This is part 2 of a multi part series on the mutation of the H1N1 influenza virus. Part one discussed the similarities of the D225G mutation of 2009 Pandemic to the D225G mutation found in the 1918 Pandemic. SEE PART 1 Also we discuss the similarities of severe symptoms and hemorrhagic pneumonia between the two pandemics. At this time all we have are similarities and more data is needed to see if the D225G mutation will lead to the catastrophic events of the 1918 Spanish Flu. What we do know is the D225G mutant strain acts in the host as it did in 1918 and we also know that the 1918 flu started off mild and few deaths and ended with severe symptoms and millions of death. So far the 2009 pandemic has started off slow and there have been few deaths. What we also know is 1918 is a different time than 2009 and we have better infrastructure, we are better educated in hygiene and we have better health care and vaccinations. Although we are in an El Nino year See Relationship to 1918 Pandemic we don’t have the same drought and famine conditions that were found in 1918. However we can travel the world faster and we have troops abroad as we did in 1918, which can lead to faster transmission around the globe.
It has been reported that 2 oil workers from Nacogdoches County Texas have died from severe complications due H1N1 infection 24 hours apart. They were roommates on the oil rigs and both were in there mid 50’s. There hasn’t been a postmortem report made available at this time, so it’s hard to say if these individuals have the mutant D225G strain. What is interesting is that these gentlemen were roommates and both dies within 24 hours of the same infection. We know the H1N1 virus is highly contagious and we know people have died from complications from an H1N1 infection. However most H1N1 infections have been mild and when you have this type of event occur we can be almost certain that these gentlemen had contracted a lethal contagious form of H1N1. When coupled with the reports out of Norway and the Ukraine about the isolation of D225G mutant and the severity of symptoms and death, we cannot rule out that these gentlemen had contracted the D225G mutant H1N1 strain.
From Recombinomics.com
Ukraine has reported 388 pneumonia deaths in the past several weeks and agency reports described 90 cases which involved total destruction of both lungs. Recently released sequences from Mill Hill in London included 4 fatal cases and all four cases had D225G, which was not present in the other six sequences which appear to be from milder cases.
Many of the fatal cases in the United States have also involved ARDS and hemorrhagic lungs, raising concerns that isolates with high levels of D225G can produce the increasing levels of such fatalities being reported throughout the northern hemisphere, including cases in Norway.
But does this mean the D225G mutant is easily transmitted? Does this mutation only happen in the host? What is the significance of a low transmission, high death rate mutant H1N1 strain?
There is an article on Virology Blog written by Dr. Vincent Racaniello titled “The D225G change in 2009 H1N1 influenza virus is not a concern” It is a well written article and supported by research and data. The premise of this article is to show that the mutation D225G in H1N1 actually helps to inhibit transmission of the mutant D225G H1N1 virus from host to host. This discovery is backed by research and data. The details are long and very technical so for simplicity we will omit these details in this article but here is the link to both the Virology Blog article and the Research article on Sciencemag.org. If we assume this data is correct then human to human transmission of D225G mutated H1N1 is severely inhibited, but not 100% and there can be some transmission taking place. Very close contact can be key in transmission, as in the 2 oil workers. We need more data out of the Ukraine and Norway to see the relationship of the people who have confirmed cases of the D225G mutation. We know that the Avian flu H5N1 is very hard to be transmitted between bird and human and human to human, however we know that close contact with the birds transmission occurred and most of the human to human transmission were between family members.
From the CDC
While most people in these clusters have been infected with H5N1 virus through direct contact with sick or dead poultry or wild birds, limited human-to-human transmission of H5N1 virus cannot be excluded in some clusters
The CDC and WHO so far claim that these mutations are spontaneous and pose no real threat to the public at this time.
The mutations appear to occur sporadically and spontaneously. To date, no links between the small numbers of patients infected with the mutated virus have been found and the mutation does not appear to spread, according to the World Health Organization.
If we assume these mutations are spontaneous within the host and they have a low transmission rate there still is a possibility that this mutation could become part of the circulating H1N1 with greater frequency. So if we end up with a mutated D225G H1N1 strain that dominates the wild type H1N1 we actually would see less infections, but we would see more severe cases and more deaths. Assuming the death rate of the D225G mutant is 5 times that of a wild type a non-mutant H1N1 strain (This number seems to be conservative based on data from the Ukraine in which 4 patients who had the mutant D225G strain all died.) and a transmission rate 5 times less than that of a wild type strain. We will use this example to show that having a low transmission rate may not be the best thing in a pandemic. These numbers are highly exaggerated and are only used for simplicity. Let’s assume we have a population of 10 million and a infection rate of 10% with the wild type H1N1 and a death rate of 1%. That would mean 1 million people would be infected and 10 thousand would die. Working with the same population we see an infection rate of 2% with the mutant D225G strain and a death rate of 5%. That would mean 2 hundred thousand infections and 10 thousand deaths. So if this D225G mutation becomes the dominate strain and can be transmitted at a much lower rate than the wild type H1N1 it could correlate to the same amount or even more deaths. Of course there are a lot of assumptions that have been made, but that is all we can do until more data is reported. What would be ideal would be for this mutation to spontaneous and limited to transmission within small clusters leaving the dominate strain the wild type H1N1.Is this how the 1918 pandemic played out? Only time and more data will tell.
We will have more on H1N1 mutations in part 3 with a look more closely at the symptoms and pathology of the D225G mutation.
D225G in Fatal H1N1casesin Norway?
Clusters of Hemorrhagic H1N1 Pneumonia in Ukraine
H1N1 mutation makes swine flu virus resistant to antiviral drugs - Tamiflu doesn't work anymore
H1N1 mutations emerging around the world - Tamiflu-resistant strain of H1N1 virus resists antivirals
Comments
Very informative. If I understand this correctly D225G does not necessarily mean that a given individual will contract a severe case if they are infected with it, as compared to the wild strain. Is this because it all depends on the G placement at position 225? From the article it appears that that between the two we are looking lots of infection , little death (Wild), or little infection, lots of death (mutant). If that is the case it seems at present there is a fight for supremacy going on. Would it be a fair assumption to suggest that because of the ever growing number of cases of D225G becoming visible that we may be at a tipping point between the two? If D225G does not match up with 1918/1919 exactly, what would be a clearer indicator that we are going down that path? Additionally since many people still have not been vacinated both healthy and otherwise, would it be a prudent move to get a Pneumovax? Thanks,
Hi Charlie.That is correct some people with a D225G mutation H1N1 infection have had only mild symptoms.This could be for many reasons.The virus didn't get deep into the lungs. They were vaccinated.The already had an H1N1 infection.Maybe a false positive for the mutation.A lot of variables to consider,but I believe that puts an even stronger emphasis on getting the H1N1 vaccination including the seasonal flu shot and a pneumococcal vaccination.Having the mutation D225G allows the virus to bind to both alpha(2,3) and alpha(2,6) linked sialic acids. The alpha(2,3)sialic acids are located on nonciliated bronchiolar cells between the respiratory bronchiole and alveolus, and on type II cells lining the alveolar wall.This type of binding will allow the virus to be more efficient in getting deeper into the lungs.The closer to O2/Co2 exchange site the more damage can be done.However wild type H1N1 can get deep in the lungs without a d225G mutation.
If the Data is correct then we could see less infections and more severe symptoms and deaths, than we would with a dominate wild type strain.I think we need more data to see were we are in regards to which is more dominate in certain clusters.I think we will find that this H1N1 of 2009 and its mutant D225G will work very close the way it worked in 1918 within its host. This does not mean we will see the results of 1918,just how they both operate.I think when we see these small cluster of mutant infections move into more clusters and into larger populations and we see a higher death rate then that of the seasonal flu these 2 variables could be a sign of bad things to come.Lets hope that day never comes.
If the Data is correct then we could see less infections and more severe symptoms and deaths, than we would with a dominate wild type strain.I think we need more data to see were we are in regards to which is more dominate in certain clusters.I think we will find that this H1N1 of 2009 and its mutant D225G will work very close the way it worked in 1918 within its host. This does not mean we will see the results of 1918,just how they both operate.I think when we see these small cluster of mutant infections move into more clusters and into larger populations and we see a higher death rate then that of the seasonal flu these 2 variables could be a sign of bad things to come.Lets hope that day never comes.
Excellent work, keep it up.
What about current H1N1 vaccine? Would it be a protection from this mutation?
This thing have already stressed my nerves to the point of nervous collapse some weeks ago. It's like a never-ending treat. And the lack of clear information is awful.
Please, could you tell me:
How much time the virus is infectious after being released to the environment?
I have read that the virus is active for 10 hours. Is that true?
If an ill person cough or sneeze over a surface (a door,a window, a book or the floor were all people walk) I can catch the flu if I touch the surface and then my eyes, nose or mouth ,even if had passed several hours?
Or that happen only if the surface is wet?
In short, what is the lifetime of the virus in surfaces like:
1)Dry steel or glass(windows and door edges)
2)Wet tissue and paper
3)Dry tissue and paper
4)Concrete and asphalt(i.e. the street floor)
5)Wood (in doors and the floor at home)
6)Plastic surfaces
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