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