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Biomedical subjects

A Alberti

Publications and source records attributed to A Alberti.

At least 325 records · Page 18Linked to original sources
PubMed1984

Polyalbumin receptors on hepatitis B virus and on 22 nm hepatitis B surface antigen (HBsAg)2 particles.

Receptors for polymerized human serum albumin ( pHSA ) were studied by solid-phase radioimmunoassay on different hepatitis B surface antigen (HBsAg) particles subpopulations prepared both from hepatitis B e antigen (HBeAg) and from anti-HBe-positive sera. HBsAg particles in HBeAg-positive serum showed higher expression of the receptor compared with HBsAg particles from anti-HBe-positive serum. Analysis of different morphological forms of virus particles was performed after separation by density-gradient ultracentrifugation. Maximum receptor expression was detected in HBV particles containing fractions while the 22-nm HBsAg particles had significantly lower receptor activity. These observations support the hypothesis of a pathogenetic role of the pHSA receptor in mediating virus access to hepatocytes. Indeed, the higher pHSA binding activity on HBV particles could allow selective attachment of the infectious virion to liver cells that bear similar albumin receptors on their surface.

Hepatitis B Antigens↗
PubMed1984

Circulating hepatocyte membrane-specific autoantibodies in chronic active hepatitis type B. Relation to virus replication activity and liver cell necrosis.

Sera from two groups of untreated HBsAG-positive patients with chronic active hepatitis on liver biopsy were tested for antibodies to liver cell membrane antigens (liver-specific protein, LSP; and liver membrane antigen, LM-Ag). Among the 14 HBeAg-positive cases, seven (50%) were positive for anti-LSP, whereas only two (13%) of 15 anti-HBe-positive cases circulated this antibody. Liver membrane autoantibody (LMA) was detected only in two sera from delta-positive patients (1 HBeAg positive and 1 anti-HBe positive). Anti-LSP-positive patients presented transaminase values significantly higher than those of the negative cases. Our data do not support the hypothesis that a liver-specific autoimmune mechanism plays a significant role in the immunopathogenesis of liver cell necrosis in anti-HBe-positive chronic active hepatitis type B. The relationship between hepatocyte necrosis and anti-LSP antibody response is confirmed.

Adult↗
PubMed1983

A beta-thalassemia lesion abolishes the same Mst II site as the sickle mutation.

Digestion of DNA from a patient with homozygous beta zero thalassemia from Calabria, Italy with the restriction endonuclease Mst II produced a pattern similar to the one obtained with sickle cell trait DNA in that the Mst II site at the beta 6 position on one chromosome was abolished. We cloned the DNA from this beta-thalassemia chromosome and performed sequence analysis. The deletion of a single nucleotide (A) at the GAG codon of the beta 6 position results in a frame shift and early beta-globin chain termination. This mutation occurs on a chromosome with a haplotype similar to two other Mediterranean beta-thalassemia lesions. The Mst II enzyme is useful for prenatal diagnosis of beta thalassemia in this population.

Base Sequence↗
PubMed1983

Evidence of non-A, non-B hepatitis in children with acute leukemia and chronic liver disease.

Eleven children with acute lymphoblastic leukemia and chronic liver disease, who had negative reactions for hepatitis B virus markers in the liver, were studied at the time of therapy withdrawal for an antigen-antibody system linked to non-A, non-B (NANB) hepatitis infection. By immunofluorescence, six of the 11 children had a positive reaction for the NANB antigen in the liver, and five of these six children also had a positive reaction for the NANB antibody in serum. Histologic lesions were more severe in patients with the NANB antigen in the liver compared with those with a negative reaction.

Adolescent↗
PubMed1983

Virus replication and liver disease in chronic hepatitis B virus infection.

Recent studies on the natural history of chronic hepatitis B virus infection have provided evidence for a close temporal relationship between the phase of active virus replication and development of liver lesions. To assess the role that virus replication plays in this phase in determining the severity of the liver disease, we studied serum levels of virus-specific DNA-polymerase activity and hepatitis Be antigen/antibody status in 48 chronic carriers of the hepatitis B surface antigen found positive for the hepatitis B core antigen in the liver. There was a remarkably evident inverse correlation between virus replication activity and liver disease activity, patients with minimal histological changes having the highest DNA-polymerase levels (mean +/- SD: 3879 +/- 2557 cpm) and those with severe chronic active hepatitis the lowest enzyme levels (419 +/- 246 cpm), while cases of chronic persistent hepatitis and of mild chronic active hepatitis had intermediate levels. Serum hepatitis Be antigen was detected in 31/32 patients with milder liver lesions and in 11/16 with severe liver lesions; the remaining five cases were anti-HBe-positive despite the presence of the core antigen in the liver. Serum levels of virus replication markers closely correlated with the distribution pattern of the core antigen in the liver. These findings indicate that in chronic hepatitis B the severity of liver disease is not directly related to levels of virus replication, thus suggesting a predominant role of host immune mechanisms.

Carrier State↗
PubMed1983

Changes in hepatitis Be antigen/antibody system in children with chronic hepatitis B virus infection.

The long-term changes in the HBeAg/anti-HBe system were examined in 55 children with chronic type B hepatitis (52 patients) or cirrhosis (three patients) during a follow-up period of two to 10 years. At the time of presentation, positive reactions to HBeAg were seen in 46 children, and to anti-HBe in nine. Spontaneous seroconversion from HBeAg to anti-HBe occurred in 13 of 38 patients (average annual rate 16%), mainly those with acute onset of hepatitis B or with features of active liver disease at presentation and with a focal distribution pattern of hepatitis B core antigen in the liver. Normalization of transaminase activity and disappearance of histologic features of activity were the rule in patients in whom seroconversion occurred, but the exception in those who maintained persistently HBeAg-positivity. In contrast to the favorable evolution of illness observed in children showing anti-HBe seroconversion, three of nine patients who had anti-HBe-positive reactions at presentation were found to have liver cirrhosis, and a fourth patient had features of active hepatitis throughout the observation period. Because delta antigen was detected in the liver in two of these patients, it is conceivable that etiologic cofactors could have influenced their course of chronic hepatitis.

Adolescent↗
PubMed1983

A 7 year survey of acute hepatitis type B.

Epidemiological and clinical features of acute symptomatic hepatitis type B were evaluated in 51 otherwise healthy children and in 13 children receiving immunosuppressive treatment for leukaemia and malignancy, who were admitted to hospital with acute hepatitis B surface antigen (HBsAg) positive hepatitis during a period of 7 years. Blood transfusions, or intimate contacts with asymptomatic HBsAg carriers or with contaminated material during repeated admission to hospital were the possible sources of infection in the immunosuppressed patients, whereas percutaneous exposure was identified as the source in a minority of non-immunosuppressed patients. Features of the acute phase of the illness differed little between the two groups of patients (acute liver failure developed in one patient with leukaemia and in two untreated children). Conversely, chronic evolution was observed in 69% of immunosuppressed patients but in only 9% of untreated children and affected only patients born to HBsAg positive mothers (two of four patients) or patients presenting with papular acrodermatitis (both patients).

Age Factors↗
PubMed1983

Virus-associated receptors for polymerized human serum albumin in acute and in chronic hepatitis B virus infection.

The receptor for polymerized human albumin, recently identified on the hepatitis B virus, was studied by hemagglutination in 89 patients with acute and chronic hepatitis B virus infection. The receptor, which was differentiated from antialbumin antibodies by immunofluorescence and hemagglutination inhibition, was detected mainly in patients with active virus replication, independently of hepatitis B surface antigen titer. Thirteen of 20 uncomplicated acute hepatitis B cases were positive at clinical onset (mean log2 titer +/- SD: 4.20 +/- 2.46) but became negative during the acute phase, while 5 patients who progressed to chronic hepatitis had significantly higher receptor titers at onset (7.0 +/- 0.0, p less than 0.01) and remained positive afterwards. In chronic hepatitis B virus infection, the receptor was detected in 17 of 30 patients with chronic active hepatitis, in 5 of 12 with chronic persistent hepatitis, and in 2 of 16 healthy carriers. Among hepatitis B e antigen positive cases a wide range in receptor levels was observed, and in longitudinal studies most patients with low initial titers seroconverted to hepatitis B e antibody while patients with higher titers remained persistently hepatitis B e antigen positive. These results indicate that the virus receptor for polyalbumin may represent a useful marker in hepatitis B e antigen positive acute and chronic hepatitis B.

Antibody Formation↗
PubMed1983

Cellular immunity to the hepatitis B virion in acute hepatitis type B.

Ten patients were studied serially during acute hepatitis type B for lymphocyte sensitization to the hepatitis B surface antigen (HBsAg) and to the complete hepatitis B virion (Dane particle). Using the lymphocyte transformation test, sensitization to purified HBsAg was not observed during the first 10 days of illness but became detectable later, being particularly evident during convalescence, while sensitization to antigens of the complete virion, other than HBsAg, was demonstrable as soon as at the onset of symptoms, often at the time of maximum liver cell damage. These results indicate that in the course of acute hepatitis type B, lymphocyte sensitization to other antigens of the complete virion precedes that to HBsAg and may be of greater pathogenetic importance.

Acute Disease↗
PubMed1982

Histological evidence of hepatitis-B-virus infection with negative serology in children with acute leukaemia who develop chronic liver disease.

A high percentage of patients with acute leukaemia in established remission develop chronic liver disease: how important hepatitis-B-virus (HBV) infection is as an aetiological factor is not clear. The presence of HBV markers in liver and serum of 23 leukaemic children with liver disease was investigated at the time of a diagnostic biopsy just before treatment withdrawal. Although, at this time, none had HBV antigens or antibodies in the serum by radioimmunoassay, HBsAg was detected by direct immunofluorescence in the cytoplasm of hepatocytes in 13 children, 7 of whom also had hepatitis-B core or e antigens in hepatocyte nuclei. This pattern of both cytoplasmic and nuclear fluorescence was present in 4 of 6 patients with the histological features of chronic active hepatitis on liver biopsy. The failure of release of viral antigens into serum and the absence of an adequate immune response were probably due to the intense chemotherapy used to induce and maintain remission, since HBV markers appeared in the serum within 15 months of stopping treatment in 8 of the children in whom viral antigens had been detected in liver tissue but in none of those whose biopsy specimens were negative by immunofluorescence. These results suggest that HBV infection may be an important cause of chronic liver disease in children with leukaemia and show that during treatment serological tests may fail to detect the presence of the virus.

Adolescent↗
PubMed1982

Virus receptors for polymerized human albumin: a prognostic marker in HBeAg-positive chronic hepatitis type B?

Seventeen out of 30 patients with chronic hepatitis type B with hepatitis B e antigen (HBeAg) in serum remained persistently positive for e antigen, while 13 seroconverted to antibody (anti-HBe) when followed over a period of one to five years. Initial levels of serum hepatitis B virus (HBV) markers, such as the hepatitis B surface antigen (HBsAg), HBeAg, and HBV-DNA polymerase (HBV-DNAP) were similar in the two groups of patients, while initial titres of the HBsAg-associated receptor for polymerized human serum albumin (pHSA), recently identified on HBV particles, were significantly higher in the patients who remained HBeAg positive (mean titre +/- SD = 2(-7.00) +/- 2(-3.2)) compared to the cases who eventually seroconverted to anti-HBe during the follow-up (2(-2.54) +/- 2(-2.14) P less than 0.001). A receptor titre above 1:64 by haemagglutination was highly predictive of persistence of HBeAg, suggesting that in patients with HBeAg-positive chronic hepatitis testing for the HBsAg-associated pHSA receptor may be useful in predicting the duration of HBe antigenaemia, with relevant clinical and prognostic implications.

Hepatitis B↗