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Biomedical subjects

E Takai

Publications and source records attributed to E Takai.

45 records · Page 3Linked to original sources
PubMed1986

A synthetic peptide vaccine involving the product of the pre-S(2) region of hepatitis B virus DNA: protective efficacy in chimpanzees.

The S gene encoding the major surface polypeptide of hepatitis B virus is preceded by the region pre-S(2) with a capacity to code for 55 amino acid residues. In the product of region pre-S(2), the sequence of 19 amino acid residues (amino acids 14-32 from the N terminus) representing an area of high local hydrophilicity is shared by viral strains of subtypes adr, ayw, and ayr; residue 22, phenylalanine, is replaced by leucine in a strain of the other subtype, adw. A synthetic peptide vaccine involving these 19 amino acid residues, when given to two chimpanzees, raised antibodies that bound to viral particles and protected the animals from challenge with 10(6) chimpanzee infectious doses of hepatitis B virus.

Animals↗
PubMed1986

Translation products of pre-S(1), pre-S(2) regions and the S gene of hepatitis B virus: susceptibility of their antigenic activities to treatment with heat, urea, formalin or pepsin.

Hepatitis B subviral particles, purified from plasma of asymptomatic carriers seropositive for hepatitis B e antigen, were treated with various conditions reported for the processing of vaccines. Thereafter, antigenic activities displayed by the translation products of pre-S(1), pre-(2) regions and the S gene were determined with monoclonal antibodies, and the reactivity for polyalbumin receptor was tested. Heating at 100 degrees C for 1.5 min and then at 65 degrees C for 10 h preserved more than 1/2 of antigenic activities representing products of pre-S(1), pre-S(2) regions and the S gene. After incubation in the presence of 8 M urea at 37 degrees C for 4 h, more than 2/3 of antigenic activities still remained. The antigenic activity of the S gene product was decreased to 2/3 and that of pre-S(2) region product to 1/3, after treatment with formalin at the final concentration of 1:4000 at 37 degrees C for 72 h, whereas the activity of pre-S(1) region product was affected drastically. Although 1/5 of the antigenic activity of the S gene product survived the digestion with pepsin for 18 h, antigenic activities of pre-S(1) and pre-S(2) region products were destroyed almost completely. Polyalbumin receptor, borne by the pre-S(2) region product, was lost by pepsin digestion also. Based on the results obtained, heating may be most appropriate for sterilizing plasma-derived hepatitis B particles for use as a vaccine, because it is reliably virucidal and would not affect the protective efficacy to an extent as the other virucidal methods would.

Epitopes↗
PubMed1985

Factors influencing postexposure immunoprophylaxis of hepatitis B virus infection with hepatitis B immune globulin. High deoxyribonucleic acid polymerase activity in the inocula of unsuccessful cases.

Hepatitis B immune globulin was given intramuscularly to 102 staff members of a dialysis unit within 48 h after the accidental needlestick exposure to blood containing hepatitis B surface antigen (HBsAg). Hepatitis B virus (HBV) infection developed in 11 of 56 persons (20%) who had been exposed to blood containing hepatitis B e antigen (HBeAg). Among 56 HBeAg-positive inocula, HBsAg-associated deoxyribonucleic acid polymerase activity in the 11 inocula that transmitted HBV infection was significantly higher than that in the remaining 45 inocula that did not (log counts per minute 3.27 +/- 0.57 vs. 2.09 +/- 1.19, p less than 0.001). These 11 HBeAg-positive inocula revealed higher hemagglutination titers of HBsAg (geometric mean 13.5 +/- 1.4 vs. 11.2 +/- 3.2, p less than 0.001). The receptor for polymerized human serum albumin was detected significantly more often in the inocula that transmitted HBV infection than those that did not (10/11 vs. 24/45, p less than 0.05). Based on the results obtained, the failure in protecting all of those exposed to HBeAg-positive blood would be attributable to a high concentration of HBV in some HBeAg-positive inocula and the inability of intramuscular injection to raise a protective level of antibody in the circulation immediately.

DNA-Directed DNA Polymerase↗
PubMed1984

Low C3b receptor reactivity on erythrocytes from patients with systemic lupus erythematosus detected by immune adherence hemagglutination and radioimmunoassays with monoclonal antibody.

C3b receptor (CR1) on erythrocytes from 23 patients with systemic lupus erythematosus (SLE) and 124 normal controls was determined by immune adherence hemagglutination (IAHA) and radioimmunoassay. The binding of radiolabeled monoclonal anti-CR1 to erythrocytes and their lysate was distributed continuously in a wide range. The majority of SLE patients showed low binding by both assays. CR1 sites on erythrocytes were determined also by Scatchard plot analysis and standardized by the number of similarly determined lectin-binding sites that served as a measure of erythrocyte surface. The numbers of standardized CR1 sites were classified as high, intermediate, and low. Thirty-six percent of control subjects had high numbers of CR1 sites, 53% had intermediate numbers, and 11% had low numbers. Of SLE patients, the numbers of CR1 sites were high in 0%, medium in 52%, and low in 48%. Negative IAHA was found in 10 controls (8%), all of whom had low numbers of standardized CR1 sites. Among 13 SLE patients with negative IAHA, 11 had low numbers of CR1 sites and the remaining 2 had low intermediate numbers. IAHA, therefore, was particularly efficient in detecting the low numbers of CR1 sites in SLE, which would impair the disposal of circulating immune complexes and accelerate the development of tissue injuries.

Antibodies, Monoclonal↗
PubMed1984

Low molecular weight (7s) immunoglobulin M antibody against hepatitis B core antigen in the serum for differentiating acute from persistent hepatitis B virus infection.

Sera from persons infected with hepatitis B virus were fractionated into 19s and 7s moieties by high performance liquid chromatography and then tested for the antibody to hepatitis B core antigen (anti-HBc) of immunoglobulin M (IgM) class by radioimmunoassay. Sera from 17 patients with acute or fulminant hepatitis invariably showed a high activity of 19s IgM anti-HBc (sample/normal ratio 30.6 +/- 13.6). In addition, they all revealed a much lower activity of 7s IgM anti-HBc (4.1 +/- 3.4). In remarkable contrast, 7s IgM anti-HBc activity was higher than 19s IgM anti-HBc activity in the sera from 5 asymptomatic carriers (10.4 +/- 2.4 vs. 1.0 +/- 0.1), 4 patients with chronic persistent hepatitis (11.7 +/- 1.4 vs. 2.1 +/- 1.4), 13 with chronic active hepatitis (13.6 +/- 3.0 vs. 6.0 +/- 5.6), and 10 with liver cirrhosis (8.9 +/- 3.4 vs. 5.4 +/- 2.4). Among these 32 cases of persistent hepatitis B virus infection, there were only 2 (6.3%) in which the 7s IgM anti-HBc was lower than the 19s IgM anti-HBc. The proportion of patients who showed the value of 7s IgM anti-HBc exceeding that of 19s IgM anti-HBc was significantly higher for persistent (30 of 32) than for acute (0 of 17) hepatitis B virus infection (p less than 0.001). On the basis of these results, the determination of IgM anti-HBc in terms of 19s and 7s subpopulations would be useful for differentiating acute from chronic hepatitis B virus infection, especially when the titer of IgM anti-HBc is not high enough to exclude a persistent hepatitis B virus infection.

Acute Disease↗
PubMed1983

Immunoglobulin M antibody against hepatitis B core antigen for the diagnosis of fulminant type B hepatitis.

We attempted to diagnose fulminant type B hepatitis by the hepatitis B core antibody of the immunoglobulin M class. Of 27 consecutive cases of fulminant hepatitis not due to drug-related causes or type A hepatitis, 11 cases with and 9 without hepatitis B surface antigen in the serum revealed a high activity of immunoglobulin M hepatitis B core antibody by radioimmunoassay (S/N ratio 36.3 +/- 20.3). The remaining 7 cases with presumed non-A, non-B hepatitis, as well as the other 4 cases with drug-related causes, did not show any detectable activity (0.99 +/- 0.16). Serums from 30 asymptomatic carriers did not reveal a high activity of immunoglobulin M hepatitis B core antibody (2.1 +/- 1.2), although titers of non-class-specific hepatitis B core antibody were invariably high. On the basis of the results obtained, immunoglobulin M hepatitis B core antibody may be applied for the diagnosis of type B etiology in cases of fulminant hepatitis with or without hepatitis B surface antigen in the serum.

Adolescent↗
PubMedDate not supplied

Antibody to the receptor for polymerized human serum albumin in acute and persistent infection with hepatitis B virus.

The antibody against the receptor for polymerized human serum albumin was determined by radioimmunoassay. The method involved the inhibition by the test serum, absorbed with HBsAg particles without the receptor, on the binding of polymerized human serum albumin to HBsAg particles with the receptor fixed on a solid support. The amount of polymerized human serum albumin captured by the receptor on HBsAg was then determined by the radiolabeled monoclonal antibody directed to an epitope specific for polymerized human serum albumin. In acute infection, the antibody to the receptor for polymerized human serum albumin appeared in the early recovery phase while HBs antigenemia and elevated transaminase levels were still present, preceding the antibody to HBsAg (anti-HBs). The antibody was detected in 4 (1%) of 358 sera from asymptomatic carriers of HBsAg containing antibody to HBeAg, and in none of 67 sera containing HBeAg. Although the antibody was found in as many as 111 (74%) of 150 sera from blood donors who had presumably acquired anti-HBs after natural infection, it was not detected in any sera from 77 recipients of hepatitis B vaccine who had seroconverted for anti-HBs. On the basis of these observations, the determination of antibody to the receptor for polymerized human serum albumin helps in further understanding the immunity to hepatitis B virus.

Acute Disease↗
PubMedDate not supplied

Antibodies to translation products of the pre-S1 and pre-S2 regions of the envelope gene of hepatitis B virus in fulminant hepatitis B.

Sera from 11 patients with fulminant hepatitis B were tested for antibodies to translation products of the pre-S1 and pre-S2 regions of hepatitis B virus of IgM, IgA and IgG classes, as well as of IgA1, IgA2 and SIgA, with solid-phase enzyme immunoassays using native viral polypeptides. Antibodies to pre-S1 region product of IgM and/or IgA class were detected invariably in six patients who still had detectable hepatitis B surface antigen in serum at the time of clinical presentation. The remaining five patients who had lost HBsAg at presentation had antibodies to pre-S region products of various immunoglobulin classes in higher titers. The five patients with fulminant hepatitis without HBsAg had higher levels of IgA antibodies to pre-S region products than the seven patients with nonfulminant acute hepatitis B who had lost HBsAg: IgA antibody to pre-S1 region product (75.6 +/- 63.8 vs. 2.9 +/- 3.2, p less than 0.01) and IgA antibody to pre-S2 region product (28.9 +/- 25.3 vs. 4.2 +/- 6.9, p less than 0.01). IgA antibodies to pre-S1 and pre-S2 region products were invariably polymeric in fulminant hepatitis B. These findings are compatible with the hypothesis that a heightened humoral antibody response to pre-S1 and pre-S2 region products occurs early during the course of fulminant hepatitis B, participating in severe hepatic injury and early clearance of virus characteristic of this disease.

Acute Disease↗