The larger entropy of the variant corresponds to longer infectious duration than the circulating incumbents. However, the mechanism of antigenic drift (as described above) then begins to operate on this newly established sub-type and so there will be a gradual decrease in infectious duration of the dominant circulating variant with time. Given that the new virus is likely to be a hybrid animal-human type, it is likely that it is less well adapted to human hosts so it might have a low R 0 . If, rather crudely, we associate infectious duration in the host with pathogenicity, directionality theory implies high pathogenicity immediately following establishment of a new sub-type followed by decreasing pathogenicity in subsequent years. That is, the new Influenza A sub-type (such as 1918, 1957 and 1968) appears to be highly pathogenic in the immediate interval following establishment, but there is a contribution to the decrease in 'flu mortality in the era following the antigenic shift by the action of competitive selection of lower entropy variants during the antigenic drift phase in the SE-Asia seeding region. When a new Influenza A virus sub-type is generated due to antigenic shift the cycle is repeated again. Clearly, there will be a decrease in the absolute influenza mortality figure (number of fatalities) during the drift phase because as time passes the overall population immunity level increases. However, the model suggests that the case fatality rate (CFR -number of fatalities per infected individuals) will decline during the drift phase due to declining pathogenicity. A decline in the CFR is observed empirically when comparing a pandemic attack year and the next subsequent epidemic [39] but there does not appear to be any detailed epidemiological analysis of long-term CFR trends during the drift phase. A recent detailed study of the epidemiology of Influenza A H1N1 in the era 1918-1951 [40] shows, Figure 2 , that during the H1N1 era there is evidence of a sustained decrease in mortality rate between 1918 (autumn wave) and 1924 and likewise between 1928 and 1944. Whilst some of this progressive weakening of the influenza epidemics is due to increasing host population immunity it is likely that there is also a contribution to declining pathogenicity resulting from the mechanisms proposed in the directionality theory. H1N1 (2009) Swine flu. In March 2009 the first reports of an epidemic of a novel influenza-like pathogen emerged in Mexico [13] . Analysis showed that the infectious agent in this on-going epidemic to be Influenza A H1N1 (swine flu) [7] . H1N1 has generated epidemics in humans in the past and was responsible for the 1918 influenza pandemic and a 1977 'flu epidemic. It is possible to explain the relentless spread of this current outbreak in directionality theory. This new variant has emerged from a 'flu type associated with pigs, but now has human-to-human transmission capability. This successful variant has a shorter infectious duration than other influenza A strains [13] which suggests that it may have emerged with a competitive advantage founded on its lower entropy DSv0 ð Þrelative to other currently circulating 'flu strains. The extent of pre-existing immunity to H1N1 (swine flu) is currently unknown, but our results suggest that in humans there may be some pre-existing protection from previous exposure to influenza virus. This possibility is also noted by Fraser et al. [13] . Alternatively it may simply be a novel pandemic strain with short infectious duration. SARS had a higher R 0 and longer infectious duration (Table 1 ) than swine flu yet did not have the same global impact, which reinforces the generic suggestion from entropic considerations that it is those emergent diseases with shorter infectious durations that appear to have the greater pandemic potential.