The Taffy Epidemic: 1941-1945

I must admit I am also confused. You say

The survivors are not the spreaders of the virus, it is those who are in the first two stages and the original source of the virus remains unknown.

But that is not what you said earlier.

But you need to remember, there may be carriers who suffer the disease, but don't die. All of the people who survive may be carriers of the disease.

Are you saying these is a large number of people who get the disease, but do not show symptons? If so, I don't think you can claim a 90% fatality rate.

Are you saying only certain people go from stage 1 to stage 2, and people who reach stage 2 have the 90% fatality? If so, how many people do not get to stage 2?

Or are you saying that most people do not catch the disease? And only the small percentage who do gets 90% fatality? If so, what is the likelihood of someone getting the disease? If you have epidemics, that implies a lot of people would get it fast.

I think Torqumada has a lot of valid points, and if you have addressed them, then I admit I am still just as confused.
 

Commissar

Banned
I must admit I am also confused. You say
But that is not what you said earlier.

It is exactly what I said in the first post.

Are you saying these is a large number of people who get the disease, but do not show symptons? If so, I don't think you can claim a 90% fatality rate.

Oh for crying out loud, pay attention. Vaccines exist for the virus, and quarantine laws are in place to contain the virus. The problem is that it is mutating faster than new vaccines can be made and spreading faster than the Health Department can quarantine the infected areas.

Since the virus mimics the cold and is relatively new, it manages to fall through the cracks of screening procedures for it and keeps kickstarting new pandemics before burning out.

It is also occurring in a time when other diseases such as tuberculosis, malaria, cholera, dysentery, polio, and small pox were top priority for elimination which helps out a bit as many hospitals are already set to isolate the victims of the virus and will ultimately play a key role in preventing mass die off.

You and Torqumanda are not reading clearly the posts and jumping to conclusions.
 
But you need to remember, there may be carriers who suffer the disease, but don't die. All of the people who survive may be carriers of the disease.

It is exactly what I said in the first post.



Oh for crying out loud, pay attention. Vaccines exist for the virus, and quarantine laws are in place to contain the virus. The problem is that it is mutating faster than new vaccines can be made and spreading faster than the Health Department can quarantine the infected areas.

Since the virus mimics the cold and is relatively new, it manages to fall through the cracks of screening procedures for it and keeps kickstarting new pandemics before burning out.

It is also occurring in a time when other diseases such as tuberculosis, malaria, cholera, dysentery, polio, and small pox were top priority for elimination which helps out a bit as many hospitals are already set to isolate the victims of the virus and will ultimately play a key role in preventing mass die off.

You and Torqumanda are not reading clearly the posts and jumping to conclusions.

I'm not reading posts and jumping to conclusions. I am applying something called science to your posts. Viruses don't mutate that fast. When viruses mutate it's just a likely that they will mutate to something that is less dangerous or less infectious as it is into something more dangerous or infectious. Again, a virus that kills off 90% of it's victims is going to burn out quickly. That's how they work in the real world. That's why Ebola hasn't wiped out the population in Africa. This might be an AH board, but this section has to deal with real world factors that have a relatively high degree of probability of happening. Having a virus that kills off 90% of those infect that runs rampant through a relatively large population (more than a few hundred or so) is about as likely as a successful Sea Lion.

Torqumada
 
Doesn't Ebola have a near 90% death rate?

The Zaire strain of Ebola has a 90% fatality rate for those infected. The last outbreak that I know of that strain was in the late 90's and resulted in the deaths of around 250 people. There are 70 million people in the Democratic Republic of Congo.

Torqumada
 

Commissar

Banned
I'm not reading posts and jumping to conclusions. I am applying something called science to your posts. Viruses don't mutate that fast.

:rolleyes: The Flu mutates every damn season forcing new vaccines to be developed and there are several different strains currently running around which makes vaccinations near useless in combating them.

Again, a virus that kills off 90% of it's victims is going to burn out quickly. That's how they work in the real world. That's why Ebola hasn't wiped out the population in Africa. This might be an AH board, but this section has to deal with real world factors that have a relatively high degree of probability of happening. Having a virus that kills off 90% of those infect that runs rampant through a relatively large population (more than a few hundred or so) is about as likely as a successful Sea Lion.

Big differences between this virus and Ebola.

Ebola has a 2 to 21 day incubation period before the sickness strikes and the first outbreaks were isolated quickly in a country that lacks mass transit.

Taffy Virus on the other hand is latent for three weeks, but is still contagious, it then enters the cold stage where the infected think they have a cold and think nothing of it while going about their business all the while spreading it to other till they enter the coma phase three weeks later.

Another factor enables this virus to spread is the mass movements occurring in this country at the time with individuals being drafted, people going to the cities for work, overcrowding, poor public education, underfunded public health facilities that are already working overtime dealing with the big name diseases of that period.

Taffy Virus is literally the straw that breaks the camel's back in this time period and allows the virus to spread rapidly.

Its not enough to apply science, you also have to look at this virus in its social-historical context.
 
:rolleyes: The Flu mutates every damn season forcing new vaccines to be developed and there are several different strains currently running around which makes vaccinations near useless in combating them..

I knew you were going to use influenza in your ignorance. Mutation is not why you need a new flu vaccine every year. The reason you need a new flu vaccine every year is due to the fact that there are so many flu viruses out there, that the vaccine produced the previous year that is still effective against that previous flu virus mixture isn't effective against the others that are still out there causing the flu this year in this year's mixture. Mutation is a factor in why this year's vaccine won't work 5 years down the line. While influenza does have a slightly higher than average rate of mutation (on the order of 1 mutation per one million replications per generation IIRC) than most viruses, there is still only a slight chance that the mutation is beneficial to the virus and detrimental to the host. It's more than likely to be detrimental to the virus, because that's how mutations actually work in nature. Even if it is beneficial to the virus, that doesn't mean it's detrimental to the host. What has actually caused the big influenza epidemics is a process called reassortment, which is a process in which viruses exchange genetic material and something that the influenza viruses seem to be very good at.

Its not enough to apply science, you also have to look at this virus in its social-historical context.

If the science doesn't add up, it doesn't matter what the social-historical context is. Roll your eyes at this all you want, it doesn't change the laws of nature. It is agreed on this site that any TLs that change the laws of nature are ASB. This is one of them.

Torqumada
 
I thought it was 100%?

A virus might kill 100% of the patients it infects in a small sample size and be 100% lethal. However, it's overall historical fatality rate is 90%. Which is why it doesn't spread very far. It runs out of hosts rather quickly.

Torqumada
 

Commissar

Banned
Part Three: The Bush Fires, Baltimore

July 8, 1941: All contact with Coast Guard Cutter Modoc is lost. The German Embassy asks the U.S. if they have any information about U-66 which has disappeared (the wreck of U-66 would not be discovered till 2003, cause of loss is unknown).

July 9, Petty Officer Spark is confirmed to have been infected with the Taffy Virus and the alarm goes out and the hospital already under quarantine procedures due to a minor small pox outbreak goes to a total lockdown with mandatory tests ordered for everyone.

At 1600, Petty Officer Sparks awakes from his coma with a normal temperature and is questioned. He would be sent back to the Coast Guard the next day and go on to serve aboard the USCGC Campbell and become another one of Famous CPO Sinbad's regular drinking crew on Liberty.

July 10:

1000 GMT: A rush shipment of Taffy Virus Vaccines arrive along with Maryland National Guard to enforce a Quarantine and Mandatory Vaccination Order prioritizing Hospital Staff followed by city officials then the General Population, signed by the Governor of Maryland, Herbert Romulus O'Conor, himself.

Sneezing in public is prohibited and surgical masks are passed out by National Guard Troops wearing surgical masks themselves. Therein lay the seed for the infection of the National Guard Troops. Surgical masks are not airtight like gasmasks. Air can and will flow into them. Hundreds of National Guard Troops will be infected due to this oversight before it is corrected with gas mask orders and more vaccines.

Out to sea, a Flight of TBD Devastators enroute to the USS Ranger are ordered back to Baltimore. A wise decision as all of them were infected and would subsequently die in the coma stage.

All pubs, bars, restaurants, and parks are closed by order of the Governor. The Harbor is also cleared and ships that had left in the past few days were by FDR's order intercepted by the USN or Coast Guard and told to drop anchor and hold positions to await medical screening. As many of these vessels were heading Halifax to join convoys for Britain, where they would be delivering food, this was a harsh blow, especially as the delay caused many of them to be picked off by German subs.

While these actions were derided as shutting the barn door after the horse had bolted, they were critical in preventing the Outbreak from reaching Canada and Britain and prevented a full blown outbreak in Baltimore. As it was nearly 45,000 Baltimore Citizens and National Guard Troops would die from the outbreak.

Unfortunately for America, the Virus had already spread beyond Baltimore and the first cases were starting to crop up elsewhere.
 

Commissar

Banned
I knew you were going to use influenza in your ignorance. Mutation is not why you need a new flu vaccine every year. The reason you need a new flu vaccine every year is due to the fact that there are so many flu viruses out there, that the vaccine produced the previous year that is still effective against that previous flu virus mixture isn't effective against the others that are still out there causing the flu this year in this year's mixture. Mutation is a factor in why this year's vaccine won't work 5 years down the line.

"Raises eyebrows" I knew you were going to pull a fast one. Picks up the CDC's report on H5N1's 12 mutations from 1996 to 2005. Specifically, in 1996 the virus was not catchable by Humans, the next year it mutated and the first Human cases started showing up.

Say again Torq. You know I do have access to Davenport University's Medical Database and I can pull up a long list of mutations of Flu Viruses over the years from the CDC and Michigan's Public Health Service.

Analysis of PB2 protein from H9N2 and H5N1 avian flu virus
, Bioinformation (Annual 2008): p41(6):

As I doubt you are a Davenport Student or Alumni, I won't bother with a direct link to the database.

Anycase the article describes mutations over several years in the PB2 protein of H9N2 and compares it with mutations of the same protein in H5N1. Its interesting to note they had the same rate of mutations and both went from mainly affecting poultry to making the species jump via mutation to infect humans.

Effect of neuraminidase inhibitor-resistant mutations on pathogenicity of clade 2.2 A/Turkey/15/06 (H5N1) influenza virus in ferrets.(Report) Pl o S Pathogens 6.5 (May 2010)
.:

The acquisition of neuraminidase (NA) inhibitor resistance by H5N1 influenza viruses has serious clinical implications, as this class of drugs can be an essential component of pandemic control measures. The continuous evolution of the highly pathogenic H5N1 influenza viruses results in the emergence of natural NA gene variations whose impact on viral fitness and NA inhibitor susceptibility are poorly defined. We generated seven genetically stable recombinant clade 2.2 A/Turkey/15/06-like (H5N1) influenza viruses carrying NA mutations located either in the framework residues (E119A, H274Y, N294S) or in close proximity to the NA enzyme active site (V116A, I117V, K150N, Y252H). NA enzyme inhibition assays showed that NA mutations at positions 116, 117, 274, and 294 reduced susceptibility to oseltamivir carboxylate (IC50s increased 5- to 940-fold). Importantly, the E119A NA mutation (previously reported to confer resistance in the N2 NA subtype) was stable in the clade 2.2 H5N1 virus background and induced cross-resistance to oseltamivir carboxylate and zanamivir. We demonstrated that Y252H NA mutation contributed for decreased susceptibility of clade 2.2 H5N1 viruses to oseltamivir carboxylate as compared to clade 1 viruses. The enzyme kinetic parameters ([V.sub.max], [K.sub.m] and [K.sub.j]) of the avian-like N1 NA glycoproteins were highly consistent with their [IC.sub.50] values. None of the recombinant H5N1 viruses had attenuated virulence in ferrets inoculated with [10.sup.6] [EID.sub.50] dose. Most infected ferrets showed mild clinical disease signs that differed in duration. However, H5N1 viruses carrying the E119A or the N294S NA mutation were lethal to 1 of 3 inoculated animals and were associated with significantly higher virus titers (P<0.01) and inflammation in the lungs compared to the wild-type virus. Our results suggest that highly pathogenic H5N1 variants carrying mutations within the NA active site that decrease susceptibility to NA inhibitors may possess increased virulence in mammalian hosts compared to drug-sensitive viruses. There is a need for novel anti-influenza drugs that target different virus/host factors and can limit the emergence of resistance.

The full article details experiments on Ferrets with seven mutations of the Wild Type H5N1 strain and documents that a third of the ferrets inoculated with the WT H5N1 E119A and N294S mutations had to be euthanize due to excessive lethargy and weight loss.

It also goes on at length about other mutations in the H5N1 Virus other nation's experiments and what drugs and vaccines they were showing resistance to, etc.

If the science doesn't add up, it doesn't matter what the social-historical context is. Roll your eyes at this all you want, it doesn't change the laws of nature. It is agreed on this site that any TLs that change the laws of nature are ASB. This is one of them.

First off, your arguments are countered and you clearly haven't kept abreast with the developments of current Flu Strains and research.

Screaming ASB won't do you any good.
 
First off, your arguments are countered and you clearly haven't kept abreast with the developments of current Flu Strains and research.

Actually you haven't countered anything and, unwittingly proved several of my points. Where do we start?

To begin with, if you are writing a TL that deals with a highly virulent infection that has a fatality rate of 90% and is as easily spread as the common flu, you might want to pick something better than H5N1 to make your arguments, since it has only infected a little more than 500 people worldwide in the last 14 years or so and has an overall fatality rate of roughly 60%.

"Raises eyebrows" I knew you were going to pull a fast one. Picks up the CDC's report on H5N1's 12 mutations from 1996 to 2005. Specifically, in 1996 the virus was not catchable by Humans, the next year it mutated and the first Human cases started showing up.

First rolling eyes and now raised eye brows? Are you developing a nervous tic there? What CDC paper are you referring to? You will find that most of the stuff the CDC and the NIH make available to the public are simplified versions of other reports. They would use a word like mutation for a general public report, because the general public understands the basics of mutation, but not reassortment. It is a well established fact that the change that happened between 1996 and 1997 was a reassortment and not a spontaneous mutation. There have been several studies that have confirmed it. Here is one of them: Kou Z, Lei FM, Yu J, Fan ZJ, Yin ZH, Jia CX, Xiong KJ, Sun YH, Zhang XW, Wu XM, Gao XB, Li TX. (2005). "New genotype of avian influenza H5N1 viruses isolated from tree sparrows in China". J. Virol. 79

Now, I'm sure that you will want to scour the Davenport University's Medical Database, but don't bother. Here is the relevant portion of the report:

Highly pathogenic H5N1 influenza virus has caused serious poultry loss, and since 1997 it has been reported to cause human deaths. It has been determined that H5N1 influenza viruses have undergone reassortment in recent years (12, 17). The Hong Kong influenza H5N1 virus that infected humans in 1997 was confirmed to be a reassortant virus that had acquired the hemagglutinin (HA) gene from A/goose/GuanGdong/1/96 (Gs/Gd/96; H5N1)-like viruses, the neuraminidase (NA) gene from A/teal/HongKong/W312/97 (Teal/HK/W312/97; H6N1)-like viruses, and the internal genes from A/quail/HongKong/G1/97(Qa/HK/G1/97; H9N2)-like or Teal/HK/W312/97 viruses (1, 5). Multiple genotypes of H5N1 were detected from 2001 to 2004, which were designated A, B, C, D, E, V, W, X, Y, Z, and Z+ (6, 12). Since 2002, genotype Z has been the dominant H5N1 virus in southern China and was responsible for the 2003-2004 outbreaks in Asia (12).

See reassortment, not mutation. (BTW, I have access to lots of databases. There is this thing called the internet. If you know where and how to look, there is a wealth of information out there. You keep your database to yourself. You seem to be proud of it)

Now, according to you, the CDC only list's 12 “mutations” in 10 years. You seem to be stating “But you said that mutation was on the order of 1 in a million and there are one or more happening every year! You're wrong!” Actually no. I said that the average is one in a million per replication per generation. Now, an infected person, or bird in the case of H5N1, infected with influenza will have millions of viruses produced during the course of the disease. For argument's sake and to keep the numbers simple, let's use 1 million per generation. The average length of a influenza generation (the serial interval) is about 3.6 days. The average run of influenza from the time of infection to the person is no longer sick is about 2 weeks. That means there is a chance that person could have on average 4 spontaneous mutations. Yes, there could be more or less, but that would be an average. So, 4 spontaneous mutations per sick individual, multiplied by hundreds of millions of infected humans or birds and the CDC only reports 12 total “mutations” (more than likely some were reassortments as the above article indicates) in 10 years that survived to be found by researchers. How can this be? That proves my point, that successful mutations that are beneficial to the virus are rare events in nature. If they were more common, as you seem to believe, then there would not be one or so beneficial mutation detected every year, but potentially millions. They aren't seen, because they aren't there. The ones that are found are the mutation's that survive the process of evolution.

Now about that article that you posted the text from. I take it, it's meant to counter my assertion that the reason last year's vaccine is not effective against this year's influenza is due to the fact that this year's viral mixture is different than the one you have been inoculated against? You are saying that the reason last year's vaccine is not useful is due to mutation, as you stated earlier in the thread?

The Flu mutates every damn season forcing new vaccines to be developed and there are several different strains currently running around which makes vaccinations near useless in combating them..

If, so why did you post an article on the resistance of H5N1 to anti-viral drugs. Viral resistance (and bacterial resistance) to medications is not a new or shocking idea, I hope you know. Oseltamivir carboxylate (Tamiflu) and Zanamivir (Relenza) are antiviral agents, analogous to antibiotics that treat bacteria, in that they act upon the viruses directly by inhibiting their reproduction through inhibiting the enzyme that controls that reproduction, instead of boosting the body's immune system, which is what vaccines do, by exposing the body to a weakened or dead form of the virus to allow it to build immunity before, and in a certain cases, during, a viral infection.

Also, you make mention that they had to euthanize a subset of their test subjects. I take it that you mean that to counteract my argument that mutations don't necessarily mean a more lethal version of the virus? Let's take a look at that article.

We generated seven genetically stable recombinant clade 2.2 A/Turkey/15/06-like (H5N1) influenza viruses carrying NA mutations located either in the framework residues (E119A, H274Y, N294S) or in close proximity to the NA enzyme active site (V116A, I117V, K150N, Y252H).

So under laboratory conditions, they created the virus combinations they were were going to use for their tests. They went for combinations they were sure would be more resistant to the anti-viral drugs, based on previous studies.

We used the eight-plasmid reverse genetics technique to generate 11 recombinant A/Turkey/15/06-like (H5N1) viruses carrying different NA mutations (Figure 1), that were proposed to affect virus susceptibility to NA inhibitors [12], [16]–[19]

They then injected these 11 viruses, including the baseline virus found in nature into ferrets and watched for the results.

From their results, they had two strains that caused an increase in the severity of the illness, but not necessarily the mortality of it's victims. We don't know if it increases the fatality rate, because the researcher euthanized the ferrets before they could potentially die of the disease process. (It was probably considered a humane thing to do, and I would agree that there is no need for an animal to suffer unnecessarily) Even then, the fatality rate could only be considered 30% maximum, which is ½ of the current human average of 60%. Of the 11 mutant strains created under laboratory conditions to be more resistant to anti-viral drugs, 2 caused the test subjects to be sicker than the ferrets injected with one of the other 10 strains (9 mutants and the wild type virus)? That's less than 17%. How does this disprove my statement that mutations don't necessarily mean an increase in lethality of the host? It doesn't. It proves actually proves my statement. If mutations commonly caused diseases to become more fatal, then certainly more ferrets would have died from the changes in the viruses genetic code. They didn't, because mutations are a rare thing and it takes certain combinations to become more fatal and those things are even rarer. Despite the best efforts of these researchers, this is the best they could do.

You also state that the author's of this study talk about the resistance of H5N1 to vaccines. The word vaccine appears twice in the article. One of those is in the reference section. The other is in the introduction when they discuss how anti-viral drugs can be used when vaccines are not available. The word vaccination appears twice in the article. Once when they are discussing what the primary means of controlling the spread of influenza and the other is in the summary when they again state that anti-viral agents are a way to control the spread of influenza when vaccination is not present.

Were there any other points? Did you just do a search in the database about something that seemed to talk about the increase in lethality of influenza and stumble across this and in your haste post it?

You haven't proven that mutations occur more frequently.
Your assertion that H5N1 jumped to humans after a mutation has been disproven.
Your article on resistance to anti-viral agents has nothing to do with our discussion of vaccines and doesn't even mention testing of these viruses against vaccines of any sort.
Your article on the resistance to anti-viral agents shows that despite the best efforts of humans and under laboratory conditions, they can only create a potentially more lethal strain of H5N1 about 1 time in 6 does not disprove my argument that mutations rarely cause an increase in the mortality rate of a disease.

I thank you for your hard work and time in proving my points. Since you have done just that, you can now agree that what you are posting is ASB and needs to be moved to the appropriate section of the board.

(If you have just come in and said “Here is my timeline: “Spanish Flu: Part Dos, about an outbreak that takes place during WW2” and maybe doubled the mortality rate, and it would have been much more believable.)

Torqumada
 
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