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- W47907525 abstract "Current explanations of the seasonality of colds and influenza are incompatible with observations of the incidence of these diseases in the tropics. Many or most wild respiratory viruses possess temperature sensitivity (with less activity at higher temperatures) and it has been suggested that this prevents them from moving down the respiratory tract and infecting the lungs and internal organs of birds and mammals. This temperature sensitivity seems to be finely balanced, and to be continuously adjusted by natural selection, but it may be lost very rapidly in laboratory cultures. Nevertheless, many biochemical studies show decreased viral activity at elevated temperatures. Overdue weight seems to have been given to early volunteer investigations into viral respiratory tract infections (VRTIs) that often used recycled viral strains. [These “pedigree” strains were established by collecting nasal secretions from volunteers with colds, and inoculating subsequent batches of volunteers with the secretions.] Clear-cut evidence that outbreaks of VRTIs are closely (and inversely) correlated with ambient temperature, and that individuals are more likely to develop VRTIs after chilling may therefore have been overlooked. In the laboratory, the following unexpected observations need to be explained: (1) persistent viral infections of cell cultures often yield spontaneously-generated temperature-sensitive (ts) viral strains, and, (2) on at least two occasions, temperature sensitivity was lost when ts influenza A strains were incubated at a low temperature (33°C) in conditions that allowed rapid replication. In this review I note that diverse viral species cause very similar VRTIs, that the incubation periods of VRTIs have frequently been underestimated, that influenza A and B may be shed by asymptomatic patients who have not seroconverted, and that colds and influenza often infect only a subset of the susceptible individuals who are exposed to them. Mechanisms where temperature fluctuations can increase viral replication and transmission are considered, and explanations of VRTI seasonality in both temperate and tropical regions are discussed. Key index phrases Respiratory tract infections, viral infections, temperature changes, influenza seasonality, viral epidemiology. Introduction epidemiological anomalies that need to be explained Before the discovery of influenza A virus in 1933, many physicians doubted that influenza was contagious [1]. For example, in 1775 Thomas Glass of Exeter wrote of influenza, 'Nor does this distemper seem to arise ... from contagion. For in this city, in the year 1729, it was conjectured that two thousand persons at least were seized with it in one night’ [1]. During the 19 century, the question of whether influenza was contagious was the subject of intense medical debate, and a major focal point of medical research [133]. Many agreed with August Hirsch, who claimed in 1883 that influenza was not communicable because it spread “quite independently of intercourse” [1]. Today, in spite of intense study and public interest, it has often been noted that influenza and other VRTIs spread in patterns that are difficult to predict or explain [2]. Hope-Simpson listed several unexplained features of the epidemiology of influenza A, including its abrupt cessation when numerous susceptible individuals remain in the population (discussed below), and its reappearance after long absences [3]. It often appears explosively over wide areas at the same time. For example, Magrassi was impressed by cases of influenza in 1948 among shepherds living in complete social isolation in open country in Sardinia, who developed influenza contemporaneously with the inhabitants of towns on the same island [113]. Hope-Simpson also noted the low attack rate of influenza A within households, often contrasting with a high attack rate within institutions [3]. For example, he found that during the “Hong Kong” (H3N2) epidemics of 1968/69 and 1969/70, 70% of infected households in Cirencester (UK) had only one case of influenza (a total of 134 households were infected) [3], and 81% of cases occurred on the first day that influenza arrived in each household. (The low attack rate within households could not be explained by the susceptibility or ages of patients; the H3N2 subtype arrived in Britain for the first time in 1968, and 70% of patients in the first two epidemics in Cirencester were adults [98].) Moreover, no serial interval, dividing introducing cases from those infected by them," @default.
- W47907525 created "2016-06-24" @default.
- W47907525 creator A5068946627 @default.
- W47907525 date "2013-10-01" @default.
- W47907525 modified "2023-09-24" @default.
- W47907525 title "An exploration of selective trends and seasonality in viral respiratory tract infections" @default.
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