Search

Background: The Regional Influenza Surveillance Group (GROG) is a French surveillance network set up in 1984. It collects virological specimens and health service based indicators on a weekly basis. Our aim was to assess the predictive value of the health service based indicators for the detection of influenza A epidemics.Methods: Virological data were used as a gold standard for defining the epidemics. For each health service based indicator, a statistical threshold was used as a test for the identification of epidemic weeks. Finally, an epidemiological criterion was defined in order to improve the specificity and the speed of detection of outbreaks.Results: Health service based indicators have a positive predictive value of around 0.80. They also advance the detection of outbreaks by between 1 and 4 weeks.Conclusions: These indicators are easy to collect and are useful for the surveillance of influenza epidemics. Such a system is the prerequisite for the rational use of preventive tools. [ABSTRACT FROM AUTHOR]

In man influenza viruses induce a cytolytic T lymphocyte (CTL) activity directed against autologous or HLA-A or -B compatible target cells infected with the immunizing virus. While only type specific CTL are characterized in man, we report here experiments showing intertypic activities of human CTL from donors vaccinated with both A and B type influenza viruses. Their peripheral blood leucocytes (PBL) restimulated in vitro with live influenza virus of one type gave rise to both anti-A and -B activities, when non-infected or Sendaï infected target cells were not lysed. These intertypic activities were restricted by HLA-A or -B antigens and were inhibited by 0KT3 antibody. When u.v.-inactivated viruses were used as restimulating antigen, no intertypic CTL were obtained. The results of competition experiments with cold targets show that no common antigens were recognized by anti-A and anti-B CTL. Moreover the restricting HLA-A or -B molecules seen in association with A or B types viruses appeared different in the same experiment, confirming that different antigens were probably involved for the agents of A and B subgroups. This influenza specific intertypic activity was therefore probably due to an intertypic stimulation of type specific CTL activities, possibly arising at the level of T helper cells. [ABSTRACT FROM AUTHOR]

Influenza A virus was found to enhance Staphylococcus aureus-induced histamine release in human leukocyte suspensions, but did not per se release histamine. This potentiating effect was found to be similar in cells from normal individuals and from patients with intrinsic asthma. The enhancement of mediator release could be due to viral neuraminidase on the surface of the virus, since a similar potentiating effect was caused by a purified neuraminidase preparation obtained from Vibrio cholerae, and the effect of virus as well as of the purified neuraminidase was completely abolished by a potent neuraminidase inhibitor. The potentiating effect of virus on bacteria-induced mediator release might be of importance for the conversion from latent to manifest asthma in upper respiratory tract infections. [ABSTRACT FROM AUTHOR]

Histamine release was examined in leukocyte suspensions from patients allergic to house dust mite, grass pollen, birch pollen or cat dander. Influenza A virus was found to enhance the antigen-induced mediator release, but did not cause release of histamine from the cells per se. Also histamine release induced by anti-IgE in cell suspensions from normal individuals was enhanced by virus. The potentiating effect of influenza A virus might be due to neuraminidase on the surface of virus, since a similar effect was caused by a purified neuraminidase obtained from Vibrio cholerae, and the effect of virus as well as the neuraminidase was completely abolished by a potent neuraminidase inhibitor. The synergistic enhancement in IgE-mediated histamine release by virus could be of significance for the conversion from latent to manifest asthma. [ABSTRACT FROM AUTHOR]

Histamine release from human basophil leukocytes was triggered by complement activation by means of endotoxins isolated from E. coli and Salmonella bacteria. Influenza A virus was found to enhance the mediator release, and the effect was caused by synergism, since virus itself did not release histamine. The potentiating effect was similar in cells from normal individuals and from patients with intrinsic asthma. The involvement of viral neuraminidase was examined by a potent neuraminidase inhibitor and this inhibitor completely abolished the potentiating effect by virus. A purified neuraminidase preparation obtained from Vibrio cholerae caused a similar potentiating effect in mediator release and the effect was abolished by the neuraminidase inhibitor. These findings indicate that viral neuraminidase is responsible for the potentiating effect of virus on the histamine release. This effect might play a role in septic conditions and possibly contribute to asthmatic attacks by infections. [ABSTRACT FROM AUTHOR]