Search PubMed⌕ Search

Biomedical subjects

C Trepo

Publications and source records attributed to C Trepo.

At least 271 records · Page 15Linked to original sources
PubMed1980

[The interaction of cellular immunity and of viral factors in the pathogenesis and the resolution of HB virus infections in hemodialysis (author's transl)].

A study of delayed cutaneous hypersensitivity (DC) was carried out in 50 chronic hemodialysis patients divided into 3 groups according to their serological response to the HB virus (HBV): 31 chronic carriers of Ag HBs (13 HBe positive and 18 HBe negative and 19 having eliminated Ag HBs, antiHbs positive). The results of DCH testing were compared in relation to the 3 patient groups. The number and sum of indurations were reduced, this being more marked in the women, in all the uraemic patients tested. Male hemodialysis patients who were carriers of Ag HBe had the weakest responses, significantly more depressed than those of the HBe positive HBe negative or anti-HBs carrier patients. The presence of Ag HBe was correlated with persistently raised transaminases. In chronic carriers of Ag HBe, hepatic cytolysis was always absent when DCH reactions were negative, and was seen only in the presence of a cellular immune reaction. These results suggest the interaction, in the hemodialysis patient, of virological factors related to Ag HBe and cell mediated immunological factors in the pathogenesis of hepatic lesions related to HBV.

Adult↗
PubMed1980

[Non-A non-B hepatitis virus: demonstration of a double antigenic and structural kinship with hepatitis B virus].

Major antigenic identity has been demonstrated by immunodiffusion between the Ag described by Shirachi and confirmed by us (NANB/e) in the serum on non A non B hepatitis and the HBe/3 specificity of hepatitis B virus (HBV). A second Ag (NANB/c) linked to the core of a new virion morphologically similar to HBV and also associated with ADN polymerase activity as recently described, has been identified and purified from an infected liver. This NANB/c Ag also cross reacts with HBc Ag. These results confirm that HBV and the NANB virus defined here belong to the same new class of DNA viruses.

Animals↗
PubMed1980

Hepatitis B core antigen in hepatocytes of patients with chronic active hepatitis.

Hepatitis B core antigen was demonstrated in the hepatocytes of 28 of 40 patients with chronic active hepatitis in whose sera hepatitis B surface antigen was not detectable by radioimmunoassay. This finding suggests that in these patients, despite hepatitis B surface antigen being undetectable in serum, the liver disease is the consequence of chronic infection with hepatitis B virus.

Adult↗
PubMed1980

Use of the cross-reactivity between hepatitis B and non-A, non-B viruses for the identification and detection of non-A, non-B 'e' antigen.

The morphological similarities between B and non-A, non-B hepatitis viruses prompted the search for common antigenic determinants between the two agents. Major antigenic cross-reactivity was demonstrated by immunodiffusion between hepatitis B e/3 and the most common circulating antigen previously reported in the serum of patients with non-A, non-B hepatitis. Since it is the equivalent of an e antigen, this antigen will be hereafter referred to as non-A, non-B/e antigen. Screening with hepatitis B e/3 antigen or anti-hepatitis B e/3 by immunodiffusion may be used as an easy and efficient way to test for non-A, non-B hepatitis in the absence of specific reagents since it detected up to 91% of non-A, non-B antigen and 86% of anti-non-A, non-B/e. Antigenic cross-reactivity may be used to look for additional viruses belonging to the hepatitis B group.

Antibodies, Viral↗
PubMed1980

Identification and detection of long incubation non-A, non-B hepatitis virus and associated antigens or antibodies.

Three distinct antigen/antibody systems supposedly associated with an HBV-like virus of non-A, non-B hepatitis have been identified. Because of previously demonstrated cross-reactivity with HBe/3 and HBc antigens and other analogies the following terminology is tentatively used. 1. The previously reported serum antigen has been redesignated non-A, non-B e antigen, since it is equivalent to HBe/3 Ag and cross-reacts with it. Non-A, non-BeAg or Ab were detected in 51/62 post-transfusion and 11/56 sporadic acute non-A, non-B hepatitis cases, and in 12/14 cases affecting staff members. In non-A, non-B chronic persistent or active hepatitis and cryptogenic cirrhosis, the prevalence was similarly high: 14/18, 22/48 and 12/18 respectively. Ten out of 26 implicated blood donors were found positive for non-A, non-BeAg accounting for 7 out of 8 post-transfusion cases. A high prevalence of non-A, non-BeAg was also found in haemophiliacs (11/48) and haemodialysed patients (6/42), whereas anti-non-A, non-Be was respectively detected in 4/48 and 6/42 of these cases. 2. Using immunofluorescence, a second antigen termed non-A, non-BcAg has been identified in liver biopsies from 55/84 non-A, non-B chronic hepatitis or cryptogenic cirrhosis cases. All 8 positive biopsies examined by electron microscopy revealed clusters of 22--25 nm intranuclear particles identical to those described in chimpanzees. Anti-non-A, non-Bc detectable by counter-electrophoresis and indirect immunofluorescence was found in the serum of all patients of which biopsy was positive for non-A, non-BcAg. Anti-non-A, non-Bc was also detected in 5/5 non-A, non-BeAg positive cases of post-transfusion hepatitis, 2--6 weeks after onset end remained positive for the 6 month follow-up period. 3. A third antigen, tentatively designated non-A, non-BsAg, has been found less frequently than non-A, non-BeAg in serum. However, it was detectable in 3/18 and 2/12 washed ultracentrifugation pellets of sera positive for non-A, non-BeAg or anti-non-A, non-Be, respectively.

Antibodies, Viral↗
PubMed1979

[Identification of a virus similar to hepatitis B virus in non-A non-B hepatitis].

Hepatitis B virus-like particles (including DANE particles) with DNA polymerase activity but negative for HBs Ag have been identified in NON-A, NON-B hepatitis sera positive for HC Ag. Although specifically associated with the particles, HC Ag is not a surface antigen of the hepatitis C virus identified here for the first time. The relationship of this agent with HBV seems obvious, and deserves further study.

Hepatitis B virus↗
PubMed1979

Detection of virus-associated antigen in serum and liver of patients with non-A non-B hepatitis.

In a search for serological markers of non-A non-B(NANB) hepatitis, sera from repeatedly transfused and convalescent patients were assayed by immunodiffusion against sera from 12 patients with early acute NANB hepatitis. A new antigen/antibody system distinct from HBsAg was demonstrated in 8 cases. To assess the specificity of the test, serial sera from 17 patients with acute hepatitis of known aetiology (10 due to hepatitis-B virus, 4 to hepatitis-A virus, 3 to drugs) were tested twice a month, together with sera from 14 NANB patients obtained during a prospective post-transfusion study. NANB antigen (Ag) was detected in at least one sample from 12 of the 14 NANB patients (86%) but in none of the other groups. NANB Ag appeared after or just before elevation of transaminase levels and was cleared before they fell to normal. 4 of 5 patients who showed seroconversion to NANB antibody (Ab) had transient hepatitis. In contrast, the alanine adminotransferase value returned to normal in only 1 of the 5 with persistent NANB antigenaemia during 6 months' follow-up. NANB Ag was also demonstrated by immunodiffusion in liver extracts from patients with chronic NANB hepatitis with antigenaemia. Fluorescein-isothiocyanate-labelled gammaglobulins with strong NANB Ab activity revealed specific nuclear fluorescence in foci of hepatocytes on cryostat sectons of these livers but in none of 6 control human livers. The results suggest that the antigen and antibody are specifically linked to NANB hepatitis of long incubation period.

Acute Disease↗
PubMed1979

[Demonstration of a serum and liver antigen in acute or chronic non A-non B viral hepatitis].

A new precipitating antigen-antibody system possibly was demonstrated by immuno-diffusion in the serum of patients suffering from non A-non B hepatitis. The antigen appears during the first four weeks of transaminases elevation. In acute cases was transient antigenemia (average 3 weeks). Antibodies appeared rapidly after the disappearance of antigen. The same antigen was also detected, by immunodiffusion and by immunofluorescence, in the liver nuclei of infected hepatocytes. This antigen specific appears for non A-non B hepatitis since it is neither found in the serum of normal subjects nor in that of patients with cirrhosis toxic or viral that hepatitis A or B. The hypothesis of a virus associated antigen is the most likely explanation.

Acute Disease↗
PubMed1979

[Absence of anti double stranded DNA antibodies in viral hepatitis (author's transl)].

The presence of anti double stranded DNA antibodies (ds DNA Ab) in the sera of patients with acute viral hepatitis and B virus chronic active hepatitis has recently been described. In contrast with these results we found no ds DNA ab, but anti single stranded DNA antibodies (ss DNA ab) in the sera from patients with these diseases. The ds DNA ab were studied simultaneously by two methods: Immunofluorescence (IF) on crithidia luciliae and Farr test. In this later case it was shown that the ds DNA preparation contained no ss DNA because it did not react with an anti ss DNA rabbit serum. Our results indicate that the above mentioned authors have been using in their Farr test a preparation of ds DNA contaminated by ss DNA, thus revealing the presence of anti ss DNA ab but not anti ds DNA ab, in the sera of their patients. On the other hand the presence of ds DNA ab has been shown in the sera of 85% of the patients with systemic lupus erythematosus and of 20,5% of the patients with non EB chronic active hepatitis. At least one part of these later are probably autoimmune diseases.

Acute Disease↗
PubMed1979

Cryptic association of e antigen with different morphologic forms of hepatitis B surface antigen.

When highly purified HBsAg particles, separated by rate zonal centrifugation into populations differing in predominant size, were tested for HBeAg, the e1 specificity was detected preferentially in association with particle fractions containing large filaments and Dane particles. These results were obtained both by agar gel diffusion and by radioimmunoassay for e antigen. The e antigen activity present in these fractions was potentiated by prior treatment of particles with Tween 80, suggesting cryptic localization of e1 specificity within or under the outer membrane. The HBeAg released by detergent treatment from a purified preparation composed predominantly of small-particle forms of HBsAg was separated by electrofocusing into a peak of nonparticulate e antigen in the pH range of 5.7--6.0. Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed three major polypeptides in this preparation with approximate molecular weights of 25,000, 55,000, and 70,000. Furthermore, two additional peaks of e antigen activity were detected which migrated in association with HBsAg particles at isoelectric points of 4.4 and 5.5--5.6. The major portion of e antigen remained in association with particles after further purification by rate zonal centrifugation.

Animals↗
PubMed1978

Different fates of hepatitis B virus markers during plasma fractionation: a clue to the infectivity of blood derivatives.

Hepatitis B surface antigen (HBs Ag) and associated particles, e antigen (e Ag) and DNA polymerase are unevenly distributed during Cohn's cold ethanol fractionation of plasmas positive for these markers of the hepatitis B virus (HBV). Most of the e Ag, Dane particles and DNA polymerase are retained in fraction III whereas the bulk of HBs Ag is recovered in fraction IV where only 22 nm spheres and short filaments are still identified. These results suggest that differences in quantitative distribution of HB virions together with alteration of infectious particles during the fractionation process may in addition to heat inactivation account for the relative hepatitis risk of the various plasma derivatives.

Blood Proteins↗