posted on Nov, 16 2007 @ 10:27 AM
It will take a number of evolutionary mutations in the genome of H5N1 for it to become human to human transmissable. In fact, one of the most basic
mutations would require that its Hemagglutinin glycoprotein structure changes in a way that would allow it to bind with cellular membrane 2' or 3'
Alpha receptors. Currently, any serotype of Influenza A (of which H5N1 belongs to) only bind with the 2' and 6' receptors, which means that not
only would H5N1 have to alter its genetic structure, but it would also have to mutate it's viral proteins. Having said this H5N1 is the first known
Influenza virus to mutate its RNA polymerase enzyme enough to not have Glutamine amino acids in its standard genetic code. It was actually able to
acquire certain genes that led it to expressing a Lysine Base amino acid, which until then were only present in human Influenza infections. This of
course took a number of years, but because of the extremely fast transcription and replication process that all RNA based viruses go through it is
entirely possible that further mutations will and could occur.
For instance, as mentioned previously it would require Hemagglutinin (HA) glycoprotein reformation, but it would also require slight alteration to its
Neuraminidase enzymes (NA). Neuraminidase is essentially a Glycoside hydrolase enzyme that helps a newly formed virus bud and release from the
infected cell. It would be pertanent for the virus to mutate both HA and NA in order to cause a longstanding infection in humans. In other words
Bird Flu's H5, or the 5th Glycoprotein of Hemagglutinin, would have to evolve enough to acquire further proteins and thus transform into H7, H10,
H12, etc. On the same order N1, or the 1st enzyme of Neuraminidase, would also have to reassemble its structure to infect human Leukocyte and
Lymphocyte cells on a massive scale thus resembling N2, N5, N10, or other combinations thereof. This would allow the mutated form of H5N1 to bind
with human cell membranes.
By the time Bird Flu completes this process it will effectively no longer be H5N1, but will mutate into a subserotype of Influenza A such as it has
already done with H5 and H7. In effect, the new strain would resemble something on the order of H7N10 or some other Influenza strain. Because of the
extremely high virulence and mutation rates associated with RNA viruses, and Influenza A strains (including H5N1) it is entirely possible that a
Panzootic infection could happen within the next few years. Nevertheless, humans have survived the onslaught of H1N1, H3N2, and even a suspected
early outbreak of H2N2. The one positive point to take from all this is that we have now known about H5N1 for a number of years and new antivirals in
development may give us enough time to contain an infection should it pass from human to human.