Maternal antibody and respiratory syncytial virus infection in infancyOne hundred newborn infants were studied prospectively for 1 year for evidence of infection with respiratory syncytial virus (RSV). The indirect membrane fluorescence technique was used to determine specific antibody in sera. Infection was shown in 29 cases. In 31 infants exposed to an RSV epidemic season, there was no evidence of infection. Maternal antenatal sera were also tested, and wide range of IgG antibody to RSV was found. Mean titre of maternal IgG antibody to RSV was significantly higher (P less than 0.001) in those mothers whose babies remained uninfected than in those whose babies had proved RSV infection before 6 months of age. Babies born to mothers with high levels of IgG antibody to respiratory syncytial virus were protected against infection with this virus during the first months of life when the risk of severe disease was greatest.
Intranuclear virus particles in human genital wart tissue: Observations on the ultrastructure of the epidermal layerA. E. G. Dunn, Marie Ogilvie|Journal of Ultrastructure Research|1968 The effect of cigarette smoke on adherence of respiratory pathogens to buccal epithelial cellsOmar R. El Ahmer, Stephen D. Essery, Abdulrahman T. Saadi et al.|FEMS Immunology & Medical Microbiology|1999 Smoking is associated with an increased risk of respiratory tract infection in adults. In children, exposure to cigarette smoke is a risk factor for respiratory tract infection and bacterial meningitis: Active smoking and passive exposure to cigarette smoke is also associated with carriage of some potentially pathogenic species of bacteria in both adults and children. The aims of the study were to determine the effect of active smoking on: (1) bacterial binding to epithelial cells; (2) expression of host cell antigens that act as receptors for some species; and (3) the effects of passive exposure to water-soluble components of cigarette smoke on bacterial binding. Flow cytometry was used to assess binding to buccal epithelial cells of the following species labelled with fluorescein isothiocyanate: Neisseria meningitidis, Neisseria lactamica, Streptococcus pneumoniae, Bordetella pertussis, Haemophilus influenzae, Moraxella catarrhalis, Staphylococcus aureus. Flow cytometry was also used to assess expression of host cell antigens which have been identified as bacterial receptors. For each species, binding to cells of smokers was significantly higher than to cells of non-smokers; however, expression of host cell antigens was similar on epithelial cells of both groups. Non-dilute cigarette smoke extract reduced binding of bacteria to epithelial cells, but dilutions between 1 in 10 and 1 in 320 enhanced binding. We conclude that smokers might be more densely colonised by a variety of potentially pathogenic bacteria. The enhanced bacterial binding to epithelial cells of smokers is not related to enhanced expression of host cell antigens that can act as receptors for some species, but possibly to components in the smoke that alter charge or other properties of the epithelial cell surface. Passive coating of mucosal surfaces with components of cigarette smoke might enhance binding of potentially pathogenic bacteria.
Characterization of surface antigens of <i>Trichinella spiralis</i> infective larvaeInfective larvae of trichinella spiralis were surface-labelled with radioactive iodine, and the products were characterized biochemically and immunochemically. The labelled material was restricted to two basic subunits: a lentil lectin-adherent glycoprotein (GP), mol. wt 47K, and a lentil lectin-nonadherent protein fraction (P), mol. wt 55K. Both of these form homologous dimers through as yet unspecified covalent bonds to yield GP90 and P105. GP is further polymerized into higher molecular weight forms by disulphide bond-dependent associations. suggesting a highly cross-linked arrangement in the cuticle. To what extent this structure contributes to the overall organization of the cuticle remains to be established. The two labelled surface molecules are immunogenic in the infected host, and do not react with a panel of sera taken from animals chronically infected with other nematode species. The approach therefore offers immediate possibilities for immunodiagnosis in nematode infections, and for a comparative immunochemical study of the surface cuticle of different stages of the same and different nematode species and for studies of the function of the nematode cuticle.
Antibodies to Respiratory Syncytial Virus Polypeptides and their Significance in Human InfectionKenneth Ward, Paul R. Lambden, Marie Ogilvie et al.|Journal of General Virology|1983 The human antibody response to respiratory syncytial (RS) virus infection was investigated using radioimmunoprecipitation analysis (RIPA). A total of nine RS virus-specific proteins, VP200, VGP95, VP68, VGP48, VPN41, VP35, VP27, VP23 and VGP20 were identified by comparing 35S- or 3H-labelled extracts of infected and uninfected HEp-2 cells, and by radioimmunoprecipitation using a hyperimmune human serum. Three glycopeptides, VGP95, VGP48 and VGP20, were identified by incorporation of [3H]glucosamine, and two of these (VGP48 and VGP20) were assumed to be part of a single disulphide-bonded polypeptide since they were precipitated by a monoclonal antibody raised against a surface protein. Human serum antibodies to three major RS virus proteins, VGP95, VGP48/VGP20 and VPN41 were measured by RIPA using radioiodinated RS virus antigens. Sera from a group of mothers whose babies escaped RS virus infection during a local epidemic showed increased antibody levels to VPN41 when compared to sera from mothers whose babies had become infected with RS virus within the first 6 months of life. In infants who remained uninfected with RS virus during the first 12 months of life the maternal gift of antibody decayed to about 50% at 3 months with traces of antibodies detected in a few sera at 12 months. The antibody levels detected in the sera of infants less than 3 months old convalescent from primary RS virus infection did not exceed the mean levels present in the serum of uninfected babies. Infants between the ages of 6 and 12 months were able to mount an IgG response to VPN41 and VGP48 but, unlike adults and older children, a particularly striking finding was their failure to produce antibodies to VGP95.