I don't know how, by reading the original article, anyone could come to the conclusion that we have manufactured H5N1. Influenza has many different
serotypes including H9N2, H5N1, H7N2, H1N1, H7N3, H10N7, which in the case of Bird Flu stand for the 5th glycoprotein of Hemagglutinin (HA) and the
1st glycoprotein of Neuraminidase (NA). On the most basic level this is what distinguishes each serotype of Influenza in that Neuraminidase is a
specific enzyme which releases new viral particles and Hemagglutinin is a Lectin (carbohydrate bound protein) which helps the virus bind to the host
cell. When antibiotic agents are administered to a patient some of them only attach to the aforementioned proteins found on the capsid and lipid
envelope, and we are able to classify each serotype by its binding factors. In other words, the distinguishing factor between say Bird Flu and
Spanish Flu is that we see certain antibiotics will only attach to the following:
Bird Flu: 5th protein of Hemagglutinin and 1st protein of Neuraminidase
Spanish Flu: 1st protein of Hemagglutinin and 1st protein of Neuraminidase
I believe this is what the original article was referring to in that they have observed one of these proteins on the viral capsid, which allows it to
cross species. With this information you can see how easy it is for many variations of one virus to occur, and this taken with the fact that
Influenza is one of the fastest replicating RNA based viruses, we can also observe how mutations occur so often. Influenza also lacks RNA polymerase
enzymes that are responsible for pinpointing errors during transcriptase, meaning that every time it replicates it only makes 1 error in every 10,000
nucleotides. Now, because the entire length of one Influenza viral RNA genome is only 10,000 nucleotides itself we see that 1 error (mutation) will
occur in every single budding virus. This means one replication cycle of H5N1 will produce a slightly different virus than its predecessor, which is
biologically consistant with RNA based viruses.
As XR500Final alluded to about Spanish Influenza being reverse engineered, this has a few meanings, but in genetics and biology it basically means to
manipulate the genome in order to transfer certain genes between viruses. In the case of Spanish Flu H1N1 Immunologists and Medical scientists will
essentially work with two mutations of the same Influenza virus and splice parts of H1 and N1 from the 1st virus into seperate DNA plasmids. Then
they will take additional pieces of HA and NA from the 2nd virus and splice them with the prepared plasmids. These plasmids are then grown in fully
matured mammalian cells, which instructs the cell to create more versions of the newly created strain and remove the virulence. Many vaccines are
engineered by this exact same process and it's quite common because it makes the vaccines even safer to handle.
On top of that, as XR500Final stated, and I'm quite curious as to where this information came from:
Dr Deagle has stated that the odds of the Spanish Flu magically migrating from having 1 receptor to having 6, and spontaneously creating itself from
nothing is like winning a million lotteries - it doesn't happen.
All viruses have the ability to alter their genetic structure and Spanish Flu (H1N1) has angenically drifted its genome and structure on numerous
occasions because of the RNA polymerase proofreading error I previously mentioned. This means that the outer glycoprotein layer of HA and NA can
drift and reassort itself from H1N1 into H2N2 and H3N2, of which it has before, but this is completely different than what "Dr. Deagle" said. In
fact, H1N1 (which is a distinct serotype of Influenza A) does not have any "receptors" on its surface, so there is something intrinsically wrong
with the above quote. Viruses are composed of an outer layer of glycoproteins and human cells are the receptors of the virus. In other words, the
receptors are found on your own cells and are composed of sialic acid linked sugars in the form of sialylglycoconjugates bearing of 2'-sialyllactose
and 3'-sialyllactose (when H1N1 crosses to humans it has 2' and 6' linkages), so there is no way for a virus to display the characteristics of
"migrating from having 1 receptor to having 6" as the above quote states.
With that information one can see why influenza continues to pose problems, and does't need the help of scientists to help its already present
pathogenic traits. Namely, because of the following:
1. Influenza's viral RNA polymerase creates too many mistakes per genome and mutates so often based on this to account for all the serotypes.
2. The main distinction between serotypes involves the number of and location of Hemagglutinin proteins and Neuraminidase enzymes on the viral
surface.
3. Each serotype uses site specific cellular receptors to bind with the host, and these receptors are located on the host cell, and not on the virus
itself.
4. Influenza subtypes, like most RNA viruses are difficult to manufacture even in controlled settings, and errors during viral transcription make it
hard to account for their variability. There is no reason to re-manufacture a virus that is already so good at fooling the best minds in the world by
itself.
[edit on 13-11-2007 by Jazzerman]
