Timing and periodicity of influenza epidemics

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2024-12-25 18:00:03

Although the annual cycle of summers and winters is a long-resolved mystery of astronomy, the annual antipodal waxing and waning of influenza epidemics is still an unresolved question in epidemiology. In 1981, R. E. Hope-Simpson, an astute British physician who maintained and analyzed detailed records of his patients and their diseases for more than three decades, observed that “Influenza outbreaks are globally ubiquitous and epidemics 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…” (1). In PNAS Deyle et al. (2) combine convergent cross-mapping with empirical dynamic modeling to elucidate the nonlinear roles of absolute humidity and temperature in explaining influenza’s “sinuous curve that runs parallel with the ‘midsummer’” across the globe (1).

Understanding interepidemic intervals and timing of outbreaks has been a focus of mathematical epidemiologists for more than 50 y (3, 4). Acute immunizing infections have internal cyclic clockworks determined by the overcompensatory predator/prey-like interaction that results from slow susceptible recruitment, through births and loss of immunity, and rapid susceptible depletion from transmission during epidemics. The internal clock depends on traits of both the pathogen and the host and determines the frequency of oscillations we expect to see in the presence of random perturbations to the disease dynamics (3). The “flu” is a recurrent menace—and sometime scourge—caused by cocirculating strains of influenza A and B viruses, which at the strain-aggregate level can be modeled using the “susceptible-infected-recovered-(re)suceptible” compartmental model (5). For influenza, the internal interepidemic period is usually in the 10- to 16-mo range depending on the infectious period and transmissibility (the basic reproductive ratio, R0) of each strain (Fig. 1A). The prediction is that, in the absence of extrinsic forcing, the flu peak would slowly drift across the seasons. When it appeared in the 2003/2004 winter, the influenza A/H3N2/Fujian strain had an estimated R0 of 2.0 (6) and an infectious period of about 3 d. With these epidemiological parameters, the natural tendency would be for the peak to be gradually delayed by 5–6 wk each year (“0” in Fig. 1A). In contrast, a time-series analysis of influenza in Israel since 2000 estimates R0 to be 2.9 (5). Combined with recent estimates of 3.8 d of significant viral shedding from volunteer studies (7), theory predicts that the influenza season should accelerate by 4–5 wk each year (“X” in Fig. 1A). Such considerations prompt the long-studied question of why—when timing of the influenza peak varies by several months among years—it is (almost) always centered in midwinter in temperate areas of the world, and 6 mo out of phase between the northern and southern hemispheres' higher latitude regions, a question to which Deyle et al. (2) contribute an important global perspective.

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