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Biomedical subjects

P W Gill

Publications and source records attributed to P W Gill.

At least 19 recordsLinked to original sources

Influenza A(H1N1): a widening spectrum?

OBJECTIVE: To study the incidence of H1N1 influenza from 1977 to 1988 in unvaccinated volunteers and the effects of continuing minor antigenic change (antigenic drift) in the virus. DESIGN: Prospective study by a group of general practitioners, backed up by virological findings. PARTICIPANTS: Mainly patients of the general practitioner group, also some doctors and members of staff. There were 287 participants during 1977-1981, and 207 at the end of 1988. INTERVENTION: Any participant deemed to be "at risk" was encouraged to be vaccinated and to withdraw from the study. BACKGROUND: In 1957, H1N1 subtype influenza had been displaced by H2N2 (Asian) subtype. In 1968, H2N2 was displaced by H3N2 (Hong Kong) subtype. During 1977, H1N1 influenza unexpectedly reappeared in Asia, and spread widely. The resurgent strain, designated A/USSR/90/77(H1N1), caused world pandemics, attacking (almost exclusively) persons who had been born since the 1950-1951 northern winter and causing negligible mortality. It did not displace the current H3N2 strain, and strains of both subtypes have continued to emerge independently. HYPOTHESIS: Antigens of A/USSR resembled closely those of the 1950-1951 H1N1 strain, which apparently was rendered antigenically inert between 1951 and 1976 (possibly frozen) and was reactivated during 1977. Antigenic drift was then resumed. MAIN OUTCOME MEASURE: The A/USSR/90/77 strain and its close successor, A/Brazil/11/78, attacked mainly the young, whose previous exposure to H1N1 antigens had been minimal or zero. Mortality during the A/USSR pandemics was negligible because death from influenza in people aged less than 30 years is rare. Would continuing antigenic drift ultimately widen the H1N1 spectrum of attack? RESULT: During the epidemic of 1988, A/Taiwan/1/86(H1N1) attacked a wider range of age groups than had A/USSR or A/Brazil. CONCLUSION: Assuming that H1N1 viruses continue to undergo further antigenic drift, an ever widening age spectrum of H1N1 attack may be expected.

Antibodies, Viral

Naturally acquired immunity to influenza type A. Lessons from two coexisting subtypes.

When the H1N1 subtype of influenza reappeared in the Northern Hemisphere during 1977, after a 20-year absence, it behaved very differently from the H3N2 subtype still in circulation. In Sydney, we studied the incidence of both subtypes of laboratory-proven influenza type A in 287 unvaccinated volunteers whose serum antibody titres were measured before and after each winter, to facilitate the detection of subclinical as well as clinical infection. During a 1977 epidemic, the A/Victoria/3/75 strain of the H3N2 subtype attacked participants of all age groups, whereas during epidemics of 1979 and 1981, the A/USSR/90/77 and A/Brazil/11/78 strains of the H1N1 subtype attacked only subjects born after 1950. The older participants apparently possessed homologous protection, acquired as a result of exposure to H1N1 more than 20 years earlier and not dependent upon strain-specific haemagglutination inhibition antibody.

Adolescent

Naturally acquired immunity to influenza type A: a further prospective study.

During the 1976 influenza epidemic, the incidence and severity of attack by A/Victoria/3/75 strain were studied in 312 participants who were divided into two groups: in Group 1 were 216 participants who had a history of laboratory-proven infection by one of the earlier strains of Hong Kong subtype; in Group 2 were 96 participants who had no known history of such prior infection. No participant in either group received influenza vaccine. The efficacy of clinical immunity, acquired as a result of prior infection by an earlier Hong Kong subtype strain, was judged by comparing the findings in Group 1 and Group 2. Incidence of laboratory-proven A/Victoria/3/75 infection was found to be 27% in Group 2 (26 cases confirmed) and 10.6% in Group 1 (23 cases confirmed). Among Group 1 members, the incidence was highest in those with the longest interval since prior Hong Kong subtype infection. Severe influenzal illness was seen in 14 of the 26 proven cases in Group 2, and in only three of the 23 proven cases in Group 1. The prior infection in these three had been by A/Hong Kong/1/68 strain in 1969-1970. Thus in Group 1, severe influenzal illness was not observed until six years or more had passed since prior infection (and three episodes of antigenic drift had intervened). Results suggested that low serum antibody levels may be unreliable as indicators of clinical immunity. Preepidemic sera of 99 members of Group 1 and 82 members of Group 2 showed no HAI antibody to A/Victoria/3/75 (titre less than 8), but the incidence of laboratory-proven A/Victoria/3/75 infection among these individuals was lower in Group 1 (19%) than in Group 2 (30.5%).

Adolescent

Naturally acquired immunity to influenza type A: a clinical and laboratory study.

After type A influenza virus had undergone major antigenic change in mid 1968, it was noted that individuals previously infected by strains of the old subtype (Asian), especially late strains, appeared to be unexpectedly resistant to clinical attack by the new subtype (Hong Kong). Prospective studies have since shown that, during the A/England/42/72 influenza epidemic of 1972, in which the incidence was approximately 7% in the community, clinical influenza due to this virus was not found in 229 subjects previously confirmed as having had A/Hong Kong/1/68 influenza, even though vaccine which had been effective against A/Hong Kong/1/68 was ineffective against A/England/42/72. During the A/Port Chalmers/1/73 influenza epidemic of 1974, clinical influenza resulting from Port Chalmers virus was not found in a closely monitored group of 176 unvaccinated subjects previously infected by A/Hong Kong/1/68 or A/England/42/72, although laboratory studies demonstrated Port Chalmers infection in five of these (2-8%). By contrast, among 99 subjects who had no such history of earlier infection, 22 developed laboratory-proven Port Chalmers influenza and most of them had typical illness.

Adolescent

Clinical diagnostic process: an analysis.

An analysis of observations made during 1,307 diagnoses by a total of 28 clinicians (503 diagnoses in real life, and 804 on simulated patients) concerned primarily the interview of patients suffering from abdominal pain. Interviews ranged from 10 to 35 questions, and from "stereotyped" procedures, in which identical (and often irrelevant) questions were asked to each patient, to "adaptive" interviews, in which specific relevant questions were put to each patient. Senior clinicians tended to ask fewer, more relevant questions than their junior counterparts; and urgent cases were dealt with in a more adaptive fashion than routine cases in outpatients. Disappointingly, there was considerable difference between real-life and simulated situations. From these results it is suggested (a) that the "diagnostic process" does not exist, (b) that any automated diagnostic system must be flexible to accommodate the wishes of a variety of clinicians, and (c) that studies based on artificial clinical situations should be treated with extreme caution.

Abdomen