It demonstrated that the likelihood of emergence and spread of equine influenza viruses was dependent on the immunity landscape characterizing the horse population, HDAC cancer and for the first time the relationship between immune escape and epidemic potential was quantified. The impact of pre-existing cellular immunity on influenza virus epidemiological and evolutionary

dynamics is less clear yet likely non-negligible. This calls for further quantitative studies on pre-existing herd immunity—both antibody- and cell-mediated—as a major component of human-to-human transmission barriers. Although acquisition of transmissibility is necessary for the crossing of the human-to-human transmission barriers, it is not sufficient to guarantee sustained spread and maintenance of influenza viruses in a susceptible

human population. The ability of influenza viruses to spread in a host population can be measured by the basic reproduction number R0, which corresponds to the number of secondary cases that arise from one infected individual in a well-mixed susceptible population [181]. R0 is defined mathematically by the product of the transmission rate and the length of the infectious period (Eq. (1)). equation(1) R0=βα+γ Here β is the transmission rate, α is the virus induced-mortality/morbidity rate BVD-523 manufacturer and γ is the recovery rate. The length of the infectious period is defined by 1/(α + γ). Only viruses with R0 above 1 will successfully spread in a well-mixed susceptible population and result in an epidemic. As the epidemic unfolds, the proportion of susceptible individuals (s) decreases as they become infected, recovered and immune, and the effective

reproductive number (Re) of the virus declines (Eq. (2)) equation(2) Re=sR0.Re=sR0. At the peak of the epidemic, Re = 1. Thereafter, Re < 1, and local stochastic extinction of the virus may occur during the epidemic trough [182]. As seen previously, the presence of pre-existing immunity in heptaminol the human population can impact influenza virus probability of emergence and epidemic dynamics. In addition, variability in susceptibility to infection and in infectiousness, e.g., associated with host age or predisposing factors, as well as variability in host behaviour that can affect transmission or infectious period can have dramatic consequences on the epidemic dynamics and maintenance of influenza virus in the human population [183]. For example, schoolchildren are considered to play a primary role in influenza virus transmission [184] and [185], and school terms and holidays in association with heterogenous mixing patterns of individuals of different age classes can be considered important drivers of influenza epidemic dynamics [186] and [187].