of hepatitis non A, non B (HNANB) revealed that a rheumatoid factor (RF)-like reaction was interfering. This RF-like reaction was not detectable by routine screening methods for RF, such as latex agglutination or the Waaler Rose test. Testing of sequential sera of chimpanzees with acute HNANB showed that this RF-like reaction was present in the acute phase of HNANB simultaneously with alanine aminotransferase (ALT) elevations. Characterization of this RF-like reaction revealed the presence of an IgM antibody against human IgG that banded in CsCl at 1.3 g/ml and at 19S in sucrose gradients. Absorption with IgG-coated latex particles and anti-human IgM gave further evidence of an RF. By testing sera of patients with different forms of acute viral hepatitis, it was demonstrated that an RF-like factor was also present in seven sera from 9 patients with acute hepatitis A, in two sera from 11 patients with hepatitis B, and seven sera from 11 patients with acute HNANB. The rise of RF in the acute phase of hepatitis A may be an effect of polyclonal stimulation of IgM producing B lymphocytes. The high prevalence of RF in HNANB remains unclear as no polyclonal stimulation of IgM has been observed.

Alanine Transaminase↗

What's new in hepatitis delta virus?

Seven years of clinical and laboratory research have provided us with a rather good knowledge of the infectious agent that causes hepatitis delta. This agent is a small RNA containing virus (hepatitis delta virus), which is functionally incomplete and needs the help of hepatitis B virus for infection and replication. It is unique also in respect to its RNA, which is smaller than the RNA of every other known RNA virus, but larger than the RNA of the viroids of higher plants. Animal experiments as well as clinical studies showed that hepatitis delta virus infection can be transmitted either simultaneously with hepatitis B, leading to a clinical picture which usually resembles that of hepatitis B alone, or as superinfection of a chronic HBsAg-carrier. The latter often leads to severe, and sometimes fatal, acute hepatitis, followed by chronic liver disease in as many as 30-40% of cases. The hepatitis delta virus is distributed world-wide, showing a high endemicity in Italy and some Arab countries, but also in certain risk groups such as intravenous drug addicts and haemophilics. Further epidemiological studies will probably reveal other foci where the hepatitis delta virus is endemic; especially in Africa, areas of high endemicity of hepatitis delta virus are suspected. Extensive research on delta agent is continuing: further clinical studies, using the highly sensitive method of DNA-RNA-hybridization for the detection of hepatitis delta virus RNA, will tell us more about the role of this virus in acute and chronic hepatitis, and future biochemical and biological research may be expected to increase our insight into the still enigmatic cooperation of the hepatitis delta virus and hepatitis B viruses.

Animals↗

[Hepatitis B and the delta agent].

The delta agent seems to be a defective RNA virus which is dependent on a helper function provided by hepatitis B-virus. Delta agent infection occurs by parenteral transmission either together with hepatitis B-virus, or superimposed on chronic HBV infection. In the first case biphasic hepatitis may result, whereas in the second case mostly an acute delta agent infection develops, which is often followed by chronic delta hepatitis. The delta agent is endemic to certain areas, and also in certain risk groups such as drug addicts, hemophiliacs and polytransfused patients. A delta agent infection should be suspected in case of acute hepatitis in a hitherto clinical inapparent chronic carrier, especially if he belongs to one of the above mentioned risk groups. There is no specific therapy for delta infection, the only prophylactic measure is vaccination against hepatitis B.

Carrier State↗

Community-acquired non-A, non-B hepatitis: clinical characteristics and chronicity.

The characteristics of 86 patients with acute non-A, non-B hepatitis were compared to 23 patients with acute hepatitis A and 76 with acute hepatitis B by medical record reviews of patients seen at 5 hospitals in Baltimore, Maryland, as part of case-control study of viral hepatitis. Results of serum aminotransferase levels, bilirubin, albumin, and prothrombin times alone could not distinguish the type of viral hepatitis because of extensive overlap. The alanine aminotransferase range for non-A, non-B hepatitis was 56 to 1819 IU/liters, for hepatitis A 250 to 1995 IU/liters, and for hepatitis B 203 to 2120 IU/liters. The ranges of aspartate aminotransferase and bilirubin for the types of hepatitis also overlapped. Fewer patients with non-A, non-B hepatitis or hepatitis A had a prolonged prothrombin time compared to patients with hepatitis B. Hepatic encephalopathy was seen only in two patients with hepatitis B. Forty-two percent of non-A, non-B hepatitis patients followed for 6 months or longer continued to have elevated alanine aminotransferase levels. Chronic alanine aminotransferase elevation was independent of the source of infection: transfusion, parenteral drug use, or all other sources. Prolonged follow-up is necessary to evaluate chronicity in patients with non-A, non-B hepatitis.

Alanine Transaminase↗

Detection of hepatitis B viral DNA in sera positive for antibody to delta antigen.

Hepatitis B virus (HBV) DNA was detected in 17 sera positive for antibody to delta antigen (anti-delta). Six sera from two patients were positive for HBV DNA. Analysis by the Southern blot technique showed identity between HBV DNA in anti-delta-positive and anti-delta-negative sera. These results show that anti-delta-positive sera contain HBV DNA, although these sera were also positive for antibodies to hepatitis B e antigen.

DNA, Viral↗

Expression of hepatitis B antigens with a simian virus 40 vector.

Recombinant DNA molecules consisting of the simian virus 40 (SV40) early region and different subgenomic hepatitis B virus DNA fragments were constructed in vitro and packaged in vivo into SV40 capsids by using a complementing SV40 helper virus. Upon infection with these virus stocks the three known hepatitis B-specific antigens were expressed under SV40 control. The surface antigen was released into the medium, and the core antigen and its derivative hepatitis B e antigen were only detected intracellularly. Size analysis of the core gene product(s) by immunoblotting revealed the presence of a single protein species identical with the 21-kilodalton core antigen isolated from human liver. The hepatitis B core antigen expressing construct did not contain a putative precore sequence, indicating that such a sequence is not needed for hepatitis B core antigen synthesis in animal cells. S1 analysis demonstrated the use of SV40 signals for initiation and polyadenylation of the core gene transcripts. In addition, a processing-polyadenylation signal was identified within the core gene.

Cell Line↗

Comparison of hepatitis B core antigens derived from human liver or synthesized in Escherichia coli and evaluation of their use in diagnostic assays for anti-HBc IgM.

Hepatitis B core antigen (HBcAg) synthesized in Escherichia coli (clone PR1-11) was compared with HBcAg purified from a liver obtained at autopsy of a patient with chronic active hepatitis B. The molecular weight determined by SDS-PAGE with subsequent transfer of the proteins to nitrocellulose paper, incubation with 125I anti-HBc and exposure to X-ray film, was about 21,000 for HBcAg synthesized in E. coli and was slightly lower for the liver-derived HBcAg. In CsCl density gradients the liver-derived HBcAg had one peak at 1.32 g/ml, and the HBcAg synthesized in E. coli had two peaks at 1.34 and 1.30 g/ml. In a comparison of the immunological activity of both antigen preparations in an enzyme immunoassay, the liver-derived HBcAg was detected only up to a dilution of 1:320, whereas the HBcAg synthesized in E. coli was detected in dilutions up to 1:100,000. With both antigens, the same percentage of sera were positive for anti-HBc IgM from patients with acute (100%), convalescent (61%), past (5%) and chronic active (29-37%) hepatitis. These results indicate that tests for anti-HBc IgM performed with HBcAg synthesized in E. coli are at least as sensitive and specific as those using liver-derived HBcAg.

Antibodies, Viral↗

Enzyme-linked immunosorbent assay for acute adenovirus infection.

An enzyme-linked immunosorbent assay (ELISA) is described for demonstrating antibodies to the hexone antigen of adenoviruses. The antigen-coated, flat-bottomed microtiter plates are incubated sequentially with dilutions of patients' sera (2 h at 37 degrees C) and peroxidase-coupled anti-human IgG (2 h at 37 degrees C). After a final washing, orthophenylenediamine is added to the plates, and the absorbance (A) measured 30 min later. The ELISA was found to be a hundred-fold more sensitive than complement fixation. An evaluation methods for determining antibody concentration is described which correlates the absorbance of sera diluted 10(-3) to the absorbance of a reference serum containing an arbitrary value (100) of antibody. This methods avoids titration of sera and day-to-day assay variations by different background reactions. A significant increase in antibody concentration of acute-phase serum over that of convalescent phase serum is observed. The ability to test sera in a single dilution and the automatic reading of results and their evaluation by computer make this assay suitable for diagnostic laboratories.

Adenoviridae Infections↗

[Laboratory procedures in adenoviruses. VIII. Immunoglobulin class-specific ELISA for the demonstration of antibodies against adenovirus hexon].

Serum pairs from 114 patients with adenovirus infections (mostly ocular disease in adults) were investigated by an ELISA, with purified adenovirus 5 hexon coated to the solid phase, diluted sera, and peroxydase-labeled antihuman IgG, IgA, and IgM antibodies. Serum dilutions of 1:3200, 1:200, and 1:100 respectively proved to be optimal to demonstrate antibody rises. Sera from infants served as negative controls. Antibody rises were found in the IgG and/or IgA test 85% of the patients, but only in 56% by complement fixation. Antibody rises in all three ELISA tests occurred mostly around the 10th day after onset of disease. Fewer antibody rises and weak reactions were found in IgM test. Moreover, IgM antibodies were present also in persons without fresh adenovirus infection. Hence, this test is not suitable for an early diagnosis. This observation is probably due to the frequent stimulation of the immune system by the genusspecific determinant alpha of the hexon by repeated adenovirus infections during life.

Adenoviridae Infections↗

[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↗