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Biomedical subjects

B Yvonnet

Publications and source records attributed to B Yvonnet.

At least 19 recordsLinked to original sources
PubMed1995

A 3-week hepatitis B vaccination schedule provides rapid and persistent protective immunity: a multicenter, randomized trial comparing accelerated and classic vaccination schedules.

Hepatitis B (HB) vaccinations given once weekly for 3 weeks can provide early seroprotection. This study compared immune responses induced by the accelerated (A; days 0, 10, 21) and classic (C; days 0, 28, 56) HB vaccination schedules. Two hundred seventy healthy subjects (95 men, 175 women) with a mean age of 23.8 years received 3 doses of GenHevac B, a recombinant vaccine produced in mammalian cells. The subjects were randomly assigned to schedules A or C. A booster dose was given 1 year later. One month after the third dose, 70% (schedule A) and 92% (schedule C) of the subjects were seroprotected and 100% (A) and 99% (C) had developed anti-pre-S2 antibodies. Before booster injections, 93% (A) and 95% (C) of the subjects were seroprotected, and 1 month after the booster, almost all subjects were seroprotected. A 3-week HB vaccination schedule with GenHevac B can confer early protective immunity lasting up to 1 year.

Adolescent↗
PubMed1994

Twelve-year follow-up study of hepatitis B immunization of Senegalese infants.

Numerous studies have documented the efficacy and safety of plasma-derived and recombinant hepatitis B vaccines. However, little is known about the long-term protection of hepatitis B vaccine, when anti-HBs declines to low or undetectable levels. This study reports results from a 9-12-year period follow up of infants immunized against hepatitis B in Senegal. At the end of the follow-up period anti-HBs were detected in 81% of children who received a booster dose at school age and in 68% of those who did not. HBsAg was detected in 19% of infants from the control group compared to only 2% of immunized infants, corresponding to a protective efficacy of 88%. The results show that long-term protection against HBsAg carriage of hepatitis B vaccination is very high and that a booster dose at school age does not significantly increase this protection.

Child↗
PubMed1993

High prevalence of mutations at codon 249 of the p53 gene in hepatocellular carcinomas from Senegal.

In hepatocellular carcinoma, mutation within the p53 gene occurs mainly at codon 249 and its frequency has been associated with exposure to aflatoxin. As Senegal is a country where liver cancer incidence is one of the highest in the world and where people are highly exposed to aflatoxin, we screened 15 liver cancer samples from this country for mutation at codon 249 of the p53 gene. Non-tumoral DNA from the patients showed a wild type genotype. Mutation at codon 249 of the p53 gene was detected in 10 of the 15 tumour tissues tested (67%). This frequency of mutation in codon 249 of the p53 gene is the highest described. These results confirmed that there is an association between countries of high aflatoxin intake and a high frequency of mutation in codon 249 of p53 gene, and that HBV alone does not contribute to these base changes.

Base Sequence↗
PubMed1993

Random-effects models, for longitudinal data using Gibbs sampling.

Analysis of longitudinal studies is often complicated through differences amongst individuals in the number and spacing of observations. Laird and Ware (1982, Biometrics 38, 963-974) proposed a linear random-effects model to deal with this problem. We propose a generalisation of this model to accommodate multiple random effects, and show how Gibbs sampling can be used to estimate it. We illustrate the methodology with an analysis of long-term response to hepatitis B vaccination, and demonstrate that the methodology can be easily and effectively extended to deal with censoring in the dependent variable.

Follow-Up Studies↗
PubMed1992

Persistent hepatitis B virus infection and hepatoma in The Gambia, west Africa. A case-control study of 140 adults and their 603 family contacts.

To determine the incidence of persistent hepatitis B virus infection and its etiologic role as a cause of hepatoma, the authors carried out a case-control investigation of 70 persons with hepatoma, 70 controls, and their families in 1981-1982 in The Gambia, West Africa. The risk of developing hepatoma after the age of 39 years was 1.4% in men and 0.3% in women. Hepatoma occurred more than twice as frequently among persons who had four or more older siblings as among persons who had less than two older siblings. The attributable risk between persistent infection with hepatitis B virus and hepatoma was 78% for individuals aged less than 50 years and 37% for persons aged 50 years or more, with an overall risk of 53%. The high prevalence of hepatitis B surface antigen and hepatitis B e antigen antigenemia in children under 15 years of age (14% of 341 children) and the positive correlation between late birth order and risk of developing hepatoma suggest that postnatal early childhood exposure to hepatitis B virus is an important risk factor. The use of a hepatitis B virus vaccine which provides durable immunity in very young children will probably prevent most cases of hepatoma.

Adolescent↗
PubMed1992

Comparative immunogenicity in children of mammalian cell-derived recombinant hepatitis B vaccine and plasma-derived hepatitis B vaccine.

Three doses of hepatitis B vaccine were given at 2, 4 and 9 months of age to 220 Senegalese infants living in the Dakar area of Senegal. Half of the infants received 5 micrograms plasma-derived hepatitis B vaccine (Hevac B) and the remainder 20 micrograms mammalian cell-derived recombinant hepatitis B vaccine (GenHevac B). Both vaccines contain S and pre-S2 encoded proteins; however, the recombinant vaccine had a much higher pre-S2 content than the plasma-derived vaccine. Adverse reactions to both vaccines were limited to mild and transient soreness at the injection site. Fever was reported in 14-21% of the infants and was likely to be related to DTP-polio vaccine which was given simultaneously. After the two first doses, seroconversion rates and geometric mean titres of anti-HBs were higher in infants receiving the recombinant vaccine than in infants receiving the plasma-derived vaccine. After completion of vaccination, all infants in both groups had protective levels of anti-HBs antibodies. The recombinant vaccine induced more rapidly antibodies directed against S and pre-S2 epitopes. Anti-pre-S2 antibodies were detected after the first injection of GenHevac B and only after the third injection of Hevac B. From the data, GenHevac B vaccine is expected to be as effective as Hevac B vaccine for controlling hepatitis B infection.

Amino Acid Sequence↗
PubMed1992

Simultaneous injection of hepatitis B vaccine with BCG and killed poliovirus vaccine.

In most developing countries, hepatitis B virus is endemic and prevention has to be carried out early in life and on a mass scale. In these regions, simultaneous administration of multiple antigens is normal practice. We have therefore investigated the interaction of hepatitis B vaccine with BCG and inactivated polio vaccine. The serological antibody response to poliovirus and HBsAg as well as the cellular immune response to tuberculin post BCG immunization were assessed. The immune responses to HBsAg, BCG and polio vaccines injected simultaneously were comparable to those observed after separate administration of each vaccine. Moreover, no increase of adverse reactions was noted. Results confirmed that HB vaccine could be introduced into the WHO expanded programmes on immunization without impairing the expected protective efficacy against the targeted vaccine-preventable diseases.

BCG Vaccine↗
PubMed1991

Scheduling of revaccination against hepatitis B virus.

Studies have shown that to maintain protection against infection after a primary course of hepatitis B immunisation, revaccination can be scheduled on the basis of an anti-hepatitis B virus surface antigen (anti-HBs) titre obtained 1 month after the booster dose. However, schemes which require post-booster testing may present practical difficulties. We applied a random-effects regression model to data from 118 Senegalese infants given three injections of hepatitis B vaccine about 6 weeks apart and a booster injection at 13 months, and show that revaccination can be scheduled on the basis of an anti-HBs titre recorded at the time of the booster dose. We also show that titre-at-booster is no less accurate in predicting future titre than 1-month post-booster titre. In several other studies the post-booster decline in anti-HBs conforms to the same mathematical description, indicating the generality of our findings.

Hepatitis B↗
PubMed1990

Hepatitis B surface antigen reactivity in man due to a new variant of hepatitis B virus.

A new type of hepatitis B virus (HBV) infection has been encountered in Senegalese infants and French adults characterized by serum hepatitis B surface antigen (HBsAg) without antibodies to the core antigen (anti-HBc). As the infection is not associated with the presence of the e antigen, it differs from HBV in its core antigen. After the loss of HBsAg, neither anti-HBc nor antibodies to HBsAg (anti-HBs) become detectable. This new infection (called HBV2 as opposed to the classical HBV1 infection) was found in infants with anti-HBs, either naturally acquired or produced by immunization against HBV. The use of monoclonal anti-HBs antibodies showed that two epitopes of HBV1 surface antigen could be detected in HBV2-positive sera. HBV DNA sequences could only be found in one of 15 HBV2-infected children using a DNA-DNA hybridization procedure; low levels of HBV DNA were also detected in 58% of the HBsAg-positive adult sera tested. If this new infection, apparently related to HBV1, is shown to cause chronic liver disease, hepatitis B vaccine should also contain surface antigen from HBV2.

Adult↗
PubMed1989

Hepatitis B virus infection in lepromatous and tuberculoid patients from Senegal.

Hepatitis B Virus (HBV) seric markers (HBs Ag, anti-HBs, and HBe Ag) were studied in 987 Senegalese leprosy patients (lepromatous: LL; tuberculoid: TT) in comparison with 6187 healthy adults (controls). Two populations of leprosy patients from ILAD (Institut de Léprologie Appliquée de Dakar) were studied: The First study (i.e.: study I) between 1973 and 1977 included 553 patients (329 LL; 224 TT). The Second study (i.e.: study II) between 1982 and 1986 included 434 patients (236 LL; 198 TT). HBV serological markers were tested by various techniques. By RIA, they were present in 98% and 96.5% in the studies I and II respectively. Each marker was studied and compared to the control population. HBs Ag detected by RIA was present in 25.5% (study I) and 23.0% (study II) when comparing to 15.2% in the control group. This marker was correlated with leprosy forms (LL and TT), age, sex, ethnic group.

Female↗
PubMed1988

[Immunogenicity of a hepatitis B vaccine obtained by genetic recombination and containing products of S and pre-S2 genes].

Immunization against hepatitis B by means of a vaccine obtained by genetic recombination on chinese hamster ovary cells was attempted in 32 adult subjects. The HBs antigen was purified from the culture supernatant and contained S and pre S2 genes products. Three 20 micrograms doses were injected intramuscularly at intervals of one month. Anti-HBs seroconversion levels and the geometrical mean of antibodies were slightly higher than those observed with plasma vaccines or genetically engineered yeast-derived vaccine. Antibodies directed against HBs appeared more rapidly and at a higher titre. Anti-pre S2 antibodies were detected after the third injection in 84 per cent of the subjects vaccinated. This recombinant hepatitis B vaccine prepared from chinese hamster ovary cells will probably be as effective as the first generation vaccines obtained by purifying the HBs antigen obtained from the blood of asymptomatic carriers.

Adult↗
PubMed1988

Anti-pre-S2 antibodies in natural hepatitis B virus infection and after immunization.

Anti-pre-S2 antibodies were detected by enzyme-linked immuno-absorbant assay using a synthetic peptide analogue of pre-S2 protein, in different groups of hepatitis-B-infected subjects, including patients presenting with cirrhosis and liver cancer, and also in infants immunized with hepatitis B vaccine. Anti-pre-S2 antibodies were not detected in hepatitis B surface antigen (HBsAg) chronic carriers, including patients with cirrhosis or primary liver cancer. Anti-pre-S2 antibodies were not detected in HBsAg-positive sera during the early phase of acute hepatitis. They were only noted upon recovery, when anti-HBs antibodies are detectable at the same time as HBsAg. After recovery, anti-pre-S2 antibodies were noted in 57% of test sera and were still detectable in 16% of anti-HBs-positive sera obtained years after HBV infection. Anti-pre-S2 antibodies were detected in 70% of infants immunized with 2 or 5 micrograms doses of Hevac B Pasteur vaccine, confirming that this vaccine contains pre-S2 antigen. Anti-pre-S2 detection was correlated with the anti-HBs antibody titre.

Carrier State↗
PubMed1987

HBsAG positive reactivity in man not due to hepatitis B virus.

A viral infection characterised by serum HBsAg positivity with serum anti-HBc negativity has been encountered in Senegal. The infection is not associated with the presence of HBeAg, so it differs from hepatitis B virus in its core antigen, but the surface antigen of the two viruses share some epitopes. After the loss of HBsAg, neither anti-HBc nor anti-HBs becomes detectable. Anti-HBs, naturally acquired or produced by immunisation, does not protect against this new infection. Chronic carriage occurs. If this new infection is confirmed to cause chronic liver disease, hepatitis B vaccine should include surface antigen from the new virus.

Carrier State↗
PubMed1987

Age- and sex-related study of hepatitis B virus chronic carrier state in infants from an endemic area (Senegal).

This report concerns hepatitis B virus (HBV) infections observed in 155 infants from Senegal, studied with a view to determining the factors involved in development of the chronic carrier state. A chronic carrier state was observed in 50.3% of the infants. This study confirms that the risk of chronic carriage is linked to age. This risk declines very rapidly with age, falling from 82% in infants under 6 months old, to 15% in children between the ages of 2 and 3 years. Spontaneous elimination of hepatitis B surface antigen (HBsAg) is uncommon in HBsAg carriers during childhood. The difference observed in chronic carriage between males and females is due to a difference in susceptibility of the two sexes to the development of the chronic carrier state: HBV infections (before 2 years of age) lead to a chronic carriage in 77% of males as against 50% of females. These conclusions are important in view of the immunisation programs being carried out against hepatitis B virus in endemic areas. For a maximum efficacy, vaccination must be carried out at birth, or shortly afterwards.

Age Factors↗
PubMed1987

Hepatitis B vaccine in infants from an endemic area: long-term anti-HBs persistence and revaccination.

Persistence of anti-HBs in 156 Senegalese infants immunized with hepatitis B vaccine was studied for periods ranging from 2 to 6 years after booster dose administration. Six years after the booster dose, 90.4% of the infants had detectable anti-HBs antibodies, with 78.1% having titers higher than 10 mIU/ml. The geometric mean titer was 60 mIU/ml. Females showed higher anti-HBs values than males. In a group of 11 infants who received no booster dose, anti-HBs antibodies were detectable 7 years after the first dose. However, the geometric mean titer was lower (26 mIU/ml). Revaccination (56 infants) led to an increase of the geometric mean titer to 469 mIU/ml 2 months later. These results show that a booster injection every 5-6 years should provide adequate protective anti-HBs levels in infants.

Antibodies, Viral↗
PubMed1986

Seven-year study of hepatitis B vaccine efficacy in infants from an endemic area (Senegal).

A booster dose of hepatitis B vaccine was given to 143 children in whom hepatitis B had not developed 1 year after initial vaccination. Over the next six years the incidence of hepatitis B in this group was 1.5% per year compared with 11.5% per year in a similar group of unvaccinated children. In the first 4 years the protective efficacy of the vaccine was 100%, but during the 5th and 6th years it fell to 67%. For maximum protection a second booster is needed, 5 years after the first.

Carrier State↗