Nitrogen processing by treatment wetlands in a tropical catchment dominated by agricultural landuse.

Agriculture is a major contributor to marine nitrogen pollution, and treatment wetlands can be a strategy to reduce it. However, few studies have assessed the potential of treatment wetlands to mitigate nitrogen pollution in tropical regions. We quantify the nitrogen removal rates of four recently constructed treatment wetlands in tropical Australia. We measured denitrification potential (Dt), the inflow-outflow of nutrients, and tested whether the environment in these tropical catchments is favourable for nitrogen removal. Dt was detected in three of the four systems with rates between 2.0 and 12.0 mg m-2 h-1; the highest rates were measured in anoxic soils (ORP -100 to 300 mV) that were rich in carbon and nitrogen (>2% and >0.2%, respectively). The highest nitrogen removal rates were measured when NO3--N concentrations were >0.4 mg L-1 and when water flows were slow. Treatment wetlands in tropical regions can deliver high removal rates of nitrogen and other pollutants when adequately managed. This strategy can reduce nutrient loads and their impacts on sensitive coastal zones such as the Great Barrier Reef.

Immunization with a DNA expression vector encoding the varicella zoster virus glycoprotein E (gE) gene via intramuscular and subcutaneous routes.

In this study we constructed a plasmid containing the gene encoding varicella-zoster virus transmembrane glycoprotein gE (VZV gE) and evaluated its utility for DNA immunization in mice. Our initial work demonstrates that intramuscular and subcutaneous injection of VZV gE DNA, without the use of costimulatory molecules or other adjuvant materials, results in the generation of antigen-specific antibodies of primarily the IgG2a subclass, indicating that this vaccine can stimulate Th1 type immunity. This is the first report of a prototype DNA vaccine for varicella-zoster virus.

Molecular epidemiology of varicella-zoster virus in East London, England, between 1971 and 1995.

The molecular epidemiology of varicella-zoster virus in London, England, between 1971 and 1995 was examined by using two informative polymorphic markers, variable repeat region R5 and a BglI restriction site in gene 54. Viruses from 105 cases of chickenpox and 144 of zoster were typed. Two alleles of R5, A and B, were found at prevalences of 89 and 6%, respectively. No difference in allele frequency between the zoster and chickenpox cases was found, and no change in the frequencies of these alleles was observed to occur over time. By contrast, a BglI restriction site (BglI+) was found with increasing frequency over time among cases of varicella (P < 0.005) and, to a lesser extent, cases of zoster. The BglI+ polymorphism was strongly associated (P < 0.0005) with zoster in subjects who had immigrated to the United Kingdom from countries with low adult immunity to varicella (LAIV). Sixty-three percent of the subjects with zoster who had emigrated from countries with LAIV carried the BglI+ virus, in contrast to 10% of adults who had grown up in countries with high adult immunity to varicella. The significance of these data, in view of the changing epidemiology of chickenpox, is discussed.

Detection of specific IgM in varicella and herpes zoster by antibody-capture radioimmunoassay.

A simple and sensitive M antibody-capture radioimmunoassay (MACRIA) is described which utilizes crude commercial VZV antigen and a single monoclonal anti-VZV antibody. This was compared to the immunofluorescence (IF) test for IgM antibody and was used to study IgM responses in sera from 261 patients with varicella and 220 patients with herpes zoster. With MACRIA, IgM antibodies were detected in all patients with varicella. The IgM antibodies appeared shortly after onset of rash, reached peak levels between 1 and 4 weeks after onset and then declined to low or undetectable levels in most, though not all, patients after 3 months. IgM antibodies were also detected in 98.2% of patients with herpes zoster, but the levels of IgM were significantly lower than after varicella and there was wider individual variation both in magnitude and duration of the IgM responses, in some cases only lasting 2-3 weeks. Comparison between MACRIA and IF showed good agreement in the detection of IgM antibodies following varicella. Discordant results were obtained with 13% of sera, of which 81% were taken either early or late after onset of rash and contained very low IgM levels. In contrast, 62 (28%) of the 220 sera from patients with zoster gave discordant results in the two tests, all except five being MACRIA-positive but IF-negative. The largest proportion of discordant results were obtained with sera taken more than 3 months after onset of rash, but 18 (29%) contained high IgM levels and were taken during the period of peak IgM responses. The diagnostic applications of the VZV MACRIA are discussed.

Reduction in immunoreactivity of varicella-zoster virus proteins induced by mycoplasma contamination.

During the study of protein differences between several strains of varicella-zoster virus (VZV), two of the strains were found to be contaminated with Mycoplasma hyorhinis. Polyacrylamide gel electrophoresis showed fourteen extra bands present in MRC5 fibroblasts infected with these strains compared to other strains of VZV. A more striking difference was observed when infected cultures were used as antigens in immunoblotting. Certain viral proteins, corresponding in molecular weight to the viral glycoproteins, showed greatly reduced immunoreactivity. Experimental contamination of a mycoplasma-free strain of VZV with the glucose fermenting M. hyorhinis produced similar effects on immunoreactivity, while contamination with the arginine-hydrolysing M. orale produced no detectable effects. Given these data, it appears likely that the glucose-fermenting species induced significant changes in the VZV glycoproteins, possibly by depletion of sugars or interference in glycosylation pathways. The implications of this are discussed.

Antibody against viruses in maternal and cord sera: specific antibody is concentrated on the fetal side of the circulation.

Paired maternal and cord sera from 100 pregnancies were tested for antibodies against herpes simplex virus, measles virus and respiratory syncytial virus by complement fixation and for antibodies against rubella virus, influenza A virus and influenza B virus by haemagglutination-inhibition. For four viruses (herpes simplex, measles, respiratory syncytial and rubella) higher levels of antibody were found in cord than in maternal sera. There was no difference between maternal and cord serum titres against influenza B virus but significantly higher levels of antibody against influenza A virus were found in maternal sera than in cord sera. This discrepancy was investigated by measuring antibodies against the surface antigens of influenza A by a complement fixation technique, and by single radial haemolysis. Both methods showed a preponderance of virus-specific antibody in cord sera. We conclude that IgG antibodies against most, if not all, viruses are concentrated on the fetal side of the circulation, but the conventional haemagglutination-inhibition techniques may fail to detect this difference.

The postnatal acquisition of factors which affect the influenza haemagglutination-inhibition test.

Levels of maternally transferred antibodies against the surface antigen of the A/Texas/1/77 strain of influenza virus showed the expected decline during infancy when measured by complement fixation (CF). However, this decline was not observed when these antibodies were measured by haemagglutination-inhibition (HI). It has been postulated that this discrepancy is due to the acquisition, in the early days of life, of non-specific serum factors which increase the HI activity of sera. The levels of these factors were determined indirectly by calculating HI:CF ratios and it was shown that the factors are rapidly acquired by children between the fifth and twentieth week of life.

The role of host responses in the recovery of mice from Sendai virus infection.

The antiviral responses in mice to intranasal inoculation with Sendai virus are described. To investigate the relative importance of the humoral, cell-mediated and interferon responses, the pathogenesis of this infection was studied in animals which were immunocompetent, T cell-deprived or immunosuppressed with cyclophosphamide. Treatment with cyclophosphamide converted the mild, self-limiting infection observed in immunocompetent mice into a severe and frequently lethal pneumonic disease. This was associated with an enhanced interferon response but no detectable antibody or cell-mediated immune response. T cell-deprived mice suffer an infection of intermediate severity associated with an increased interferon response, a normal humoral immune response and no cell-mediated immune response. The implications of these results in relation to the role of the antiviral responses in recovery from Sendai virus infection are discussed.