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 3,975 women who were consecutively delivered at two Nottingham teaching hospitals between May 1993 and July 1994.
To investigate the clinical and serological responses to an inactivated influenza vaccine (split-virion A/Singapore/6/86-like strains H1N1 (15 ug HA), A/Beijing/353/89-like H3N2 (15 ug HA) and B/Yamagata/16/88-like strain (15 ug HA): MFV-JECT, Merieux, UK) in persons with HIV infection, diabetes, obstructive lung diseases, elderly adults and healthy volunteers. Forty-nine HIV-infected persons received 2 doses of the vaccine at one-month intervals; 34 healthy volunteers, 30 elderly persons, 29 with insulin and non-insulin diabetes and 14 with obstructive airways diseases were vaccinated with one single dose between October 1992 to January 1993. Serological testing of antibody responses was done using haemagglutination assay.
View Article and Find Full Text PDFNo single established cell line was found capable of substituting for primary baboon kidney (PBK) or primary rhesus macacque kidney (PRK) cells for detection of human viruses. Although a panel of cell lines could detect influenza, parainfluenza, and enteroviruses, which are among the most important viruses encountered in routine diagnostic laboratories, the sensitivity of this panel was not as high as that of PBK or PRK cells. However, in a promising complementary approach, PBK and PRK cells have been immortalised successfully by oncogene transfection, and some of the resulting cell lines have retained susceptibility to human viruses, and may be suitable for routine diagnostic use.
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December 1995
This report summarises the information obtained by surveillance of influenza in England and Wales from October 1994 to June 1995 (weeks 40/94 to 25/95). Influenza B viruses were responsible for most infections, with moderate activity occurring throughout the winter, peaking in February. Influenza A became more active towards the end of the winter, and laboratory reports reached a peak in May (week 21/95).
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