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Biomedical subjects

F Deinhardt

Publications and source records attributed to F Deinhardt.

At least 217 records · Page 12Linked to original sources
PubMed1981

Anti-HBc of IgM-class, HBeAg and anti-HBe in acute and chronic hepatitis B.

The presence and persistence of IgM antibody against hepatitis B core antigen (anti-HBc IgM) and the correlation with other HBV markers were studied in 42 patients, all of whom had acute HBsAg-positive hepatitis but whose subsequent diseases differed. All patients initially had anti-HBc IgM. In 13 out of 15 patients with uncomplicated acute hepatitis, anti-HBc IgM disappeared within 6 months after onset of the disease. In five out of 12 patients, who in spite of transient HBsAg developed chronic liver disease, the anti-HBc IgM persisted for more than 2 years. Among 15 patients with persistent HBsAg, anti-HBc IgM was present from 7 months to more than 8 years. Seroconversion from HBeAg to anti-HBe was observed in seven patients and in five of these anti-HBc IgM disappeared during the follow-up period. These results indicate that anti-HBc IgM can be used as a serological marker of recent or ongoing HBV infection.

Adolescent↗
PubMed1981

Immunoglobulin M antibodies to hepatitis B core antigen: evaluation of enzyme immunoassay for diagnosis of hepatitis B virus infection.

In acute and chronic hepatitis B, antibodies of the immunoglobulin M (IgM) class against the hepatitis B core antigen (anti-HBc IgM) have been demonstrated. For the determination of anti-HBc IgM, a sensitive enzyme immunoassay with anti-mu-coated flat-bottomed microtiter plates is described and evaluated. The specificity of the anti-HBc IgM test system was proven by pretreatment of presumed anti-HBc IgM-positive samples with anti-mu to block anti-HBc IgM. The test system was highly sensitive. In the acute stage of hepatitis B, anti-HBc IgM could be demonstrated in serum dilutions up to 10(-7) (mean titer, 10(-5)), and in sera from patients with chronic hepatitis B, the mean titer was 10(-3). In a study of unselected patients whose sera were sent at irregular intervals for testing, anti-HBc IgM persisted in a high percentage (52%) for at least 13 to 18 months after onset of illness despite the fact that these patients eliminated hepatitis B surface antigen (HBsAg) and produced antibodies to HBsAg (anti-HBs). By using the anti-HBc IgM test as an additional aid in the diagnosis of acute HBsAg-negative hepatitis, the hepatitis B etiology could be established in 13 of 42 patients (31.4%). Investigations of the prevalence of anti-HBc IgM in different groups of patients with chronic hepatitis B infection showed 89.4% anti-HBc IgM-positive results in patients with chronic active hepatitis B, 60% in patients with HBsAg-negative chronic active hepatitis, 58.2% in patients with primary liver carcinoma and markers of hepatitis B infections, and 34.9% in healthy carriers of HBsAg.

Antibodies, Viral↗
PubMed1981

Comparison of two different enzyme immunoassays for detection of immunoglobulin M antibodies against tick-borne encephalitis virus in serum and cerebrospinal fluid.

Two enzyme immunoassays for the detection in immunoglobulin M (IgM) antibodies against tick-borne encephalitis virus were compared, employing a solid phase coated either with antigen or with mu-chain-specific antiserum to human IgM. The latter IgM-capturing assay system proved to be more sensitive, and its superiority was especially prominent when high titers of tick-borne encephalitis virus-specific IgG antibodies in addition to specific IgM antibodies were present in the sample. The application of this test is a valuable extension of the diagnostic tools for the rapid diagnosis of tick-borne encephalitis by IgM detection. Since specific IgG does not interfere, diagnosis can be readily established when patients have already developed high titers of IgG antibodies relatively late after the onset of the disease.

Antibodies, Viral↗
PubMed1981

Characterization and classification of virus particles associated with hepatitis A. III. Structural proteins.

Hepatitis A virus was purified from fecal samples collected at various times in the incubation period of patients with naturally acquired hepatitis A. The proteins of particles banding at around 1.34 g/ml in CsCl and sedimenting at about 160S were radioiodinated in vitro and separated by electrophoresis on polyacrylamide gels in the presence of 0.1% sodium dodecyl sulfate and 8 M urea. Under these conditions, the capsid proteins resolved into four polypeptides with molecular weights of approximately 31,000, 24,500, 21,000, and 9,000, respectively. A fifth protein of about 40,000 daltons in size and assumed to be equivalent to the precursor polypeptide VP0 of the picornaviruses was present in particles sedimenting at only 150 to 155S and banding at around 1.33 g/ml in CsCl. The physicochemical characteristics of these particles are consistent with those of the provirion structures of picornaviruses. In several of the fecal samples, these particles represented a considerable fraction of all particles present. The significance of this finding with respect to the antigenicity of hepatitis A antigen extracted from stool specimens is discussed.

Capsid↗
PubMed1981

Retinoid-induced growth inhibition of herpesvirus-transformed marmoset lymphoblastoid cell lines.

The in vitro proliferation of herpesvirus-transformed marmoset lymphoblastoid cell lines (LCL) was inhibited by retinoic acid and retinyl acetate. Both Herpesvirus-ateles-and Herpesvirus-saimiri-transformed LCL with T-cell characteristics and Epstein-Barr-transformed LCL with B-cell markers were more sensitive to retinoic acid than to retinyl acetate. Inhibition of LCL proliferation was dependent on retinoid concentration and became apparent only after 3-4 days of exposure. In vitro assays for marmoset LCL sensitivity to retinoids may indicate the potential usefulness of these compounds in the chemoprevention of virus-induced lymphoma in vivo.

Animals↗
PubMed1981

Spontaneous generalized Herpesvirus hominis infection of a lowland gorilla (Gorilla gorilla gorilla).

A 13-day-old lowland gorilla died from a generalized herpesvirus infection shortly after the onset of clinical signs. The pathologic-anatomical findings were compatible with those described for generalized herpes simplex infection in the human neonate. Electron microscopic examination of lung tissue revealed the presence of herpesvirus which was identified with the fluorescent antibody technique as Herpes simplex virus type I. Tests with related sera of the herpes group (varicella, herpesvirus-B) revealed no specific immunoflourescence.

Animals↗
PubMed1981

[Epstein-Barr virus--a clinically relevant feature of nasopharyngeal carcinoma? (author's transl)].

Nasopharyngeal carcinoma (NPC) has been linked to Epstein-Barr Virus (EBV) by seroepidemiological evidence and by the regular proof of EBV-DNA in the epithelial tumor cells. We have been able to study the serological parameters of 62 NPC patients of the local ENT-Clinic. All patients were kaukasians in contrast to a previous study by Henle et al. Our results emphasize the remarkable predominance of EBV-IgA antibodies to viral capsid antigen (VCA) and early antigen (EA) in NPC patients and prove the value of the test for the initial diagnosis of the disease. Follow-up studies with subsequent serological tests strongly suggest that this test is related to the stage of the disease. We have also found NPC-typical serological EBV-IgA titers in 3 lymphoepithelial carcinomas of the tonsil and the soft palate. Similar titers have been found in two cases of poorly differentiated carcinomas of the base of the tongue. All these tumors arise in the lymphoepithelial tissue of Waldeyer's ring. We conclude that possibly some carcinomas of Waldeyer's ring are similarly related to EBV as nasopharyngeal carcinomas are.

Aged↗
PubMed1980

Herpesvirus saimiri: protective effect of attenuated strain against lymphoma induction.

An attenuated strain of Herpesvirus saimiri (A-HVS) induced a persistent, latent infection in common marmosets. Virus was recovered from circulating lymphocytes of infected animals and antibody response to virus-specified antigens was demonstrated over 3-12 months PI. A-HVS-infected common marmosets and animals without previous A-HVS exposure were challenged with oncogenic HVS (125-825 PFU); marmosets without A-HVS infection developed malignant lymphoproliferative disease and died 3 weeks PI whereas all persistently-infected animals have survived 38-43 months post challenge.

Animals↗