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R E Hope-Simpson

Publications and source records attributed to R E Hope-Simpson.

At least 19 recordsLinked to original sources
PubMed1987

A new concept of the epidemic process of influenza A virus.

Influenza A virus was discovered in 1933, and since then four major variants have caused all the epidemics of human influenza A. Each had an era of solo world prevalence until 1977 as follows: H0N1 (old style) strains until 1946, H1N1 (old style) strains until 1957, H2N2 strains until 1968, then H3N2 strains, which were joined in 1977 by a renewed prevalence of H1N1 (old style) strains. Serological studies show that H2N2 strains probably had had a previous era of world prevalence during the last quarter of the nineteenth century, and had then been replaced by H3N2 strains from about 1900 to 1918. From about 1907 the H3N2 strains had been joined, as now, by H1N1 (old style) strains until both had been replaced in 1918 by a fifth major variant closely related to swine influenza virus A/Hswine1N1 (old style), which had then had an era of solo world prevalence in mankind until about 1929, when it had been replaced by the H0N1 strains that were first isolated in 1933. Eras of prevalence of a major variant have usually been initiated by a severe pandemic followed at intervals of a year or two by successive epidemics in each of which the nature of the virus is usually a little changed (antigenic drift), but not enough to permit frequent recurrent infections during the same era. Changes of major variant (antigenic shift) are large enough to permit reinfection. At both major and minor changes the strains of the previous variant tend to disappear and to be replaced within a single season, worldwide in the case of a major variant, or in the area of prevalence of a previous minor variant. Pandemics, epidemics and antigenic variations all occur seasonally, and influenza and its viruses virtually disappear from the population of any locality between epidemics, an interval of many consecutive months. A global view, however, shows influenza continually present in the world population, progressing each year south and then north, thus crossing the equator twice yearly around the equinoxes, the tropical monsoon periods. Influenza arrives in the temperate latitudes in the colder months, about 6 months separating its arrival in the two hemispheres. None of this behaviour is explained by the current concept that the virus is surviving like measles virus by direct spread from the sick providing endless chains of human influenza A.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1986

The method of transmission of epidemic influenza: further evidence from archival mortality data.

Evidence for influenza-associated excess mortality in the three centuries before the 20th has been sought from parish burial registers in Cumbria, Devon, Dyfed, East Anglia, Gloucestershire and Northumbria, compared with inter-epidemic years. Most of the registers showed excess of burials concordant with eight historic influenza epidemics. Comparison of the dates of these epidemics, deduced from the burials data in different areas, showed a rate of spread difficult to reconcile with direct person-to-person spread of influenza from the sick. An alternative explanation based on development of latency of the virus in the sick person and subsequent seasonal reactivation is discussed.

Disease Outbreaks↗
PubMed1984

Age and secular distributions of virus-proven influenza patients in successive epidemics 1961-1976 in Cirencester: epidemiological significance discussed.

A general practice population of around 3900, under continuous clinical and laboratory surveillance, experienced 20 outbreaks of influenza between March 1960 and March 1976. Four epidemics were caused by subtype H2N2 type A viruses, seven by subtype H3N2 type A viruses and nine outbreaks by type B viruses. The age of every person proved virologically to have influenza is related to the age structure of the community and to the phase of the epidemic in which the virus-positive specimens were collected. Children 0-15 years old suffered a higher incidence rate than adults 16-90+. Pre-school children 0-4 suffered the highest rate of infection by viruses of both influenza A subtypes, whereas older schoolchildren 10-15 suffered the highest rate of type B infections. Despite these high incidence rates neither pre-school nor schoolchildren appear to have been the major disseminators of any of these influenza viruses in the community. Adults of all ages suffered a high rate of infection even into extreme old age, and the indiscriminate age distribution among adults was sustained in the successive epidemics. Such age-patterns are not those caused by a highly infectious immunizing virus surviving by means of direct transmissions from the sick, whose prompt development of the disease continues endless chains of transmissions. An alternative epidemic mechanism--whereby the virus does not spread from the sick but becomes latent in them, reactivating seasonally so that they later infect their companions--would produce age patterns similar to those recorded here for influenza patients. The suggested mechanism is illustrated by a simple conceptual model and the influenzal age patterns are discussed in relation to the recycling of influenza A subtypes.

Adolescent↗
PubMed1983

Recognition of historic influenza epidemics from parish burial records: a test of prediction from a new hypothesis of influenzal epidemiology.

On the current conception of the epidemiology of epidemic influenza, as caused by a mechanism of direct spread of the virus from the sick, epidemics must have travelled much more slowly in former times than at present. In contrast, a new hypothesis involving virus latency with seasonal reactivation predicts that in previous centuries influenza epidemics would have spread across the country at much the same speed as in the twentieth century. The study of burial registers in Gloucestershire parishes reported in this paper shows that lethal influenza epidemics at least as early as the sixteenth century can be recognized and dated as at present by the characteristic brief but large excess mortality that they cause. Examples are given showing that the character of the excess mortality caused by lethal influenza has not changed significantly over the centuries, a finding that supports the prediction of the new hypothesis but would not be expected on the current conception of influenzal epidemiology. In each century, influenzal excess mortalities in Gloucestershire parishes coincided with the date of the relevant influenza epidemic as recorded from widely different parts of Britain, thus further supporting the prediction of the new hypothesis as against current conceptions.

Burial↗
PubMed1981

The role of season in the epidemiology of influenza.

Four types of observations have been used to illustrate the seasonal characteristics of epidemic influenza: (1) The experience of a small population during 28 consecutive years, 1946-74, (2) world influenza outbreaks 1964-75 reported to the World Health Organization, (3) the experience of two widely separated localities at about the same latitude, 1969-74, and (4) the experience of two places at latitudes 30 degrees + on opposite sides of the Equator, 1968-74. The following tendencies are shown. (1) Outbreaks of influenza even in the small community came at approximately the same season almost every year. (2) Outbreaks are globally ubiquitous and epidemic loci move smoothly to and fro across the surface of the earth almost every year in a sinuous curve that runs parallel with the 'midsummer' curve of vertical solar radiation, but lags about six months behind it. Such findings exclude the mediation of seasonal control by any agencies of local distribution, and suggest a direct effect of variations in some component of solar radiation on virus or human host. (3) Antigenic variations in influenza A virus tended to have the same seasonal characteristics as epidemicity. This suggests that epidemicity and virus variation are two facets of one seasonally controlled process. None of these seasonal characteristics can be explained by the current concept of influenzal epidemiology. A new hypothesis recently proposed and recapitulated in the Appendix offers a possible explanation. The primary agency mediating seasonal control remains unidentified.

Australia↗
PubMed1981

Streptococcus pyogenes in the throat: a study in a small population, 1962-1975.

A general practice population of around 6700 was kept under clinical and laboratory surveillance from 1962 to 1975. Illnesses totalled 18703 in three morbidity classes: sore throat (Throats) 4451, acute febrile respiratory diseases (FRD) 4934, acute non-febrile respiratory diseases (Non-FRD) 9318. Specimens were examined for beta-haemolytic streptococci (BHS) from 37.1% of these illnesses: from Throats 33.3%, from FRD 67.8%, from Non-FRD 22.6%, and 515 specimens were collected from a miscellaneous ("Other') class consisting of healthy persons and ailments that could not have had a streptococcal component. Strains of BHS were isolated from 7448 specimens as follows: group A (Streptococcus pyogenes) 353, group C 36, group G 15, other groups 274. Group A strains were isolated from specimens at the following rates: Throats 16.7%, FRD 2.4%, Non-FRD 0.9%. Other 1.4%. The last two classes reflect the carrier rate in the general community, which must be deducted to obtain the streptococcal morbidity in the other classes. Carriers thus accounted for 6% of the strains isolated from the Throats class and for 42% of those from FRD illnesses. No consistent seasonal trend of prevalence was detected. Long-term fluctuations in prevalence over several years affected all groups and most group A serotypes. Serotyping was performed on 304 strains from 1963 to 1975. The commonest types found were T-types 4 and 12 and M-type 12. Immunity against re-infection by identical strains appeared to be fairly strong and also against heterotypic strains that shared a T-antigen, but little protection was conferred against re-infection by group A strains with no shared M- or T- antigen. R-28 antigen is considered here as a marker epidemiologically equivalent to an M-antigen. Epidemicity, as measured by a simple estimate of aggregation, appeared to be low and there were differences between and within serotypes. The infecting organism appeared to linger in the pharynx, sometimes for several months, after a streptococcal illness.

Adolescent↗
PubMed1981

Parainfluenza virus infections in the Cirencester Survey: seasonal and other characteristics.

Parainfluenza viruses were isolated 165 times during 14 years surveillance of the illnesses of a general practice population of around 3700. Type 1 isolations numbered 57, type 2 isolations 22 and type 3 isolations 86, representing annual rates of 33, 13 and 50 infections respectively per 10000 of population. Type 4 parainfluenza virus was not isolated. Three major classes of illness gave the following rates: sore throats (Throats) nine, acute febrile respiratory diseases (FRD) 23, acute non-febrile respiratory diseases (non-FRD) 71. The illnesses caused by the three types isolated were similar. Type 1 infections were most abundant in November and type 2 infections in December, and only 11.4% of these types were isolated in the warm semester April through September. Type 3 infections were seasonally bi-modal, with a winter peak in January and an even greater prevalence (66% of the total) in the warm semester. Type 3 infections in the warmer months and in the later years of the Survey were usually more severe. Type 3 virus may therefore be heterogeneous, one subtype possessing and the other lacking the genetic mechanism of "cold-season' prevalence. Geographical discontinuity between summer and winter isolation strengthens the case for the existence of the two subtypes of type 3 parainfluenza virus. Type 3 infections caused the majority of the infections in very young infants. Type 2 infections were widely distributed at all ages. Females were attacked more often than males: type 1, 68.4%; type 2, 63.6%; type 3, 53.5%. Type 3 infections in males outnumbered those in females up to 60 years of age, whereas female predominance became apparent in types 1 and 2 before 10 years of age. All types were widely and sparsely distributed, areas of prevalence changing from year to year. Recurrences occurred only twice, both with type 3 infections. Six persons suffered both a type 1 and a type 3 infection, and one person suffered both a type 2 and a type 3 infection.

Adolescent↗
PubMed1979

Epidemic mechanisms of type A influenza.

The antigenic varieties of influenza A virus isolated from 1968 to 1976 in a surveillance of a small, rather remote population were similar to those from England and Wales as a whole, despite frequent antigenic changes during the period. Household studies in the first two H3N2 influenza A epidemics found low attack rates within households, a high proportion (70%) of affected households with only one case of influenza, similar distributions of affected households in the two epidemics by the number of cases of influenza and similar distributions of the influenza cases by the day of their onset in the household outbreak. No serial interval could be demonstrated by cumulating household outbreaks. More than one minor variant was causing influenza contemporaneously in the same villages in several seasons, and different variants were on one occasion found on successive days in bedfellows. The regular occurrence of epidemics in winter was often accompanied by the disappearance of the epidemic variants and their replacement, after a virus-free interval, by new variants. These epidemiological findings seem best interpreted on the following tentative hypothesis. Influenza A sufferers do not transmit the virus during their illness; instead it rapidly becomes latent in their tissues so that they become symptomless carrier-hosts and develop specific immunity. Next season an extraneous seasonally mediated stimulus reactivates the latent virus residues so that the carrier-host becomes briefly infectious, though symptomless. Antigenic drift occurs because particles reconstituted to be identical with the progenitor virus cannot escape the specific immunity it has provoked in the carrier host. He can shed only mutants also determined by the progenitor virus. From the assortment of mutants shed by the carrier-host, his non-immune companions select that (those) which is best fitted to survive, and it rapidly causes influenzal illness. Epidemics consist largely or entirely of such persons sick with influenza caused by reactivated virus caught from symptomless carrier-hosts.

Antigens, Viral↗
PubMed1975

Postherpetic neuralgia.

Postherpetic neuralgia was studied in a general-practice population (3,600-3,800) for 26 years, 1947-1972. Postherpetic neuralgia followed 46 (14.3 per cent) of the 321 cases of zoster. No neuralgia occurred after zoster in those under 30 years old. The incidence was strongly associated with age, the highest, 34.4 per cent of the zosters, being in people over 80 years old.Women, especially between 50 and 69 years old, suffered more zoster than men, and women with zoster suffered more postherpetic neuralgia.The incidence of neuralgia was not affected by the anatomical location of the zoster. The duration of neuralgia was unrelated to the age of the patient. Cranial neuralgias lasted much longer on average than neuralgia in other sites. Lumbar and sacral neuralgia were short-lived.

Adolescent↗