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Biomedical subjects

F Bonino

Publications and source records attributed to F Bonino.

At least 217 records · Page 12Linked to original sources
PubMed1976

Complement fixing hepatitis B core antigen immune complexes in the liver of patients with HBs antigen positive chronic disease.

One hundred and fifty-two biopsies from serologically HBsAg positive and negative patients with liver disease were studied in immunofluorescence: for the presence of the surface (HBs) and the core (HBc) antigenic determinants foeterminants of the hepatitis B virus, of immunoglobulins and complement (C) deposits, and for the capacity to fix human C. Circumstantial evidence is presented suggesting that HBc immune-complexes are a relevant feature in the establishment and progression of chronic HBSAg liver disease. C fixation by liver cells was shown in all HBC positive patients with chronic hepatitis; an active form was present in every case, except two with a persistent hepatitis, an inverse ratio of HBc to C binding fluorescence being noted between active chronic hepatitis and cirrhotic patients. HBc without C fixation was observed in only three patients in the incubation phase of infectious hepatitis. IgG deposits were often found in HBc containing, C fixing nuclei. No C binding or IgG deposits were observed in acute self-limited type B hepatitis, in serologically positive patients with normal liver or minimal histological lesions, with and without HBs cytoplasmic fluorescence in their biopsy, or in serologically negative individuals.

Adolescent↗
PubMed1975

[Chronic hepatitis: diagnostic and therapeutic problems].

The morphological criteria for diagnosing chronic hepatitis are discussed and criticised. A classification closer to clinical reality than that of De Groote et al 1968 is then proposed. Personal experience in differential laboratory diagnosis between the various forms of chronic hepatitis by means of comparative evaluation of an enzymogram and the measurement of certain proteins in the serum is then reported. Case examples are given to emphasise the possibilities of the immunological approach to the problem of active chronic hepatitis. Finally, the cardinal points of therapy are reviewed.

Adult↗
PubMedDate not supplied

The delta agent: HBsAg particles with delta antigen and RNA in the serum of an HBV carrier.

The hepatitis B virus-associated delta antigen was detected in the serum of a young female drug addict with acute hepatitis and a previous history of hepatitis B surface antigen carrier. Delta antigen was associated with a 35- to 37-nm subpopulation of hepatitis B surface antigen particles which banded at a density of 1.25 gm per cm3 of CsCl and contained a small RNA of approximately 5.5 X 10(5) molecular weight. This report demonstrates that delta antigen is associated with a unique subpopulation of hepatitis B surface antigen particles and small RNA in human serum.

Adult↗
PubMedDate not supplied

Hepatitis B virus DNA in the sera of HBsAg carriers: a marker of active hepatitis B virus replication in the liver.

Sera and liver biopsies from 30 Italian patients, carriers of HBsAg for at least 3 years, were examined for markers of hepatitis B virus (HBV) infection by serological assays and immunofluorescence. Biopsies were analyzed for HBcAg, HBsAg, and delta antigen by immunofluorescence; sera were assayed for HBsAg/anti-HBs, HBcAg/anti-HBc, HBeAg/anti-HBe, delta/anti-delta, HBV-specific DNA polymerase activity and the presence of HBV DNA. HBcAg, HBeAg, and DNA polymerase tests were positive in the sera of 71, 86, and 57%, respectively, of carriers with intrahepatic HBcAg. HBV DNA was detected in 100% of patients expressing HBcAg in the liver with a strong correlation between the concentration of serum DNA and the intensity of HBcAg immunofluorescence in the liver. HBV DNA was detected in the sera of 63% of carriers with intrahepatic delta where the other markers of HBV replication (HBeAg, DNA polymerase) were undetectable. The assay for serum HBV DNA appears to be an excellent noninvasive method for detecting active replication of HBV in HBsAg carriers.

Carrier State↗
PubMedDate not supplied

Cytoplasmic tubular structures in liver of HBsAg carrier chimpanzees infected with delta agent and comparison with cytoplasmic structures in non-A, non-B hepatitis.

Electron microscopic observations were carried out on five HBsAg carrier chimpanzees infected with delta (delta) agent and two chimpanzees infected with human non-A, non-B hepatitis. The cytoplasmic tubular structures, which have been recognized in the liver of chimpanzees infected with human non-A, non-B hepatitis, were found also in the liver of HBsAg carrier chimpanzees infected with delta agent. The quantity of the cytoplasmic structures in serial studies was associated with SGPT elevation rather than with expression of delta antigen in sera and liver tissues. This indicates that the cytoplasmic structures reflect a pathologic change of the hepatocytes in chimpanzees infected with delta agent or human non-A, non-B hepatitis. These and other similarities between the two agents suggest a similar nature.

Animals↗
PubMedDate not supplied

The spectrum of complement-fixing antinuclear antibodies in patients with hepatocellular carcinoma.

Sera from 230 hepatocellular carcinoma patients were tested for antinuclear antibodies by anticomplement immunofluorescence in 16 types of transformed, diploid or primary cells of human, monkey, chimpanzee or rat origin. As controls, we tested 85 sera from patients with chronic liver diseases, 48 sera from patients with nonhepatic cancers and 164 sera of normal controls. Exactly 11.2% of all cancer patients but only 3.6% of noncancer patients had complement-fixing antinuclear antibody that reacted with all substrates. Only sera from hepatocellular carcinoma reacted with subsets of the tumor cell substrates. These sera reacted with hepatocellular carcinoma cells and nonhepatic cancer cells (antitumor) or only with one or more of the human hepatocellular carcinoma cell lines, PLC/PRF/5, Hep3B and Mahlavu, that were derived from HBsAg-positive patients (antihepatocellular carcinoma). Three of these reacted only with hepatitis B virus DNA-positive cells (PLC/PRF/5 and Hep3B) that contained "hepatitis B-associated nuclear antigen," 1 reacted only with hepatitis B virus DNA-negative Mahlavu cells, 1 reacted with PLC/PRF/5 and Mahlavu and 3 reacted with all 3 cells. The nuclear antigen in Mahlavu was expressed as a homogeneous fluorescence that spared the nucleoli, was present in a lower percentage of cells than hepatitis B-associated nuclear antigen and was more thermostable than hepatitis B-associated nuclear antigen. However, it resembled hepatitis B-associated nuclear antigen in kinetics of expression and susceptibility to digestion with DNase, RNase and proteinase K. The nature of the nuclear antigens in the hepatocellular carcinoma cells is poorly understood but one possibility is that they may represent the expression of viral or tumor-related genes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMedDate not supplied

Type D hepatitis: the clinical significance of hepatitis D virus RNA in serum as detected by a hybridization-based assay.

Hepatitis D virus is a defective human pathogen that requires hepatitis B virus for its replication. A hybridization-based assay for the 1.75 kb RNA genome of hepatitis D virus was developed using as probe a radiolabeled transcript of a cloned cDNA fragment (pKD3 hepatitis D virus DNA). Sera from 120 chronic carriers of HBsAg with confirmed hepatitis D virus infection were analyzed for the presence of hepatitis D virus RNA. Serum hepatitis D virus RNA was detected in 43 of 74 (58%) patients with chronic liver disease; some patients were positive for hepatitis D virus RNA in multiple samples over a period of several years. Serum hepatitis D virus RNA was present in 17 of 28 (61%) patients during the acute phase of clinical hepatitis and was not detected after recovery from acute disease or in 18 asymptomatic chronic HBsAg carriers with antibody to hepatitis D virus. The presence of hepatitis D virus RNA correlated with other known markers of active hepatitis D virus replication; all chronic active liver disease patients with serum hepatitis D virus RNA were positive for antihepatitis D antigen IgM, and 34 of 37 (92%) had hepatitis D antigen in their liver biopsy specimens. The assay for hepatitis D virus RNA provides a direct and noninvasive method for the detection of hepatitis D virus in serum and will be useful in the study of the natural history of type D hepatitis, the identification of chronic hepatitis D virus carriers likely to transmit hepatitis D virus and the selection and monitoring of patients for potential antiviral therapy.

Acute Disease↗
PubMedDate not supplied

A histological study of hepatitis delta virus liver disease.

The histopathology of hepatitis delta virus disease was studied in carriers of HBsAg with chronic hepatitis delta antigen-positive hepatitis and in serial biopsies of patients with acute hepatitis delta virus hepatitis that progressed to chronicity. There was no histologic feature distinctive of hepatitis delta virus from other types of viral hepatitis. Biopsy specimens of patients with chronic disease exhibited portal and periportal inflammation with piecemeal necrosis, conforming to a picture of aggressive hepatitis often accompanied by cirrhosis. Characteristic was a marked intralobular infiltration by mononuclear cells and a degenerative eosinophilic change of the hepatocytic cytoplasms conducive to the formation of acidophilic bodies. Liver specimens from patients with hepatitis delta virus hepatitis exhibited aspects of focal, confluent and bridging necrosis. The disease progressed to chronicity irrespective of the original histological features. The expression of intrahepatic hepatitis delta antigen was reduced in the phase of the acute hepatitis but increased in parallel with the development of chronic active liver disease. In late-stage cirrhosis, expression of hepatitis delta antigen was usually low.

Acute Disease↗
PubMedDate not supplied

Serial passage of hepatitis delta virus in chronic hepatitis B virus carrier chimpanzees.

Five consecutive passages of hepatitis delta virus in hepatitis B virus carrier chimpanzees were performed in order to further characterize the infectious and pathogenic nature of this naturally occurring defective virus. Three animals received identical inocula at fourth passage in order to assess individual animal variation as a factor in the course of infection and disease. Acute hepatitis delta virus infection occurred in all hepatitis B virus carrier chimpanzees as demonstrated by coincident intrahepatic hepatitis delta antigen, serum hepatitis delta antigen and serum hepatitis delta virus RNA followed by seroconversion to antibody to hepatitis delta antigen. In all animals, acute hepatitis was temporally associated with hepatitis delta virus infection and was self-limited. The incubation period to hepatitis shortened with passage, whereas biochemical and histologic evidence of liver diseases increased. The marked increase in liver disease with passage was not associated with increasing markers of hepatitis delta virus replication or expression, thus indicating that adaptation to the chimpanzee by serial passage resulted in increased hepatitis delta virus virulence. The duration of hepatitis due to hepatitis delta virus infection in three chimpanzees which received the same inoculum varied from 1 to 8 months. The observations of passage adaptation and individual host variation in this experimental model of hepatitis delta virus disease parallel known pathogenic variations in human hepatitis delta virus infection.

Animals↗
PubMedDate not supplied

The immunological diagnosis of HBsAg liver disease by combined screening for the e system in the serum and the HB core and surface antigens in liver biopsy samples.

Serological screening for HBeAg and anti-HBe, combined with the immunohistochemical localization of the hepatitis B core and surface antigen in 110 HBsAg carriers, established different immunological profiles indicative of the liver status and prognostic of the future absence or progression of the disease. Intrahepatic HBcAg and serum HBeAg appeared the most sensitive indexes of chronic and progressive liver disease, anti-HBe and large amounts of cytoplasmic HBsAg suggest, instead, the asymptomatic carrier state without liver damage. Only the nuclear localization of HBcAg in immunohistochemical studies was a reliable prognostic indicator of transition to chronicity; absence or presence of serum HBeAg was of no help in predicitng the outcome of acute HBsAg hepatitis.

Acute Disease↗
PubMedDate not supplied

Interferon treatment of chronic hepatitis B surface antigen (HBsAg) carriers. A description of the activation profiles of natural killer cells obtained with different schedules of administration in three subsets of carriers.

By monitoring immunobiological parameters known to be influenced by interferon (IFN), the natural killer (NK) cell activity of 10 low replication (anti-HBe) virus B-DNA (HBV-DNA) hepatitis patients receiving rIFN alpha-A, of 5 anti-HBe/delta positive hepatitis patients treated with rIFN alpha-2, and of 6 high replication (HBeAg) HBV-DNA hepatitis patients on lymphoblastoid IFN was followed-up during therapy. Overall, strong and significant (p less than 0.01) shift to increase segregated with the low replication subset; the delta positive subset was non-significantly increased (0.30 greater than p greater than 0.2); the high replication subset was depressed in a nearly significant (0.10 greater than p greater than 0.05) manner. Kinetic studies showed the activation of the first subset to follow an early steep rise and a subsequent plateau as fitted with a quadratic curve (p = 0.02); an early rise and a depression at 2 months delineated a complex cubic model (p = 0.06) in the high replication subset. The profound NK depression was clinically witnessed by a sharp rise of the aminotransferases and following drop of viremia. The study shows that i. discrete patterns of NK response as amenable to mathematical models may associate to differential patterns of virus B replication in patients responding to IFN; ii. point(s) on the NK curve may acquire clinical meaning as they coincide with a consensual or opposite shift of a clinical index.

Adult↗
PubMedDate not supplied

The e antigen and antibody in the serum of patients with HBsAg-positive liver disease and in asymptomatic carriers.

Serum samples from 103 HBsAg positive and 69 negative patients were examined in Ouchterlony double diffusion in agarose for the presence of e antigen and anti-e antibody. e antigen was found in 66% of the cases of active chronic hepatitis, 18% of those of active cirrhosis, and 12% of those of acute hepatitis. Anti-e antibody was found only in asymptomatic chronic carriers; it occurred in 56% of HBsAg-positive individuals with normal livers at biopsy. No e reactivity was found in 6 subjects with inactive disease and in 3 with chronic persistent hepatitis. The e system seems a valuable diagnostic tool utilizing the presence of the antigen to differentiate patients with chronic progressive disease from healthy carriers who, in contrast, often have circulating anti-e antibodies; its clinical value, however, is at present limited by the low sensitivity of the technique used for antigen detection. A significant association between e antigen and the intrahepatic expression of the core determinant of the HB virus was observed inthis study, suggesting they have a similar role in pathogenicity and infectivity; the association between anti-e antibody and HBsAg appeared uncertain, HBsAg being present in the liver irrespective of e reactivity.

Acute Disease↗
PubMedDate not supplied

Antibodies against the human pancreas in acute and chronic liver disease.

Different immunofluorescence reactions in the exocrine pancreas were observed with the sera of patients with acute and chronic liver disease. In the majority of cases the antibody, frequently associated with the antibody against the smooth muscle, reacted with diffuse organ-specific antigens in the cytoplasm; in one patient it reacted with fibrillar antigens in the cells, while in another case the fluorescence was due to antibodies against non-specific ribosomal antigens. The occurrence, nature and significance of these reactions are discussed.

Acute Disease↗
PubMedDate not supplied

Nucleic acid hybridization in viral hepatitis research.

Nucleic acid hybridization is extremely important in viral hepatitis research and the newly emerging techniques are now becoming an indispensable resource also in the diagnostic laboratory. This paper provides information on methods currently used for detection of viral nucleic acids with special emphasis on the importance of hepatitis B virus DNA in the serum. Herein, we describe the procedures for preparation and labeling of DNA probes and the principles that regulate dot, slot and Southern blot hybridization. Advantages and shortcomings of filter hybridization are discussed together with the alternative approaches to it. Finally, a collection of laboratory protocols is presented in Appendix #1.

DNA Probes↗
PubMedDate not supplied

Application of nucleic acid hybridization to the hepatitis delta virus research.

Cloning and sequencing of the genome of hepatitis delta virus (HDV) represented a remarkable progress in the knowledge of HDV infection and made available cDNA and RNA probes which can be successfully used to identify HDV-RNA in biological specimens. We review here the methods currently used for detecting HDV nucleic acids and report the most recent advances of the molecular biology of HDV. Finally, we examine the number of compelling reasons for the diagnostic laboratory to pursue this technology. Testing for HDV-RNA has become essential for the screening and the follow-up of both chronic HDV carriers, undergoing antiviral therapy and patients with terminal disease, eligible for liver transplant.

Hepatitis D↗
PubMedDate not supplied

The impact of molecular biology in the diagnosis and management of viral hepatitis.

In recent years molecular biology techniques allowed an extraordinary progress in knowledge of hepatitis viruses. New informations have accumulated on the mechanisms of virus replication and on the pathogenesis of liver damage. In the clinical setting, simple noninvasive methods that use the same technological approach provide a useful diagnostic tool for infections of hepatitis B virus (HBV) and hepatitis delta virus (HDV). Using these tests we may define whether a carrier of hepatitis B surface antigen has a liver damage due to HBV or HDV or to other, non-virological causes. Detection of HBV-DNA and HDV-RNA in serum and liver can also be used as a guide for prognosis and therapy.

Animals↗