SUMMARY Four thousand and one hospital staff were screened for hepatitis B virus (HBV) markers in a vaccination programme in Hong Kong. The seropositivity rate for HBsAg, anti-HBs and anti-HBc were significantly higher in the 3160 existing hospital staff than in 841 new recruits. Of the subjects negative for HBV markers, 605 were randomized to receive three doses of either 10 or 20 μg of the Merck Institute vaccine (HB-VAX). Compared with the 20 μg dose, vaccination with the 10 μg dose results in equal immunogenicity and efficacy at the completion of the three injections but induced a slower response rate and lower anti-HBs titres with the first two doses. The commonest side-effect of local soreness was less with the 10 μg dose. We conclude that (1) hospital staff working in high endemic areas should be vaccinated on recruitment and (2) the 10 μg dose of HB-VAX can replace the recommended 20 μg dose for adults, being cheaper and as efficacious.
Summary. A defect in specific T cell immunity has long been assumed to be the central mechanism of persistent Hepatitis B virus (HBV) infection. Recent studies on HBV transgenic mice have suggested, however, that functional deficit of dendritic cells (DC) was an underlying cause for the T cell dysfunction. The functions of monocyte‐derived DC were determined by studying 75 subjects that included chronic hepatitis B patients with low or high HBV load; antibody to hepatitis B surface antigen (anti‐HBs) positive individuals who had recovered completely from previous acute HBV infection; healthy donors who had received hepatitis B vaccination and were anti‐HBs positive; and immunologically naïve to HBV or the vaccine individual. Impaired interactions between monocyte‐derived DC and T cells were shown in chronic HBV infection patients, especially in those with active virus replication. The dysfunctions included: (i) failure of DC to increase human leukocyte antigen (HLA‐II), B7 expression and interleukin‐12 secretion in responses to hepatitis B surface antigen (HBsAg), (ii) defective induction of T cell proliferative response to HBsAg, (iii) failure to activate T cells to produce cytokines and (iv) deficit in the induction of antigen specific cytotoxic T lymphocytes (CTLs). In vitro treatment of DC with tumour necrosis factor‐ α improved HLA‐II and B7 expression, as well as Th cell and CTL responses. It is concluded that defective DC‐T cell interactions may account for the specific T cell immune defects in chronic HBV infection. Immunotherapy that aims at restoring DC functions could offer a new opportunity for effectively managing persistent HBV infections.
To reveal Herpes simplex virus 2 specific IgG and to determine their avidity the ELISA test-kit was constructed using recombinant protein gG2 (PSC SPC Diaproph-Med). Using this test-kit the distribution of specific antibodies with different avidity indexes was investigated in practically healthy donor samples. It is possible to use the mentioned ELISA test-kit for confirmation of primary infection, and also for differentiation of primary infection, chronic disease and virus reactivation. Thus, this ELISA test-kit could be an additional tool in herpetic infection diagnosis.
The authors present up-to-date information concerning different inducers of different interferon types in vivo and in vitro. Interactions between the structure and interferon-inducing activity of high and low molecular weight inducers are in the focus of this paper. There are also a lot of data, concerning different biological properties of interferon-inducing compounds. Different aspects of inducers use as antiviral and immunomodulating drugs are also discussed.
The paper deals with the study of production of tumour necrosis factor (TNF), the key mediator of inflammation and immune responses of the organism, under experimental and staphylococcus infection (Staphylococcus aureus, st. 209) on mice of C57B16 line. It is established that staphylococcus infection of animals lead to TNF induction. Dynamics of this cytokinin synthesis by peritoneal macrophages and splenocytes under the infection of mice with S. aureus in different doses differed in time and as to absolute values. In animals infected by staphylococcus in a dose of LD30 the TNF production was high as compared to the control for 72 h after the infection and was normalized on the 4-6th day of the experiment. When using staphylococcus in a dose of LD50, spontaneous production of this cytokinin was higher than that in the control for the whole period of observation.
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