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Notes: Objective To determine whether maternal influenza virus infection in the second and third trimesters of pregnancy results in transplacental transmission of infection, maternal auto-antibody production or an increase in complications of pregnancy.Design Case-control cohort study.Population Study and control cohorts were derived from 3975 women who were consecutively delivered at two Nottingham teaching hospitals between May 1993 and July 1994. A complete set of three sera was available for 1659 women.Methods Paired maternal ante- and postnatal sera were screened for a rise in anti-influenza virus antibody titre by single radial haemolysis and haemagglutination inhibition. Routine obstetric data collected during and after pregnancy were retrieved from the Nottingham obstetric database. Cord samples were tested for the presence of IgM anti-influenza antibodies, and postnatal infant sera were tested for the persistence of influenza-virus specific IgG. Paired antenatal and postnatal sera were tested against a standard range of auto-antigens by immunofluorescence.Main outcome measures Classification of women as having definite serological evidence of an influenza virus infection in pregnancy (cases) or as controls.Results Intercurrent influenza virus infections were identified in 182/1659 (11.0%) pregnancies. None of 138 cord sera from maternal influenza cases was positive for influenza A virus specific IgM. IgG anti-influenza antibodies did not persist in any of 12 infant sera taken at age 6–12 months. Six of 172 postnatal maternal sera from cases of influenza were positive for auto-antibodies. In all cases the corresponding antenatal serum was also positive for the same auto-antibody. There were no significant differences in pregnancy outcome measures between cases and controls. Overall, there were significantly more complications of pregnancy in the cases versus the controls, but no single type of complication achieved statistical significance.Influenza infection in the second and third trimesters of pregnancy is a relatively common event. We found no evidence for transplacental transmission of influenza virus or auto-antibody production in pregnancies complicated by influenza infections. There was an increase in the complications of pregnancy in our influenza cohort.

Notes: Summary The effect of 1-adamantanamine hydrochloride (1-AH) on the multiplication of three strains of rubella virus in RK-13 tissue cultures was studied. At a concentration of 25μg/ml. the compound depressed the yield of infective virus, reduced the cytopathic end-point titres and inhibited the formation of rubella virus microplaques. The inhibition of microplaques was the most sensitive method of detecting the antiviral activity of 1-AH and concentrations as low as 10μg/ml. were effective. Whilst 25μg/ml. of 1-AH did not produce obvious toxic effects, 40μg/ml. caused cytoplasmic vacuolation and decreased the rate of cell divison of RK-13 cultures. Inhibition of rubella virus CPE by 1-AH was more marked in virus strains poorly adapted to growth in RK-13 cultures. Studies on the mode of action of 1-AH indicate the absence of direct virucidal action and the compound neither decreased the rate of adsorption of virus to RK-13 cells nor inhibited release of intracellular virus from infected cells. The compound appeared to act at an early stage in the growth cycle and was not effective in inhibiting subsequent virus multiplication if added later than 5 hours after infecting tissue cultures with rubella virus.

Notes: Summary Tumour transplantability in weanling hamsters was investigated for six differentin vitro cell generation levels of SV40 induced hamster tumour cells. Transplantability varied from 23% at the 55th cell generation of tumour cells to 71% at the 53rd cell generation. No direct relationship was demonstrated between the percentage of hamsters developing tumours and the cell generation level. The incidence of tumours occurring in the first month after inoculation of tumour cells varied from 7% to 17% and was greatest in animals inoculated with the largest number of tumour cells. At six months, the incidence of tumours was reversed; 37 % of hamsters inoculated with 5000 tumour cells had developed tumours and 55% of the animals which received 1000 cells had tumours. Immunization of hamsters with various normal cell extracts before transplantation of SV40 tumour cells enhanced tumour development. Immunization of hamsters with adenovirus types 5, 12 and 31, CELO virus and human wart virus did not induce transplant immunity against SV40 virus induced tumour cells: transplantation immunity was only found in hamsters immunized with SV40 virus.

Notes: Summary Newborn hamsters were inoculated with SV40 virus to produce subcutaneous tumours and during the subsequent tumour incubation period they were immunized with homologous and heterologous viruses. The incidence of tumours in animals given only the single tumour producing dose of SV40 virus was 50%. In the group of hamsters subsequently immunized with further doses of SV40 virus the tumour incidence was reduced to 4.8%. The incidence of SV40 tumours was not reduced significantly when hamsters were immunized with adenovirus types 12 or 31, or human wart virus. However, immunization with chick embryo lethal orphan (CELO) virus reduced the incidence of SV40 induced tumours to 5.6%. No serological relationship between SV40 virus, CELO virus and adenovirus type 12 could be demonstrated by specific cross-neutralization tests.

Notes: Summary Genetic analysis of influenza B virus strains isolated during concurrent epidemics (February–March 1982) in three physically separated schools was carried out using the RNA:RNA hybridization technique. The data supports the hypothesis that the influenza B virus epidemics in each school were initiated by different viruses and the variability of the strains in a closed community was found to be minor though some variants were detected.

Notes: Summary Electrophoretic migration rate differences were detected in high resolution SDS polyacrylamide gels for nucleoprotein (NP), matrix protein (M), non structural protein (NS1), haemagglutinin (HA) and, less regularly, for the polymerase polypeptides P1, P2 and P3 induced by different influenza A viruses. The technique allowed parental assignation of the corresponding genes in certain recombinant viruses including A/PR/8/34 (H0N1)—A/HK/117/77 (H1N1), A/Okuda/57 (H2N2)—A/HK/119/77 (H1N1) and A/Leningrad/76 (H3N2)—A/Leningrad/46 (H0N1) recombinants, thus considerably extending the technique which had been applied previously to A/PR/8/34—A/HK/68 (H3N2) only. Agreement in gene assignment between three recombinants of the former group and 11 of 17 recombinants in the A/Okuda/57—A/HK/119/77 group was noted when the data obtained using the polypeptide method was correlated with a direct genetic analysis by others using RNA:RNA hybridisation techniques. The polypeptide method appears to have wide application for the initial rapid analysis of influenza A virus recombinants obtained using parents of different influenza subtypes although complete analysis of the total genome requires the use of RNA hybridisation techniques. Two additional virus induced proteins are described, a phosphorylated form of NS 1 and a non structual polypeptide with a molecular weight of 16 K daltons.

Notes: Summary An electron microscopic immunogold labelling technique employing monoclonal antibodies has been applied to the antigenic analysis of influenza A and B viruses. Reassortant influenza A H3N2 viruses containing haemagglutinin molecules from viruses isolated between 1968 and 1982 were analysed with a panel of monoclonal antibodies raised against viruses which appeared over the same period. The immunogold labelling technique clearly demonstrated the antigenic drift in the haemagglutinin molecule that occurred between 1968 and 1982. When the technique was applied to the examination of viruses from a more geographically restricted influenza epidemic in a semi-closed community, antigenic variants were found. Furthermore the technique enabled the identification of distinct antigenic variant subpopulations within a single clinical isolate. Analysis of the HA of MDCK cell or egg grown virus by this procedure provided data to support the hypothesis that the host cell exerts selective pressure on subpopulations of virus resulting in the emergence of antigenic variants.