Influenza: its control in persons and populations.
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Adult↗
Biomedical subjects
W P Glezen
Publications and source records attributed to W P Glezen.
Antipyretic use among children during the 1983 influenza season.
We conducted a telephone survey in Houston in March 1983 to assess the level of aspirin use among children during the influenza season. We completed interviews of 200 households with 346 children aged 12 years or younger. Fifty-two percent of the 346 children experienced at least one acute illness in the preceding three months. Fever was measured with a thermometer in 114 ill children, 103 of whom had at least one measured temperature of 37.7 degrees C or greater. Fourteen percent of these 103 children received aspirin only, 61% received acetaminophen only, and 20% received both. Among a subgroup of 44 children with temperatures of at least 39.4 degrees C, 11% received aspirin only, 59% received acetaminophen only, and 27% received both. Only 60% of the 200 parents interviewed had heard of Reye's syndrome. Forty-two percent knew of the association between Reye's syndrome and aspirin use. The survey suggests that acetaminophen has replaced aspirin as the major antipyretic used by children in Houston. If the decline in aspirin use in Houston is representative of the population in the United States, and if aspirin is causally related to Reye's syndrome, the incidence of Reye's syndrome may decline.
Acetaminophen↗
Influenza B and staphylococcal pneumonia.
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Adult↗
Acute respiratory disease hospitalizations as a measure of impact of epidemic influenza.
Current measures of the health impact of epidemic influenza focus on analyses of death certificate data which may underestimate the true health effect. Previous investigations of influenza-related morbidity either have lacked virologic confirmation of influenza virus activity in the community or were not population-based. Community virologic surveillance in Houston, Texas has demonstrated that influenza viruses have produced epidemics each year since 1974. This study examined the relationship of hospitalizations with acute respiratory disease to the occurrence of influenza epidemics. Discharge records of 13,297 acute respiratory disease hospitalizations that occurred between July 1978 and June 1981 were obtained from 11 hospitals with 48.4% of hospital beds available in Harris County (metropolitan Houston). The correlation of adult acute respiratory disease hospitalizations with established indices of community acute respiratory disease morbidity was strong (r = 0.74) and indicated that the peak of adult acute respiratory disease hospitalizations followed the peak of influenza virus isolations by one week. Only 23.2% of persons hospitalized were 65 years of age or older, compared to 60-70% of persons who die during influenza epidemics. Although the highest rates of acute respiratory disease hospitalizations occurred among infants and persons aged 65 years or older, the rates for adults 45-64 years and preschool children aged 1-4 years were greater than 1 per 1,000 persons. Surveillance of acute respiratory disease hospitalizations can improve the measurement of serious morbidity associated with epidemic influenza, and can better define the characteristics of persons at risk for development of illness requiring hospitalization.
Adolescent↗
Serological evidence of Hantaan virus infection in the United States.
We found low titers of fluorescent antibodies against Hantaan virus, the etiologic agent of Korean hemorrhagic fever, in sera from 7 of 1,035 patients with febrile illnesses of unknown origin and from 6 of 664 blood donors in the United States. All but 1 of these individuals possessed neutralizing antibodies against Hantaan virus. This was a 31-year-old research technician who had worked with laboratory rodents with virus-induced tumors, but had not traveled abroad, suggesting that infection with Hantaan virus or a closely related agent was locally acquired. However, the precise source of his infection remains unclear.
Adult↗
Parainfluenza virus type 3: seasonality and risk of infection and reinfection in young children.
In Houston the temporal occurrence of infections with parainfluenza virus type 3 has evolved from an endemic to an epidemic pattern. Continuous virological surveillance for six years demonstrated that most infections occurred the late winter or spring after influenza virus activity. At least two-thirds of children observed in the Houston Family Study were infected with this virus in each of the first two years of life, and the risk of illness was about 30/100 children per year. After two years of age, the infection and illness rates dropped to 32 and 8 per 100 child-years, respectively. Most lower-respiratory-tract disease was associated with primary infection, and the risk for infection was greater during the second year for the smaller proportion of children who escaped infection during the first year. The risk during the first year may have been modified by passively acquired maternal antibody.
Adolescent↗
Acquisition of serum antibodies to specific viral glycoproteins of parainfluenza virus 3 in children.
A radioimmunoprecipitation assay was used to study antibody responses to parainfluenza virus 3 glycoproteins in human sera. The method was not only more sensitive than the neutralization test for the detection of antibody but also provided semiquantitative assessments of the antibody response to both glycoproteins in a single assay system. Anti-hemagglutinin-neuraminidase titers were consistently higher than anti-fusion levels in the same serum specimen. Thirteen children were monitored serologically and virologically from birth until 12 months or more after their primary infection with parainfluenza virus 3. At 1 to 3 months after infection, a significant increase in the level of antibody to the hemagglutinin-neuraminidase protein developed in 12 children; of these, 9 showed rises in the level of fusion protein. In 11 of the children, antibody titers continued to rise and the geometric mean titers to the hemagglutinin-neuraminidase protein was highest in sera collected 8 to 10 months after primary infection. Reinfection as the reason for these progressive increases in antibody levels could only be confirmed for four of the children. Three other children had reinfections after the 10-month sera were obtained; in each instance the only antibody responses were to the fusion protein.
Age Factors↗
Reactive airway disorders in children. Role of respiratory virus infections.
The knowledge of pathogenetic mechanisms of reactive airway disorders of children has advanced to complex interactions that involve respiratory virus infection, both antigen-specific and nonspecific chemical mediation, and neurogenic bronchoconstriction. Most of the clinical correlations have been derived from fragmentary studies which involved groups of children defined by one or only a few variables. To progress beyond this point, longitudinal studies are needed of infants and children for whom all of the variables are defined so that the interrelationship of these factors can be unraveled. Essential components of these studies would be that the subjects be tested for evidence of atopy, that the etiology of lower respiratory infections be determined, and that methods to follow pulmonary function be employed. These studies would require that relatively large numbers of children be followed from early infancy through childhood and that noninvasive procedures be employed for testing the various parameters in order to maintain compliance. Some investigators have suggested that the T-lymphocyte regulation of the immune response to certain antigens is altered in persons with atopy. Further research is needed to determine the genetic basis of this response. Furthermore, patients with asthma appear to have altered function of the autonomic nervous system. More information is needed to determine if this altered response (beta adrenergic subsensitivity versus alpha adrenergic and cholinergic hypersensitivity) is a cause, or a coexistent defect, or a result of atopic asthma. Finally, does hyperresponsiveness of the airways to non-specific irritants exist without underlying atopy? Most of the data presented above indicate that in its severe forms it, at least, coexists with allergen-induced asthma.(ABSTRACT TRUNCATED AT 250 WORDS)
Asthma↗
Trivalent, inactivated influenza virus vaccine in children with sickle cell disease.
School-aged children with sickle cell disease who were administered a single dose of trivalent, inactivated influenza virus vaccine had serum antibody titers comparable to titers achieved in the two-dose trials carried out in 1978. The proportion exhibiting titers of 1:32 or greater ranged from 84% to 68% for the three antigens. Preschool children with sickle cell disease received two doses of the same vaccine four weeks apart and their postimmunization titers to each of the antigens were slightly lower. The vaccine, which contained 15 micrograms of hemagglutinin to each of three influenza viruses, A (H1N1), A (H3N2), and B, in a volume of 0.5 mL, was adequately immunogenic for schoolchildren who probably had been primed by previous natural infection. Younger children who received the same quantity in two divided doses four weeks apart had slightly lower but acceptable titers and tolerated the injections with few side reactions.
Anemia, Sickle Cell↗
Viral pneumonia as a cause and result of hospitalization.
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Adolescent↗
Influenza B virus infections in the community and the family. The epidemics of 1976-1977 and 1979-1980 in Houston, Texas.
Influenza B virus epidemics occurred in Houston, Texas, in 1976-1977 and 1979-1980. Among families with young children followed longitudinally in the Houston Family Study, 112 infections were detected during 511 person-years of observation. The infection rates for the two epidemics were similar--24 per cent and 20 per cent--although the two epidemics differed greatly in the community. The first epidemic was much more intense with a mid-winter peak that produced school absentee rates above 12 per cent for four consecutive weeks. The indolent epidemic of 1979-1980 smoldered from late September to mid-April with a peak during the second week of March for which school absenteeism did not exceed 8 per cent. In the Houston Family Study population, the combined infection rate for the two outbreaks was highest at 35 per 100 person-years for school children aged 6-19 years. Preschool children aged 7 months-5 years and adults had infection rates of 31 and 16 per 100 person-years, respectively. Preexisting neutralizing antibody titers greater than or equal to 3.5 log2 protected against influenza B infection and illness. Preschool children above 6 months of age, school age children, and parents introduced infection into the family at rates of 15, 15, and 9 per 100 person-years, respectively. Three second introductions were observed. The secondary infection rate was highest among school aged children at 61 per 100 persons at risk.
Adolescent↗
Antigenic analysis of H1N1 viruses isolated in the Houston metropolitan area during four successive seasons.
We evaluated the antigenic stability of viruses within the H1N1 subtype, using 307 isolates spanning four winter seasons. The isolates from each seasonal period appeared relatively homogenous in hemagglutination inhibition tests employing ferret antisera. However, a panel of seven monoclonal antibodies to A/USSR/90/77 detected extensive micro-heterogeneity. Antigenic variation occurred in the hemagglutinin antigen within a few weeks after the initial appearance of A/USSR/90/77-like strains in 1977-78 season as evidenced by low reactivity to one or several of the monoclonal antibodies. By the end of the season, few of the isolates reacted with the complete panel. Antigenic heterogeneity of the hemagglutinin was detected among H1N1 viruses throughout each epidemic interval. Some of the antigenic changes detected by monoclonal antibodies appeared on isolates in succeeding years, but others were restricted to a few strains isolated during a given year. The cumulative nature of some of these antigenic changes was indicated by the observation that 20 (19%) of 107 isolates examined in the fourth season failed to react with five of the monoclonal antibodies. Strains similar to most reference variants from around the world circulated in the Houston community.
Antibodies, Monoclonal↗
Surveillance of influenza in Houston, Texas, USA: gradual transition from A/Victoria/75 (H3N2) to A/Texas/77 (H3N2) predominance and antigenic characterization of "intermediate" strains.
Influenza epidemics in Houston, Texas, USA, during the winters of 1975-76, 1976-77, and 1977-78 were attributed to A/Victoria/3/75 (H3N2), B/Hong Kong/5/72, and A/Texas/1/77 (H3N2)-like viruses, respectively. Both A/Victoria and A/Texas viruses were detected towards the end of the 1976-77 epidemic and throughout the 1977-78 epidemic. To determine if there had been a gradual transition in the predominant strain, 267 viral isolates from the 1975-76 epidemic were tested for A/Texas virus. Eight specimens (3%) that appeared to contain A/Texas antigens were cloned and retested with specific antisera prepared in guinea-pigs and ferrets. One virus was identical to A/Texas/1/77 virus, two reacted like A/Victoria/3/75 and five reacted equally well with antisera prepared against A/Victoria/3/75 and A/Texas/1/77 viruses (bridging strains). The six viral isolates containing A/Texas antigens were obtained at different times during the epidemic, from all parts of the city, from males and females aged between 1 and 20 years.Characterization of type A influenza virus isolates obtained during the 1976-77 and 1977-78 epidemics revealed a progressive increase in the frequency of viruses containing A/Texas antigens, from 2.2% in 1975-76 to 32% in 1976-77 to 70% in 1977-78. Thus, both type A (H3N2) variants were present in the Houston community in 3 successive years.An antigenic analysis of the bridging viruses was performed by competition radio-immunoprecipitation assays and by reactivity with a set of monoclonal antibodies prepared against A/Texas/1/77 virus. These assays confirmed the identity of the A/Texas isolate with the prototype virus and indicated that the bridging strains shared antigenic determinants with both A/Vic/75 and A/Tex/77 viruses, but were more closely related to A/Victoria/3/75 virus.It seems clear that new variants of a subtype of type A influenza may not immediately displace the existing variant and that seeding in a community and transition from predominance of one variant to another may be a gradual process.
Adolescent↗
Aspirin and Reye's syndrome.
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Adolescent↗
Mortality and influenza.
Systematic virologic surveillance in Houston over the past seven years has revealed that influenza virus infections have been epidemic during each respiratory disease season. The peak of the occurrence of acute respiratory illnesses that caused patients to seek medical care always coincided with the peak of influenza virus activity. The peak number of deaths attributed to pneumonia or influenza followed the peak of influenza virus activity by about two weeks. This relationship was constant even though the time of the epidemic peak ranged from as early as the third week of December to as late as the second week of March. No increase in deaths occurred in the absence of influenza virus activity. Therefore, the methods used to predict base-line mortality that show a seasonal rise in the absence of influenza activity may be inaccurate and, if so, lead to underestimation of mortality associated with influenza virus infections.
Adolescent↗
The influenza herald wave.
For three successive years (1976-1979), the community surveillance system of the Influenza Research Center identified a wave of influenza virus infections which occurred during the latter half of one epidemic period and which heralded the epidemic virus for the following year. Recognition of the herald waves required consistent and continuous sampling of respiratory illnesses occurring among persons who constituted a substantial proportion of the population of over two million people in Harris County, TX. The herald wave infections consisted of only 0.4-2.0% of the 2500 to 3000 respiratory illnesses examined for virus. During the first two epidemic periods, the herald wave was easily detected as a wave of influenza B virus infections occurring during an influenza A virus epidemic and then a wave of influenza A virus infections during an influenza B virus epidemic. The third herald wave was obscured because it consisted of a small number of infections caused by viruses antigenically like A/Brazil/11/78(H1N1) which occurred at the end of the outbreak caused by influenza A/USSR/90/77 (H1N1). The herald wave infections were detected among persons who lived in widely scattered areas of the county and who were representative of all age and socioeconomic groups. the herald wave phenomenon has the obvious benefit of providing information about the virus most likely to produce an epidemic during the next respiratory disease season. Under optimal conditions, this could allow six to nine months to prepare and administer control measures.
Humans↗
Serious morbidity and mortality associated with influenza epidemics.
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Age Factors↗
Evidence of interferon production in the hamster lung after primary or secondary exposure to parainfluenza virus type 3.
Experimental infection of the hamster respiratory tract with parainfluenza virus type 3 has been used to study the pathogenesis of viral pneumonia and the host response to infection. In this study, hamsters inoculated intranasally with parainfluenza virus type 3 produced local interferon, which was detected in lung washes obtained by in situ lavage. Interferon activity was present as early as 2 days after infection, and titers correlated directly with the quantity of virus recovered in lung washes. Parainfluenza virus type 3 was sensitive to the antiviral state induced in vitro by the lung wash interferon. Infectious virus induced interferon in cultures of immune and nonimmune lung wash cells, primarily alveolar macrophages. A secondary response of immune, mixed cultures of lymphocytes and alveolar macrophages, stimulated with inactivated virus, produced low concentrations of interferon, perhaps type II. Lymphocyte-alveolar macrophage cultures produced a pH and temperature-sensitive interferon in response to mitogen induction, characteristics of type II or immune interferons in the human and murine systems. Interferon may be an early defense involved in recovery from primary infection with parainfluenza virus type 3, and may contribute to resistance to reinfection.
Animals↗