Oh, bloody h- I just lost my entire reply to this - now attempting to reconstruct it. <mutters dire imprecations...all those sites! All that time!>
> Dan Minette <[EMAIL PROTECTED]> wrote: > > Behalf Of Deborah Harrell > > The acting was bad, the plot had some major holes, > > some of the science was more-than-iffy - but it > was > > interesting to watch, and if it made people think > > ahead just a little bit, that might actually be > > helpful: > > > http://www.webmd.com/content/article/121/114487.htm > I didn't see the movie but did see the ABC nightline > on the facts. I was > also in this debate before, and have looked up some > facts. > > They had some of the real life counterparts of > people in the movie (the > secretary of HHS and the governor of Virginia, as > well as CDC scientists on > Nightline. The most criticized part of the show was > the end, when the > second wave of the flu killed 100%. The CDC > scientist said while nothing > was impossible in biology, this was very very > unlikely. That makes sense. Even Ebola isn't that deadly. > If such things happened once every 100,000 years, > the odds on humans still being here would be rather >low. But that may be what happened to cheetahs - see * below (and darnit I was right about the virus being ~12K years ago <still very vexed>). Also see **, which I may have posted before, about a theory that a viral infection in the Scandanavian area may have conferred resistance to the Black Death (which may not have just been plague bacillus), and perhaps to HIV. (I was incorrect about that being 10K years ago; it's more like 2500-5K years ago.) > If the 1918 flu epidemic is the template for the > next one, then the death > rates are vastly overstated. In some countries, the > death rate approached > 10%. But, in the US it was less than 1%...0.6% > IIRC. I'd argue that the > state of medicine and nutrition had a lot to do with > the difference. >From Wiki: http://en.wikipedia.org/wiki/Spanish_Flu "...Global mortality rate from the flu is estimated at 2.5% 5% of the human population, with 20% of the world population suffering from the disease to some extent. It spread across the world killing 25 million in six months; some estimates put the total killed at over twice that number, possibly even 100 million. An estimated 17 million died in India, about 5% of India's population at the time. In the Indian Army, almost 22% of troops who caught the disease died of it. In US, about 28% of the population suffered, and 500,000 to 675,000 died. In Britain 200,000 died; in France more than 400,000. The death rate was especially high for indigenous peoples; entire villages perished in Alaska and southern Africa. In the Fiji Islands, 14% of population died during only two weeks, and in Western Samoa 22%. In Japan, 257,363 deaths were attributed to influenza by July 1919, giving an estimated 0.425% mortality rate..." >From http://www.stanford.edu/group/virus/uda/ "...The effect of the influenza epidemic was so severe that the average life span in the US was depressed by 10 years. [I saw 12 years on another site.] The influenza virus had a profound virulence, with a mortality rate at 2.5% compared to the previous influenza epidemics, which were less than 0.1%. The death rate for 15 to 34-year-olds of influenza and pneumonia were 20 times higher in 1918 than in previous years (Taubenberger). People were struck with illness on the street and died rapid deaths. One anectode shared of 1918 was of four women playing bridge together late into the night. Overnight, three of the women died from influenza (Hoagg)... "...With one-quarter of the US and one-fifth of the world infected with the influenza, it was impossible to escape from the illness. Even President Woodrow Wilson suffered from the flu in early 1919 while negotiating the crucial treaty of Versailles to end the World War (Tice)..." >From the CDC [detailed article; has links to most of the footnoted articles, also lots of graphs]: http://www.cdc.gov/ncidod/eid/vol12no01/05-0979.htm "...An estimated one third of the world's population (or ≈500 million persons) were infected and had clinically apparent illnesses (1,2) during the 19181919 influenza pandemic. The disease was exceptionally severe. Case-fatality rates were >2.5%, compared to <0.1% in other influenza pandemics (3,4). Total deaths were estimated at ≈50 million (57) and were arguably as high as 100 million (7). The impact of this pandemic was not limited to 19181919. All influenza A pandemics since that time, and indeed almost all cases of influenza A worldwide (excepting human infections from avian viruses such as H5N1 and H7N7), have been caused by descendants of the 1918 virus, including "drifted" H1N1 viruses and reassorted H2N2 and H3N2 viruses. The latter are composed of key genes from the 1918 virus, updated by subsequently incorporated avian influenza genes that code for novel surface proteins, making the 1918 virus indeed the "mother" of all pandemics...With the appearance of a new H2N2 pandemic strain in 1957 ("Asian flu"), the direct H1N1 viral descendants of the 1918 pandemic strain disappeared from human circulation entirely, although the related lineage persisted enzootically in pigs. But in 1977, human H1N1 viruses suddenly "reemerged" from a laboratory freezer (9). They continue to circulate endemically and epidemically. Thus in 2006, 2 major descendant lineages of the 1918 H1N1 virus, as well as 2 additional reassortant lineages, persist naturally: a human epidemic/endemic H1N1 lineage, a porcine enzootic H1N1 lineage (so-called classic swine flu), and the reassorted human H3N2 virus lineage, which like the human H1N1 virus, has led to a porcine H3N2 lineage. None of these viral descendants, however, approaches the pathogenicity of the 1918 parent virus..." > Further, we'd probably lose fewer people now than we > did then for the same type of pandemic because: > > 1) We have better nutrition and general health. Few > are starving in the US. > 2) We don't have rampant TB. If you look at the TB > deaths in the years > following the flu, they dropped noticeably. One > argument was that the flu > resulted in an "early harvest" of TB deaths of > people who appeared fairly healthy but had TB. >From Wiki: "...In September 2000, Noymer and Garenne published a study that poses an etiological theory explaining the unusual W-shaped mortality age profile of the virus. This profile is characterized by a mode in the 25 34 year age group. Usually, influenza has a U-shaped profile, being most deadly to the young and the old. Additionally, after the pandemic the difference in life expectancy between men and women decreased (women had a historically longer life expectancy). Noymer and Garenne have causally linked these two anomalies to an interaction with tuberculosis, a predominantly male disease of young adulthood..." > 3) We are much better prepared to fight bacterial > pneumonia, etc. than we were before 1920. > 4) We do have some Tamiflu.....by 2008 it will be > enough to dose an expected 25% infection rate. CDC: "...Despite the extraordinary number of global deaths, most influenza cases in 1918 (>95% in most locales in industrialized nations) were mild and essentially indistinguishable from influenza cases today. Furthermore, laboratory experiments with recombinant influenza viruses containing genes from the 1918 virus suggest that the 1918 and 1918-like viruses would be as sensitive as other typical virus strains to the Food and Drug Administrationapproved antiinfluenza drugs rimantadine and oseltamivir..." > Given this, it's probable that the death rate from a > pandemic that's the > equivalent of the Spanish flu would be lower. I'd > guess to the 0.25% level or so. <grin> Did you peak at this PBS site? http://www.pbs.org/wnet/secrets/case_killerflu/index.html "...Flu mortality rates typically linger around 0.1 percent (despite the widespread availability of flu vaccines and modern antiviral drugs, 36,000 people still die every year in the United States from complications of the flu); in the 1918 flu, the rate was twenty-five times higher, with deaths usually the result of secondary bacterial pneumonia or bronchitis..." [Actually, a large number were probably killed primarily; very few bacteria will cause first symptoms -> death in less than 24 hours.] > It's harder to speculate on worse flu's, but if the > exponential tail rule > for pandemics works like the symptoms rule (30% get > sick, 4% get very sick > but only 0.6% died), then a death rate of >1% would > require a once in a millennium flu or worse. Wiki again: "...In October 2002, the AFIP together with a microbiologist from the Mount Sinai School of Medicine in New York started to reconstruct the Spanish Flu. In an experiment published in October 2002, they created a virus with two 1918 genes. This virus was much more deadly to mice than other constructs containing genes from contemporary influenza virus. The experiments were conducted under high biosafety conditions at a laboratory of the US Department of Agriculture in Athens, Georgia. The February 6, 2004 edition of Science magazine reported that two research teams, one led by Sir John Skehel, director of the National Institute for Medical Research in London, another by Professor Ian Wilson of The Scripps Research Institute in San Diego, had managed to synthesize the hemagglutinin protein responsible for the 1918 outbreak of Spanish Flu. They did this by piecing together DNA from a lung sample from an Inuit woman buried in the Alaskan tundra and a number of preserved samples from American soldiers of the First World War. The teams had analyzed the structure of the gene and discovered how subtle alterations to the shape of a protein molecule had allowed it to move from birds to humans with such devastating effects..." > It doesn't mean that it won't be a problem. Our > standards for governmental > response to a crisis is much higher than it was in > the early 20th century, > and I'd expect the response to fall short. Even if > we have a US full of New > Orleans, we should not expect a 1% death rate. However, this from the CDC is sobering: "...Even with modern antiviral and antibacterial drugs, vaccines, and prevention knowledge, the return of a pandemic virus equivalent in pathogenicity to the virus of 1918 would likely kill >100 million people worldwide. A pandemic virus with the (alleged) pathogenic potential of some recent H5N1 outbreaks could cause substantially more deaths..." * http://www.cheetah.org/lm_papers/coronavirus.pdf ...Cheetahs are known as the worlds fastest land animal but also for their extreme genetic uniformity, a consequence of their escape from extinction some 12,000 years ago. Remarkably, unrelated cheetahs accept skin grafts from nonrelatives, a characteristic of highly inbred laboratory strains of mice or rats [8]. The most likely explanation for the high mortality in cheetahs is their genetic uniformity, particularly at immune genes like the MHC. This may have rendered the species susceptible to an emerging virulent strain that had evolved to circumvent the defenses of the first victim. If this hypothesis is correct, the greater genetic diversity of domestic cats and humans may reduce the severity of the epidemic, and also contribute to the occurrence of rare genetically determined SARS-CoV super-spreaders who can infect with high virulence. This explanation emphasizes the critical role of intrinsic genomic diversity among immune defense genes in any fatal epidemic... ** http://jmg.bmjjournals.com/cgi/content/full/42/3/205 "HIV strains are unable to enter macrophages that carry the CCR5-{Delta}32 deletion; the average frequency of this allele is 10% in European populations. A mathematical model based on the changing demography of Europe from 1000 to 1800 AD demonstrates how plague epidemics, 1347 to 1670, could have provided the selection pressure that raised the frequency of the mutation to the level seen today. It is suggested that the original single mutation appeared over 2500 years ago and that persistent epidemics of a haemorrhagic fever that struck at the early classical civilisations served to force up the frequency to about 5x105 at the time of the Black Death in 1347." http://www.sbs.utexas.edu/genetics/Fall05/Handouts/TheScientist-Plague-HIV-Resistance-2005.pdf ...Sue Scott and Chris Duncan from the University of Liverpool have suggested that the bacterium Y. pestis held to be the causative organism for bubonic plague since the 19th century may not have been responsible for the epidemic after all. In their book, 'Biology of Plagues' (Cambridge University Press, 2001) they proposed that the culprit was most likely a filovirus, similar to the Ebola virus. This theory is based on evidence that emerged after sifting through old parish records of the many towns affected by the plague and then tracking how the disease spread throughout Britain and Europe. So how does this link to increased resistance to HIV? In a study published in the American Journal of Human Genetics (Am J Hum Genet 1998, 62:1507-1515) Stephen O'Brien and colleagues at the US National Cancer Institute, used coalescence theory to interpret modern haplotype genealogy. They found that a genetic mutation that gives its carriers protection against the HIV virus became relatively common among white Europeans about 700 years ago the same period that the Black Death swept into Europe. The team also concluded that the geographic cline of the mutation frequencies and its recent emergence were consistent with a strongly selective historic event (such as an epidemic of a pathogen), driving its frequency upwards in populations whose ancestors survived the Black Death. The mutation occurs on the gene for CCR-5, a receptor on the surface of macrophages. When a person becomes infected with HIV, the virus latches onto CCR5 and another protein CD-4 to be transported inside the macrophages... ...The Danish group rejected the idea that the mutation became more prevalent as a result of the Black Death because the epidemic began in Sicily (in the South) and spread north to Scandinavia. This direction of travel would have predicted that the prevalence of the mutation would have become higher in the South than in the North, which is the reverse of what actually happened. Assuming that the mutation arose in Scandinavia, Eugen-Olsen's team concentrated on determining the time of the major spread of the mutation by examining bones found in Denmark, dating from the last Ice Age, around 8000 BC to 1950 BC. In particular, they focused on the time between 1800 and 2600 BC, a Mesolithic period of massive change and migration. Their findings suggested that the CCR-5-∆32 mutation was already highly prevalent in Denmark before the Black Death. Rasmussen reported: "There is support in the fact that the distribution of the Single Grave Culture in Northern and Middle Europe matches that of the high prevalence of 32∆." This meant that an epidemic decimating the Stone Age population could explain the archaeological observations as well as the distribution of the 32∆ mutation... Debbi Whew Boy Maru __________________________________________________ Do You Yahoo!? Tired of spam? Yahoo! Mail has the best spam protection around http://mail.yahoo.com _______________________________________________ http://www.mccmedia.com/mailman/listinfo/brin-l
