SUMMARYIn the spring term of 1985 there was a protracted outbreak of upper respiratory tract febrile illness consistent with a clinical diagnosis of influenza in a boys' boarding school, which lasted from 23 January to 29 March. Although influenza virus infection was confirmed in 89% of cases in the first half of the term, 53% of the cases which occurred in the second half of the term had no evidence of infection with influenza virus. Between 5 February and 31 March 28 boys presented with skin rashes consistent with a clinical diagnosis of erythema infectiosum; 68% of these were associated with parvovirus B19. Investigation of the cases of clinical influenza with no identified respiratory pathogen revealed a 58% infection rate with B19. B19 DNA was identified in either throat swabs or acute stage bloods of nine pupils with influenza-like symptoms.Cohort studies revealed that 44% of pupils aged 15–16 years were immune before the outbreak compared with only 17% of pupils aged 11–12 years. Infection in the younger group was common and was associated with influenzalike illnesses as well as rashes. Forty-eight per cent of those who did not report any symptoms were also infected with B19.

A study of influenza in residential schools provided the opportunity to assess the significance of antibody as a predictor of immunity. Five hundred and fifty-six pupils from 8 schools were included in the investigations, and the outcome for these children in 27 naturally occurring outbreaks of influenza was analysed. The outbreaks comprised 5 caused by strains of influenza A H3N2, 10 caused by strains of influenza A H1N1, and 12 caused by strains of influenza B. On 8 occasions a second outbreak of the same serotype occurred in a school. There was a general correlation between the presence of antibody to the outbreak strain and protection from infection. For each of the three influenza virus serotypes the infection rate in those with no detectable antibody was approximately 80%. Those with past experience of the virus but no antibody to the outbreak strain experienced lower infection rates (62% overall) but the infection rates were lowest in those with intermediate and high level antibody to the challenge strain (18% overall). Vaccine was used by three of the schools. The effect of antibody derived from recent experience, either natural or vaccine-induced, on subsequent challenge with a drifted strain i.e. one showing antigenic drift away from the previous strain, was compared. Intermediate or high level antibody to the challenge strain in those who had experienced a recent natural infection was associated with a low infection rate (9%). A similar level of antibody produced in response to vaccination was associated with a significantly higher infection rate (23%: P less than 0.025).(ABSTRACT TRUNCATED AT 250 WORDS)

Amantadine was used in a boarding school to control an outbreak of influenza A H3N2. Of 859 pupils 79% took amantadine and almost all of them completed the course (100 mg per day for 15 days). While amantadine was being taken the number of clinical cases of influenza was considerably fewer than that predicted on the basis of previous outbreaks of influenza A at the school. However, during the month following the course of amantadine, the outbreak continued with many clinical cases confirmed by virus isolation. The advantages and limitations of amantadine prophylaxis are discussed.

Subunit influenza vaccination in adults with asthma: effect on clinical

Seventy-eight influenza A (H3N2) viruses isolated from a single epidemic in a semi-closed community involving 203 clinical cases were characterized using a panel of monoclonal antibodies to virus haemagglutinin (HA). Thirty groups of antigenically distinguishable viruses were detected but the majority (41%) of the viruses belonged to two serological groupings, designated 11 and 17. Viruses in serological group 11 were present throughout the outbreak. The greatest diversity of antigenic variants occurred at the time of the epidemic peak. Antigenic differences among the HAs of the viruses were also detected using polyclonal human and animal antisera. The electrophoretic mobility of virus-induced structural and non-structural polypeptides and of the RNA of viruses of representative serological groups was similar or identical, suggesting that new introductions of viruses did not occur during the progress of the epidemic. The evolution of influenza A (H3N2) epidemics even in small communities appears to be complex, although a contribution to the observed antigenic microheterogeneity of the HA by spontaneous variants arising in the laboratory cannot be excluded.

Three outbreaks of influenza caused by influenza A H1N1 occurred in a boys' boarding school in 1978, 1979 and 1983. The serological response to infection with variants of the H1N1 virus was studied by radial haemolysis and haemagglutination inhibition after primary infection and reinfection. The persistence of this antibody was also studied. Infection in 1978 resulted in the production of persistent antibody to both the haemagglutinin and neuraminidase of the homotypic strain. Antibody which cross-reacted with later variants of the virus was less frequently produced, the peak response was delayed and such antibody persisted less well. Infection in 1979 resulted in a similar response to that observed in 1978 after primary infection. Reinfection resulted in a broad response in all cases. In 1983 all infected boys produced antibody which reacted with the homotypic strain but only approximately one-third of primary infections produced antibody which reacted with the A/USSR/92/77 strain. The neuraminidase of the A/USSR strain failed to detect one third of the primary infections. Reinfection again resulted in a broad response.

Following its reintroduction in 1978 influenza A H1N1 spread widely in the child population. By the autumn of 1979, 75% of 11-year olds entering a boys' boarding school had detectable antibody. The protective effect of previous experience could be assessed during two outbreaks in the school. In the first outbreak in 1979, 90% of those known to have been infected in the previous year were protected against reinfection. In 1983 after strains of the H1N1 subtype had undergone antigenic drift a large outbreak occurred. It was estimated that past infection conferred protection against clinical influenza in 55%. Where past infection resulted in the presence of antibody which reacted with the outbreak strain the attack rate was further reduced. A large number of sub-clinical infections was detected in all groups.

Twenty-nine boys in a boarding school were present during a large outbreak of influenza A H1N1 in 1978 when 27 were infected, 21 with clinical influenza. These boys were bled annually and were still in school when another outbreak of influenza A H1N1 occurred in 1983. Twenty-three of them were reinfected but only nine had symptoms. These results are compared with the experience of a similar group of boys in the early years of the influenza A H3N2 era.

An outbreak of pharyngoconjunctival fever caused by adenovirus type 3 was studied in a boarding school for 800 boys aged 11-18 years. A total of 96 clinical cases were confirmed by laboratory tests. Clinical infection rates were higher in the younger boys but total infection rate did not vary with age. Previous infection provided 88% protection against reinfection. The techniques of virus isolation, complement fixation and neutralization were compared in the diagnosis of cases. Virus isolation diagnosed 86% of confirmed cases. Where acute sera (collected at onset) and convalescent sera (collected within one month) were available complement fixation and neutralization tests each diagnosed 96% of cases.

SUMMARYA radial haemolysis test designed to detect antibody specifically directed against the neuraminidase is described and compared with currently available techniques for the routine diagnosis of infection with influenza viruses.Paired sera were available from two outbreaks of influenza A, one with the N1N1 subtype and the other with the H3N2 subtype. This technique confirmed diagnosis in 92% of cases diagnosed by other laboratory methods.

Detailed antigenic analysis using a panel of monoclonal antibodies was carried out on the haemagglutinin antigen of 53 influenza B viruses isolated from an epidemic in a single school. Thirteen distinguishable antigenic groupings of influenza B viruses could be detected but 26 of the viruses were in two groups (III and IV) which co-existed during the entire epidemic. Antigenically distinguishable influenza B viruses were isolated from an epidemic in a second nearby school. Influenza B viruses isolated from the two schools could be further distinguished by different electrophoretic mobilities of NS1 polypeptides and of genes 1, 2, 3 and 6, whereas viruses from a single school epidemic were very closely related as regards these biochemical characteristics. The findings are consistent with the hypothesis that the outbreak was initiated by a single individual who excreted antigenic mutants of which predominantly two spread and co-existed during the epidemic, although the additional occurrence of random mutations during the evolution of the epidemic cannot be excluded.

In the first outbreak of influenza A HiNi in a boys' boarding school it was estimated that 90 per cent of the boys were infected, 50 per cent with clinical influenza and 40 per cent with minor or no symptoms. The only adult infected was a 21-year-old member of the catering staff. A second outbreak occurred in the following year, mainly affecting boys who had recently joined the school and who had no antibody to HiNi. There was some evidence of re-infection in boys involved in the first outbreak.

The technique of radial haemolysis (SRH) was used to assess the response to infection with different strains of influenza B virus, to determine the persistence of antibody following such infection and to examine sera from boys entering school at age 11 years. The technique detected 95% of infections and in primary infection the antibody response was mainly to the infecting strain. Re-infections resulted in a broad response, both to the homotypic strain and to strains more distantly related. Antibody to the homotypic strain persisted for at least 3 years but in some individuals the reaction with heterotypic strains tended to become weaker--resulting in zones of incomplete lysis--or was lost. Examination of the sera collected on entry to the school showed that about 60% of the boys bled before B/Hong Kong became widespread in the United Kingdom had antibody to strains representative of those isolated in the 1960s and few boys had antibody to B/Hong Kong. After 1974 antibody to B/Hong Kong and later strains became more common while antibody to earlier strains was less frequently detected. The significance of the results as an estimate of past experience is discussed.