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Biomedical subjects

A Alberti

Publications and source records attributed to A Alberti.

At least 361 records · Page 20Linked to original sources
PubMed1979

Effects of human leucocyte interferon on hepatitis B virus replication and immune responses in patients with chronic hepatitis B infection.

Eight patients with chronic hepatitis B infection (seven with chronic active hepatitis and one with chronic persistent hepatitis) were treated with daily intramuscular injections of human leucocyte interferon for periods of 5 to 8 weeks and in one case for 5 months. In one patient there was a marked fall in virus-associated DNA polymerase activity and in the number of DNA containing viral particles during each of two courses of interferon. Hepatitis Be antigen (HBeAg) also disappeared, the aspartate transaminase levels fell and liver histology improved. In the four other patients with detectable DNA polymerase activity there was an early fall but this was transient and in one of these patients there was a continuing rise in activity despite treatment. One other patient became HBeAg negative but hepatitis B surface antigen (HBsAg) titres were mostly unaffected by treatment. A marked decrease in T-lymphocyte mediated cytotoxicity towards HBsAg coated target cells was demonstrated and raises the possibility that an immunosuppressant action of interferon may offsets its direct anti-viral action but may also account for the improvement in liver function which occurred in some patients.

Adult↗
PubMed1978

Detection of a new antibody system reacting with Dane particles in hepatitis B virus infection.

Antibodies in the serum reacting with antigens on the surface of radiolabelled Dane particles distinct from hepatitis B surface and core antigens (HBsAg and HBcAg) were detected, using a double antibody precipitation assay, in 12 out of 15 patients early in the course of acute type B hepatitis and at the time of disappearance of circulating Dane particles. No such antibody activity was found in 15 of the 16 patients with HBsAg-positive chronic active hepatitis, 13 of whom had complete Dane particles in the serum. In a group of 16 asymptomatic HBsAg carriers (without Dane particles in serum) antibody activity was shown in nine. This demonstration of antibodies precipitating Dane particles may be relevant to the clearance of circulating hepatitis B virions and the termination of infection in acute type B hepatitis. Their absence in all but one of the cases of chronic active hepatitis might explain why the virus infection persists in this group of patients.

Acute Disease↗
PubMed1978

Expression of HBsAg on the membrane of hepatocytes in chronic carriers of hepatitis B virus infection.

Liver cell membrane localization of hepatitis B surface antigen (HBsAg) was investigated in 31 asymptomatic chronic carriers by a direct immunofluorescence technique. A close relationship was found between absence of inflammatory liver disease, presence of large amounts of HBsAg in the liver and expression of the antigen at the hepatocyte surface. Capping of HBsAg after the addition of anti-HBs serum could be inhibited by factors (temperature, metabolic inhibition) that are known to influence viral antigenic mobility at the cell surface. In two patients with chronic active hepatitis as well as in some cases showing histological features of focal parenchymal necrosis, HBsAg could be detected in the cytoplasm of a few scattered hepatocytes but never at the surface of the cells. Both the cases with CAH and one with focal parenchymal necrosis had IgG bound to the liver cell membrane. These findings are in agreement with the hypothesis that the absence of liver damage in HBsAg healthy chronic carriers is related to immune tolerance to the antigen. In chronic active liver disease the presence of IgG on the membrane of hepatocytes suggests a possible role of blocking antibodies directed against viral antigens expressed at the hepatocyte surface.

Adolescent↗
PubMed1978

Full and empty Dane particles in chronic hepatitis B virus infection: relation to hepatitis B e antigen and presence of liver damage.

Circulating complete and defective hepatitis B virus forms, as represented by full, DNA polymerase-positive and empty, DNA polymerase-negative Dane particles, respectively, were investigated in sera from patients with chronic hepatitis B virus infection and related to the presence of e antigen and antibody and to the histological findings on liver biopsy. Complete hepatitis B virus particles were detected in the serum of all patients postive for e antigen, their percentage ranging from 15 to 61% of the total Dane particle population. Although most of these cases had chronic persistent or chronic active hepatitis, complete viral particles were also found in serum of 3 healthy carriers of hepatitis B surface antigen who had e antigen. These results indicate that e antigen is a marker of active virus replication and support its association with infectivity. It is also associated with liver damage because production of complete virus is a feature of chronic hepatitis. In the presence of anti-e, detection of Dane particles in serum appeared to be related to the histological findings. Most of the healthy carriers had no Dane particles in serum, whereas 80% of the cases with chronic liver disease had circulating Dane particles. However, in contrast to the cases with e antigen, 98 to 100% of Dane particles in these cases appeared to be defective in nucleic acid material on electron microscopy after positive staining. All of the patients with chronic active hepatitis in this group had progressed to cirrhosis and it is possible that production of complete virus particles is reduced in the later stages of the illness.

Carrier State↗
PubMed1977

T-lymphocyte cytotoxicity to HBsAg-coated target cells in hepatitis b virus infection.

The cytotoxic effect of peripheral lymphocytes on chicken red blood cells (ChRBC) coated with purified hepatitis B surface antigen (HBsAg) has been studied as an in vitro parameter of cell-mediated immunity in acute and chronic infection with hepatitis B virus. Using this technique, the mean cytotoxic index of lymphocytes from patients with acute hepatitis B (29.13 +/- 20.88) was significantly higher than that obtained with lymphocytes from control subjects (6.53 +/- 3.75). Only 33.3% of the patients with HBsAg-positive chronic active hepatitis exhibited lymphocyte cytotoxicity to HBsAg-coated target cells and the mean cytotoxic index (11.66 +/- 6.60) was in these cases significantly lower than that found in acute hepatitis B. Healthy chronic carriers of HBsAg failed to show lymphocyte cytotoxicity to target cells. The effector cells detected in acute hepatitis B by this in vitro assay have been demonstrated to be T-lymphocytes, as T-cell depleted subpopulations lacked cytotoxic activity. Target cell lysis could be blocked by addition of HBsAg-coated unlabelled ChRBC as well as of purified HBsAg in the culture tubes. It is suggested that damage to the liver cells in acute hepatitis B is related to the presence of cytotoxic T-lymphocytes reacting with HBsAg on the surface of infected hepatocytes. An inadequate lymphocyte response to the antigen may be responsible for the persistence of the infection in the liver with varied clinical manifestations and associated hepatic lesions.

Acute Disease↗
PubMed1976

[Infection due to hepatitis B virus and host immune response].

Cell-mediated immunity (CMI) to hepatitis B surface antigen (HBsAg) was investigated in patients who recovered from acute hepatitis B and in chronic carriers of the antigen, either with or without liver disease. The study was performed using leucocyte migration inhibition test and purified HBsAg. In antigen-negative post-hepatitis patients the frequency of cellular immunity to HBsAg (63.6%) showed a significant difference to controls. On the other hand, only one out of 5 antigen-positive post-hepatitis patients showed sensitisation to HBsAg; four out of these cases had chronic hepatitis at liver biopsy. In HBsAg-chronic carriers, with or without liver disease, the frequency of CMI to HBsAg was not significant to controls. A significant correlation was noted between inflammatory activity and inhibition of migration. Our results suggest that a normal cellular immune response to HBsAg is necessary for the recovery from acute hepatitis B and for the clearance of the virus. In HBsAg-chronic carriers this response seems to be absent or inadequate, leading to the state of healthy chronic carriers or to the evolution to HBsAg-chronic hepatitis, respectively. The high frequency of CMI in HBsAg-negative chronic active hepatitis, suggests that hepatitis B virus infection may play a role in the ethiology of the disease.

Antibodies, Viral↗
PubMed1976

[Liver-specific proteins and autoimmunity in inflammatory liver diseases].

Cell-mediated immunity to a liver specific membrane protein (LP1) has been studied in patients with different types of liver diseases, using the leucocyte migration inhibition test. A high frequency of cellular sensitization to LP1 was detected in untreated chronic active hepatitis, with no significant differences between HBsAg-positive and negative cases. Inhibition of migration is a long-lasting reaction in the spontaneous evolution of the disease, while immunosuppressive treatment normalizes the test only in cases with complete remission. In viral hepatitis B cell-mediated immunity to the liver specific membrane protein can be detected in the acute phase of the disease as a time-limited reaction, exhausted with the clearance of the virus from the liver. An inhibition of migration with LP1 was found also in some cases of HBsAg-positive post-hepatitis patients, in chronic persistant hepatitis, mainly HBsAg-positive, and in asymptomatic chronic carriers of the antigen B. Most of these cases showed a progression to chronic active hepatitis, in clinical and histopathological prospective studies. Our results suggest that cell-mediated immune response to liver specific antigens plays a major role in the pathogenesis of chronic active hepatitis. Moreover the evaluation of these reactions in chronic liver diseases may help in the diagnosis and in the control of the immunosuppressive therapy. Hepatitis B virus infection must be considered one of the possible cause responsible for the rising of autoimmunity to the liver.

Autoantibodies↗
PubMed1976

Liver cell surface localization of hepatitis B antigen and of immunoglobulins in acute and chronic hepatitis and in liver cirrhosis.

This paper describes immunofluorescence studies on liver cell surface localization of hepatitis B surface antigen (HBsAg) and of IgG in acute and chronic hepatitis and in cirrhosis. In acute hepatitis B, HBsAg was found at the surface of hepatocytes in an early phase of the disease, but not during the recovery. This finding is consistent with the hypothesis that immune reactions to HBsAg may be responsible for the liver cell lysis. In HBsAg-positive chronic hepatitis and cirrhosis the antigen was found in the cytoplasm, but not on the surface of the hepatocytes, while in HBsAg-negative cases the antigen could not be detected in the liver cells. Both in HBsAg-positive and in HBsAg-negative chronic active hepatitis (CAH) and cryptogenic cirrhosis IgG bound to the membrane of the hepatocytes could be detected, suggesting a role of antibodies in the pathogenesis of the disease.

Acute Disease↗
PubMed1975

Organ-specificity and diagnostic value of cell-mediated immunity against a liver-specific membrane protein: studies in hepatic and non-hepatic diseases.

In chronic active hepatitis (CAH, n=58) 70% of the HBsAg negative and 48% of the HBsAg positive cases showed a CMI against human liver specific proteins (HLPI). Using HBsAg as antigen only 12% of the HBsAg negative and 24% of the HBsAg positive cases gave a CMI response. On the basis of HBsAg and autoantibodies in the serum CAH patients could be divided into 4 subgroups. A close correlation between CMI against HLPI, sex, ANA and HL-A-8 could be detected. In a follow-up study of patients with acute virus B hepatitis (n=62) CMI against HBsAg was detected in 60% of the cases in the acute phase of the disease but in 15% only 3-6 months after the onset of the illness (n=40). In patients who developed a chronic HBsAg carrier status 3 of 5 cases remained persistently positive with HLPI as antigen in the migration inhibition test. - In non-hepatic diseases in which immunological abnormalities may be present (malignant diseases n=46, diabetes mellitus n=27, active tuberculosis, n=18 and untreated systemic lupus erythematodes, n=5) only 26% of patients with malignant diseases showed a migration inhibition with HLPI. - Using different antigens such as human liver specific proteins (HLP), rabbit liver specific proteins (RLP), brucella suis antigen and tuberculin it was possible to demonstrate the validity of the two-step migration inhibition test to detect CMI. The results with different antigens in hepatic and non-hepatic diseases demonstrated that cell-mediated immunity of HLPI is an organ specific immune reaction which is associated with acute and chronic active liver diseases as a time limited or long-lasting phenomenon. Positive reactions in some tumor patients suggest that different mechanisms may elicit an autoimmune reaction against liver antigens.

Antibodies↗
PubMed1975

[Frequency of antigen associated to hepatitis due to virus B (HBAg) and of antibody (HBAc) in healthy subjects and during of course of acute and chronic hepatitis. Radioimmunologic study].

Among the several methods employed for the detection of hepatitis B antigen (HBAg) and hepatitis B antibody (HBAb), radioimmunoassay is considered to be the most sensitive and specific. This paper describes a radioimmunoprecipitation test (RIP) for HBAg and HBAb standardized in our laboratory; it consists of a double-antibody precipitation test in a micro-titer system employing 125I-labeled HBAg. The test is compared with double immunodiffusion (ID) and with counterimmunoelectrophoresis (CEP) in the detection of HBAg and HBAb in healthy persons and in patients with acute and chronic liver disease. RIP is 20,000 times more sensitive than ID and 2,500 times than CEP when HBAg is tested, and 40,000 times more sensitive than ID and 10,000 times than CEP for the antibody detection. Moreover the method is reproducible and specific for HBAg and HBAb. With this test the frequency of HBAg in healthy persons was 0% in subjects without any known contact with antigenic material, 0.80% in hospital personnel and 1.17% in high risk personnel (laboratory technicians, blood products workers, ecc.). In acute viral hepatitis the frequency of HBAg was 90% at the admittance to the hospital and 70% at the dimission, while CEP detected a frequency of 85% and 20% respectively. In chronic liver disease the frequency of HBAg with the RIP method was 83.3% in chronic persistent hepatitis, 42.8% in chronic aggressive hepatitis, 23% in cryptogenic cirrhosis and 16.6% in alcoholic cirrhosis. The frequency of HBAb detected with RIP was 4.50% in subjects without any known contact with antigenic material, 6.45% in hospital personnel, 0.41% in high risk personnel, 20% in acute viral hepatitis at the admittance to the hospital and 50% at the discharge, 25% in chronic persistent hepatitis, 14.2% in chronic aggressive hepatitis, 15.3% in cryptogenic cirrhosis and 50% in alcoholic cirrhosis. The high frequency of antibody in healthy persons with no history of hepatitis or parenteral exposure to blood transfusion suggests a widespread diffusion of hepatitis B infection and the possibility of a nonparenteral route transmission. The frequency of HBAg and HBAb in chronic liver disease as detected by a very sensitive method rises the question of a possible role of hepatitis B virus in the pathogenesis of the disease.

Acute Disease↗