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Biomedical subjects

B Flehmig

Publications and source records attributed to B Flehmig.

80 records · Page 5Linked to original sources

[Epidemiology, clinical data and immune response of an epidemic of hepatitis A (author's transl)].

Almost all members of an affected family (46 persons) were followed up for a year after contracting hepatitis A during an epidemic in a rural area. Sixteen children, one juvenile and a 42-year-old woman had been infected. A mild subclinical course was present in about a third. All but one person in the studied population who were over 25 years had antibody titres from an earlier hepatitis A infection. As result, those who fell ill were almost exclusively children and juveniles with an average age of 15 years. Contagion rate within the family was 56.7% for those not immunised. Antibodies against hepatitis A virus of the IgG class rose in the majority of patients between the sixth and twelfth month of the infection. There was a significant correlation between the titre after one year and maximal GPT and bilirubin levels in the acute phase of the illness.

Adolescent↗

Hepatitis A-virus particles in stools of patients from a natural hepatitis outbreak in Germany.

During a hepatitis outbreak in Southern Germany 27 nm particles were visualized by immune electron microscopy in stools of two patients. These particles were sereologically identical or similar to hepatitis A-virus particles identified in the USA. The buoyant density of these particles was 1.34 g/cm3 as shown by cesium chloride density centrifugation. The particles were first observed in small numbers in a stool obtained 11 days, and in large numbers in stools obtained 6 and 7 days before the onset of jaundice. Few particles were seen on the day of the onset of jaundice and none thereafter. In both patients a sereoconversion to hepatitis A-virus as judged by immune electron microscopy could be demonstrated.

Disease Outbreaks↗

Seroepidemiological investigation of patients and family contacts in an epidemic of hepatitis A.

Serial blood and faecal samples were collected from patients and family contacts during an outbreak of hepatitis A in a village and tested by a solid-phase competitive type radioimmunoassay for hepatitis A antigen and hepatitis A antibody. The amount and duration of excretion of hepatitis A antigen was correlated with the severity of the illness. In 2 severe clinical cases, hepatitis A antigen was demonstrated in faecal extracts 11 days before the onset of jaundice and continuing for 10 days thereafter, with maximum shedding during the late incubation period. Faecal antigen was demonstrated in low concentrations for only 2 days in a patient with mild disease and in a person with subclinical infection. There was an inverse correlation between the incidence of infection and prevalence of hepatitis A antibody and age. Of 24 infections, 19 (79%) occurred in persons in the age group 0 to 20 years, a group in which only 6% of individuals had pre-existing antibody. Hepatitis A antibody was present in the serum of 3 persons in low titres of 1:20 to 1:40 on the day jaundice developed. The antibody titres increased very rapidly during the following 2 weeks of illness and slowly during the following months, reaching titres of 1:900 to 1:3500. In a separate study, a mean antibody titre of 1:591 was found in 13 patients, 12 years after clinical hepatitis A with jaundice.

Adolescent↗

Influenza virus: association of mouse-lung virulence with plaque formation in mouse kidney cells.

In genetic recombination experiments with the mouse-lung-adapted human influenza A/Engl/1/61 (H2N2) and an avian influenza strain A/Rostock/34 (FPV) (Hav1N1) which is avirulent for the mouse lung, recombinants in which hemagglutinin and neuraminidase were either segregated (Hav1N2; H2N1) or not segregated (Hav1N1) were selected. The recombinants were studied for mouse-lung virulence and their ability to propagate in mouse kidney cells, mouse embryo fibroblasts, chick embryo kidney cells and chick embryo fibroblasts. An association between plaque formation in mouse kidney cells and mouse-lung virulence was found.

Animals↗

Functional significance of neuraminidase in the replication cycle of influenza viruses.

An influenza A strain with temperature sensitive neuraminidase was used for investigation of the functional significance of neuraminidase in different stages of the replication cycle. Heat inactivation of the neuraminidase does not diminish infectivity. Therefore, neuraminidase is not necessary for adsorption, penetration, and uncoating. At temperatures which inhibited neuraminidase activity there was also a reduction of intracellular haemagglutinin production but based on observations with a recombinant strain this was considered to be the consequence of a separate ts defect. Using quantitative haemadsorption to determine virus-dependent alteration of the cellular membrane no evidence was found that neuraminidase is involved in this process. However, release of haemagglutinin was considerably reduced if neuraminidase activity was diminished by temperature elevation. This function of the enzyme in the latest stage of the replication cycle can be substituted by V. cholerae neuraminidase.

Culture Techniques↗

Cell-mediated cytotoxicity in hepatitis A virus infection.

We studied cell-mediated cytotoxicity to hepatitis A virus-infected cells in seven patients with acute type A hepatitis and two controls. Skin fibroblast cultures obtained from the skin biopsies of seven patients after acute hepatitis A virus infection and from two persons without history of current or past hepatitis A virus infection were inoculated with hepatitis A virus. Infection of fibroblast cultures always resulted in an inapparent, persistent infection with production and release of infectious hepatitis A virus. Peripheral blood lymphocytes were collected from the same patients at different times after onset of icterus and were stored in liquid nitrogen. Cytolytic activity of peripheral blood lymphocytes was determined by a microcytotoxicity assay using autologous 51Cr-labeled hepatitis A virus-infected and uninfected target cells. Cytotoxic peripheral blood lymphocytes capable of lysing autologous hepatitis A virus-infected skin fibroblasts were detected in all patients with hepatitis A but were not demonstrable in the controls without antibodies against hepatitis A virus. The clinical course of the hepatitis A virus infection was normal in five patients; and in these patients, cytolytic activity of peripheral blood lymphocytes against hepatitis A virus-infected autologous targets peaked 2 to 3 weeks after onset of icterus. A clinically protracted form of the disease with persistent elevation of aminotransferases for at least 5 months after onset was present in two patients. In these cases, the highest cytolytic activity was demonstrated in peripheral blood lymphocytes collected 8 to 12 weeks after onset of icterus.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗

Isolation of single stranded DNA from purified hepatitis A-virus.

Hepatitis A-virus was purified from human stools by three purification steps. Virus was identified by radioimmunoassay and purity monitored with immune electron microscopy. Virus particles, serologically and morphologically identical, banded in CsCl in two density ranges at 1.31-1.34 g/cm3 and at 1.41-1.43 g/cm3. Virions of density 1.31-1.34 g/cm3 were shown to contain single-stranded DNA of different size classes. Class I 1.33 kb, class II 4.61 kb in addition a small amount of molecules was detected with lengths up to 15 kb.

DNA, Single-Stranded↗

[A trial of a hepatitis A cultured inactivated vaccine on rhesus macaques].

In this work experimental model of hepatitis A virus (HAV) infection in macaques rhesus was used. In 6 seronegative monkeys immunized with the inactivated vaccine (3 injections of 0.3 micrograms of viral protein each at an interval of 1 month) pronounced antibody response was observed. The dynamics and titers of anti-HAV antibodies were similar to those in 5 rhesus macaques which received the active virus. But, in contrast to the latter, no IgM antibodies were detected in the immunized animals. Three months after the end of immunization the monkeys were resistant to challenge with a HAV strain pathogenic for humans (10(3) - 10(4) ID50). The monkeys had no morphological changes in the liver and no rise in the serum alanine-amino transferase activity, but exhibited transient excretion of the virus in feces, as well as stimulation of anti-HAV antibodies (in the absence of IgM antibodies). The vaccine under test proved to be safe, immunogenic and produced a protective effect.

Animals↗