from memory...
normal is about 100,000 to 500,000 people in flu season world wide.
1918 H1N1 was about 70-110 million last count.
H2N2 was about 3 million.
and H2N3 was about 2.5 million.
Considering swine flu is H1N1, its spreading faster than the 1918 outbreak and kills people in nearly the same time... and were all young enough not to have a resistance to H1N1... we might to the individual HA1 or NA1, but unlikely to both... Usually swines are just a "storage" unit for influenza and haven't usually been seen as a vector. So overall unlike SARS or bird flu, this is actually spreading human to human, so its quite a concern... And remember while AIDS has killed 30 million people world wide since 1970, influenza far surpasses any other biological pandemic/disease.
Below, an essay I wrote last year for micro about influenza. It pretty much explains that its impossible to completely combat a flu pandemic because influenza reassortment is an on going thing.
Quote:
It has been estimated by the World Health Organization (WHO) that the next influenza pandemic could result in 2 million to 7.4 million deaths world wide.
Discuss the origins of the 1918, 1957 and 1968 pandemic influenza viruses.
Influenza is a RNA virus that contains 8 negative sense genomic strands, 2 surface glycoproteins - hemagglutinin and neuraminidase, and a enzyme - polymerase. The virus itself is the cause of seasonal flu disease and occasionally is the cause of world wide pandemics. The World Health Organization (WHO) has estimated the next pandemic may result in up to 7.4 million deaths world wide. It therefore has been an essential part of influenza research to understand the causes of the last three influenza pandemics. This essay will go into brief detail on the origins of the great 1918 pandemic, the 1957 pandemic and the most recent 1968 pandemic.
The 1918 influenza pandemic, caused by an influenza strain designated as H1N1, was possibly responsible for 50 to 100 million deaths according to recent accounts. Reid et al. (1999) discusses two possible theories of the H1N1 hemagglutinin origin. One theory is that it originated from an avian source, and with little or no mutation it was able to go straight into the circulating human influenza. However this theory is near impossible to determine as avian influenza of the time no longer exist. The other theory was determined from examining frozen samples of human lung tissue. This theory stated that the 1918 influenza A virus was derived from an avian source that, rather than being transferred directly to humans, used swine as a medium. Reid et al. (2000) went on to sequence the genome of the 1918 neuraminidase glycoprotein and discovered that it was similar to avian neuraminidase. More recently the genome of the polymerase has been sequenced as well. It has been shown that it is of avian origin, and not the circulating avian type, but a different one (Pappas et al., 2008). Essentially these three sources heavily indicate that the 1918 influenza pandemic was created from an avian influenza entering directly into the circulating human influenza or used the swine influenza as a transport medium.
A new strain emerged in 1957, H2N2, taking over from seasonal H1N1 flu outbreaks (Glezen, 1996). From the genomic sequencing the hemagglutinin of the 1957 H2N2 pandemic, it too was found to have close ties with the hemagglutinin of an avian source (Sch?ffr et al, 1993). This led to the finding that the origin of the 1957 H2N2 hemagglutinin was found to have gone through a genetic reassortment of the influenza A ss(-)RNA genome. Reassortment is the mixing of two virus genomes that have infected the one cell. This results in the creation of a completely new strain of virus that contains parts of both the genomes. It included parts of hemagglutinin-2 from humans/swine and parts of the hemagglutinin-2 from avian waterborne life. Shu et al. (1996) found that genetic reassortment of avian and human strains could feasibly result in the emergence of new pandemic and interpandemic strains. This was the case for the pandemic in 1957. Shu et al. (1996) went on to point out that in ?interpandemic periods the reassortants have no survival advantage, and the circulating interpandemic influenza viruses in humans do not appear to accumulate avian influenza virus genes.?
The 1968 influenza A pandemic was characterised by the emergence of a new reassorted strain, H3N2. Gillian (1981) notes that H3N2 was not derived from mutations in the current circulating human influenza. However, it was found that instead the reassortment of current H2N2 influenza A viruses that were circulating had become reassorted with avian H3 influenza viruses. Kawaoka et al. (1989) studied the polymerase of the 1968 H3N2 and discovered that its genomic sequence came from an avian origin that was transferred into swine influenza. This has led to the understanding that polymerase reassortment from avian influenza origin to human or swine influenza is more than frequent than first thought. The primary point learnt from the genomic sequencing of the 1968 H3N2 virus, is that the majority of its sequence actually comes from its predecessor, H2N2 (Shu et al, 1996). The hemagglutinin-3 glycoprotein is the main change from the H2N2 stain to H3N2 stain. It is believed that it was a smaller pandemic because there was little genomic change to the neuraminidase glycoprotein, and thus the human population had already built up a small defence against it (Shu et al, 1996).
While the 1918 Influenza A pandemic was the result of an avian influenza entering directly into the circulating human influenza A population, it must be noted that the more recent pandemics (1957 and 1968) are the result of a reassortment of human and avian influenzas. A new influenza pandemic could be just around the corner. If another pandemic occurred which was derived entirely from an avian origin like that in 1918, mass deaths will occur. Under the current circumstances, all countries will be affected, medical supplies will be inadequate and deaths world wide will be inevitable. Alternatively, if a new pandemic is caused by reassorted human and avian influenzas, we can hope that it would not be quite as potent. Either way, with no vaccine developed for resisting influenza strains at this time, they will remain a large threat to the human species.
References
Gillian, M. A. (1981). Sequence relationships among the hemaggluttinin genes of 12 subtypes of influenza A virus. Proc. Natl. Acad. Sci. USA 78, 7639-7643.
Glezen, P. W. (1996). Emerging Infections: Pandemic Influenza. Epidemiol Rev 18, 64-76.
Pappas, C., Aguilar, P. V., Basler, C. F., Sol?rzano, A., Zeng, H., Perrone, L. A., Palese, P., Garc?a-Sastre, A., Katz, J. M., & Tumpey, T. M. (2008). Single gene reassortants identify a critical role for PB1, HA, and NA in the high virulence of the 1918 pandemic influenza virus. PNAS 105, 3064-3069.
Reid, A. H., Fanning, T. G., Hultin, J. V. & Taubenberger, J. K. (1999). Origin and evolution of the 1918 "Spanish" influenza virus hemagglutinin gene. PNAS 96, 1651-1656.
Reid, A. H., Fanning, T. G., Janczewski T. A. &Taubenberger, J. K. (2000). Characterization of the 1918 "Spanish" influenza virus neuraminidase gene. PNAS 97, 6785-6790.
Sch?ffr, J. R., Kawaoka, K., Bean, W. J., S?ss, J., Senne D. & Webster, R. G. (1993). Origin of the Pandemic 1957 H2 Influenza A Virus and the Persistence of Its Possible Progenitors in the Avian Reservoir. Virology 194, 781-788.
Shu, L. P., Sharp, G. B., Lin, Y. P., Claas, E. C. J., Krauss, S. L., Shortridge, K. F. & Webster, R. G. (1996). Genetic reassortment in pandemic and interpandemic influenza viruses. European Journal of Epidemiology 12, 63-70.
Kawaoka, Y., Krauss, S. & Webster R. G. (1989). Avian-to-human transmission of the PB1 gene of influenza A viruses in the 1957 and 1968 pandemics. J Virol 63, 4603?4608.