Immunogenicity and safety of yeast-derived recombinant hepatitis B vaccine (Heberbiovac HB) in South African children.
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Biomedical subjects
Publications and source records attributed to S Aspinall.
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BACKGROUND: Because baboons are being considered as a source of xenografts for human liver transplantation in patients with hepatitis B virus- (HBV) induced cirrhosis to forestall infection of the graft by the virus, we undertook a study to ascertain if baboons are resistant to HBV infection. METHODS: Six chacma baboons were inoculated with serum containing HBV and were followed for 52 weeks to detect transmission of infection. RESULTS: Anti-HBc was detected in the serum of four baboons 16 weeks after inoculation. Virions, small spherical particles, and tubular forms were seen at this time in the serum of the one baboon studied by transmission electron microscopy. HBV DNA was detected by polymerase chain reaction in the serum of the same four baboons throughout the period of follow-up, as well as in liver tissue obtained after 52 weeks. The specificity of the DNA was confirmed by Southern hybridization. Nucleotide sequences showed complete sequence identity between the HBV DNA in each of the baboon sera and one of the two HBV genotypes inoculated. Serum transaminase levels tested at 4-weekly intervals were always normal and histological examination of liver tissue after 52 weeks showed no evidence of chronic hepatitis. Examination of squash preparations of liver tissue by electron microscopy in one baboon revealed core-like particles. CONCLUSIONS: Chacma baboons are susceptible to HBV infection and appear to develop a chronic carrier state. The use of xenografts from baboons should preferably be avoided, but if they are used again for HBV-infected patients it would be prudent to treat the patients as if they had received an organ from a human donor.
Virus-like particles (VLPs) of the high-risk human papillomavirus (HPV) types 16, 18, 31, 33, and 45 were used as antigen in enzyme-linked immunosorbent assay (ELISA) to determine the prevalence of serum IgG in a group of San people originally from Namibia, now residing in South Africa. The San children had low seroprevalence to all VLP types, but 26/115 (22.6%) of the children were seropositive to at least 1 VLP type. Among the adults, seroprevalence was significantly higher. The seroprevalence of antibodies in 101 San women to VLP-16 was 16.8%, VLP-18 18.8%, VLP-31 12.9%, VLP-33 17.8%, and VLP-45 22.8%. Five of the 11 men were seropositive: 2 for VLP-31, 1 for VLP-18, 1 for VLP-33, and 1 for VLP-45. Seroreactivity appeared to be type specific, except possibly to VLP-18 and -45. Of the adults, 50.5% were seropositive to at least 1 VLP type and 24.8% were seropositive to >1 VLP type. From this study, it is concluded that the San people are exposed to HPV-16, -18, -31, -33, and -45, with antibodies to VLP-45 being the most prevalent.
STATEMENT OF PROBLEM: Hepatitis B infection (HBV) is a significant hazard in the dental environment because the virus may be transmitted through contaminated dental instruments. PURPOSE: This study determined whether cold disinfectants can inactivate HBV DNA and HBV surface antigens on diamond burs contaminated with HBV and whether ultrasonication can increase the antiviral properties of these agents. MATERIAL AND METHODS: Sterile dental diamond burs were contaminated with serum from a patient who tested positive for HBV surface antigen and hepatitis B viral DNA. The burs were air dried and placed in solutions containing either Cidex, Asepsys, TBS, Rotagerm, Virkon disinfectants, or a control phosphate buffered saline. Burs were divided into 2 groups and disinfected for 15 minutes. The first group was ultrasonicated; the second group was not ultrasonicated during disinfection. All the burs were transferred to phosphate buffered saline and ultrasonicated to remove any remaining viral particles. The ultrasonicate was tested for the presence of HBV surface antigen with a microparticle enzyme immunoassay and for hepatitis B viral DNA with a chemiluminescent molecular hybridization assay. RESULTS: TBS did not require ultrasonication to inactivate viral DNA and surface antigen. Rotagerm and Virkon inactivated surface antigen and viral DNA only with ultrasonication. Cidex and Asepsys inactivated viral DNA but not surface antigen with ultrasonication. CONCLUSION: The chlorine containing compound TBS was the most active disinfectant tested and did not require ultrasonication to destroy HBV. The remaining disinfectants should be used with ultrasonication to inactivate HBV.
AIM: To investigate the age related prevalence of hepatitis G virus (HGV) infection and its mode of transmission in relation to hepatitis B (HBV) and C (HCV) co-infection in South African blacks. METHODS: Reverse transcriptase polymerase chain reaction was performed to detect active infection, using primers for the 5'-NCR, NS5a, and NS3 regions. Antibodies to HGV envelope-2 protein (anti-E2), which measures past infection, were also sought. RESULTS: The overall prevalence of active infection was 116/580 (20%). A higher prevalence was noted in HBsAg carriers (28/106; 26.4%) and HCV positive subjects (25/82; 30.5%). In contrast to developed countries, active and past infection was seen in 12.9% and 12.1% of the general population, respectively (subjects negative for HBsAg and anti-HCV markers and with normal alanine aminotransferase values), with a total prevalence of 21.1% (52/248). Viraemia and anti-E2 were almost mutually exclusive. The distribution of viraemia by age was: < or = 15 years, 20/223 (9.0%); 16-35 years, 42/147 (28.6%); > or = 36 years, 37/151 (24.5%), with a significant difference (p = 0.001) in age related prevalence. A similar trend was observed for the prevalence of past infection in the general population. CONCLUSIONS: HGV infection begins in childhood and increases with age in South Africa, but transmission is largely independent of HBV and HCV. No association was found between HGV viraemia and hepatitis, or with co-infection with either HBV or HCV.
A 17 year-old boy with chronic hepatitis B who developed left-sided muscle wasting is reported. When other possible known diseases as the cause of the neurogenic muscle disease were excluded it was hypothesised that there was a relation between the chronic hepatitis B infection and the neurogenic muscle disease. An immunopathogenesis could be explained by the presence of HBsAg in the cerebral spinal fluid.
BACKGROUND: A low-cost, 'flash' heat-inactivated hepatitis B vaccine with enhanced immunogenicity allowing for a relatively low dose (Hepaccine B; Cheil Foods and Chemicals, Korea) was introduced into the South African Expanded Programme on Immunisation during 1995 to immunise infants against hepatitis B. To determine the seroresponse of this vaccine in South Africa, a country with a high hepatitis B virus (HBV) prevalence, a field trial was conducted in a rural health clinic. METHODS: The immunogenicity of Hepaccine B, containing 1.5 micrograms/0.5 ml, was studied in 186 black infants attending the Soshanguve III clinic, north-west of Pretoria. Infants receiving three consecutive doses in the anterolateral thigh at 6, 10 and 14 weeks were monitored. The doses were administered concurrently with their routine oral polio vaccine (OPV) and diphtheria, pertussis and tetanus (DPT) immunisations. Vaccine side-effects were recorded. Blood specimens were collected 3 months after the final vaccination. Sera were tested for antibodies to hepatitis B surface antigen (anti-HBs) by IMx AUSAB (Abbott Laboratories, USA). Levels of anti-HBs were determined by comparison with standard reference preparations and expressed in mlU/ml. RESULTS: Side-effects of the vaccine were minor, with limited local reaction at the site of administration. The anti-HBs seroconversion rate was 93.0%, based on a titre of > or = 10 mlU/ml with a geometric mean titre of 257.58 mlU/ml. CONCLUSIONS: Administration of 1.5 micrograms dose of Hepaccine B at 6, 10 and 14 weeks is safe and highly immunogenic in black South African infants, and this vaccine is suitable for use in countries with high HBV prevalences such as in Africa. The use of an economical hepatitis B vaccine would greatly facilitate the prevention of hepatitis B in these countries.
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Different hepatitis C virus (HCV) genotypes may be associated with viral load, severity of liver disease, hepatocellular carcinoma, geographical location and sensitivity to interferon. In this study the prevalence of HCV-RNA and distribution of HCV genotypes was investigated in anti-HCV-positive patients admitted to Ga-Rankuwa Hospital during 1994 and 1995. One hundred and forty-nine sera from three groups of anti-HCV-positive patients (N = 78) were analysed. These included: (i) patients with various liver diseases; (ii) patients admitted to the renal unit; and (iii) a miscellaneous group of patients for whom HCV antibody screening was requested. Twenty-six patients (33%) tested positive for viral RNA. Restriction fragment length polymorphism (RFLP) analysis of these patients showed that HCV genotypes 1, 2 and 5 were present. Type 2 (35%) was the dominant genotype in the region served by Ga-Rankuwa Hospital. In a large proportion of viral RNA-positive patients (27%), the polymerase chain reaction product could not be digested with one of the sets of enzymes, and therefore could not be classified into genotypes 1 to 6. Further studies are now in progress to enhance our current knowledge of the epidemiology of HCV infection.
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Serum hepatitis B virus (HBV) DNA is now the most important and reliable marker for monitoring hepatitis B viral replication. Quantitative detection of HBV DNA in serum is based on commercial standardized molecular hybridization test systems. We compared two hybridization assays, the Digene Hybrid Capture assay (Digene Diagnostics, Beltsville, MD) and the Abbott HBV DNA assay (Abbott Laboratories, North Chicago, IL, USA) with the polymerase chain reaction (PCR) technique, for detection and quantitative measurement of serum HBV DNA. Forty-two patients with various HBV serological marker profiles were included in this study. The patients were divided into four groups according to their HBV DNA values after HBV DNA determination in the serum by the Abbott assay. For each patient HBV DNA was then determined by the Digene assay and by PCR. In the case of Digene and PCR there was a 97.6% correspondence in the outcome of the two methods, whereas in the Abbott assay and PCR there was only 69% correspondence. The McNemar test of symmetry showed no statistically significant difference between the Digene assay and PCR, whereas there was a significant difference (P < 0.01) in the Abbott assay and PCR. For low positive HBV DNA values between 1.5 and 20 pg ml-1 the Abbott assay yields inconclusive results. Differences observed between the two hybridization assays underline the need for standardization of HBV DNA quantitation.
In an effort to control hepatitis B virus (HBV), the prevalence rates of the virus need to be ascertained in different regions or populations. As a baseline for a hepatitis B immunisation programme, the seroprevalence of HBV markers was determined in 400 San Bushmen from a community who were translocated from Northern Namibia to South Africa. HBsAg was detected in 6.8% while 57.0% showed one or more markers of HBV infection. The balance of the population (43.0%) showed no evidence of previous exposure to HBV. The HBV exposure rate of 57.0% is intermediate to high with reference to internationally reported figures and protection of seronegative individuals through immunisation is recommended. Individuals without possible natural immunity against HBV such as those with anti-HBc or anti-HBs as a sole marker may provide insight into the circulation of HBV mutants in this community, since these sole markers could be seroconversion in response to a mutant HBV strain.
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A community based sero-epidemiological study was undertaken to determine the age specific prevalence rates of hepatitis A virus (HAV) and hepatitis B virus (HBV) infection in a band of Bushmen in the West Caprivi, Namibia. All children tested and all but two of the adults tested showed the presence of anti-HAV antibodies. Nineteen individuals (18%) were positive for HBsAg and 65 (61%) individuals had serologic evidence of past exposure to HBV infection.
Serological markers for evidence of past exposure to hepatitis B virus (HBV) and hepatitis C virus (HCV) were investigated in a cohort of refugees from Mozambique. Serological markers for past exposure to HBV were detected in 56% of the population and, in addition, 13.2% carried the HBV surface antigen. Anti-HCV antibodies could be confirmed in 3.2% of the population and occurred mostly in the older individuals. Only one anti-HCV antibody positive individual was positive for HBsAg. Immunity to rubellavirus had reached 85% by 11 years of age.