H1N1 occasionally returns to its deadly roots: “

Deep lung infections are becoming more common as the virus spreads across America again.

Despite being nicknamed “swine flu,” H1N1v, or H1N1/2009, is a triple-threat of influenza. It is one-third avian, or bird, flu; one-third swine flu; and one-third human flu.

And to even call this new pandemic strain “swine” flu really is a misnomer, since we gave the pigs the virus to begin with. As Shope and others proved many years ago, pigs caught H1N1 from humans back in 1918, probably in the Midwest, probably Iowa. Swine H1N1 is the closest antigenic match to the 1918 pandemic strain that there is, because it has not been subject to all the mutations that human H1 has.

The pigs should probably sue for defamation of character.

OK, that’s out of the way. As I just mentioned, this pandemic virus is 1/3 human flu, 1/3 bird flu and 1/3 swine flu with antigenic similarities to 1918’s pandemic virus. And I believe that, in some people, those last two parts of this strain occasionally flare up and cause severe lung infections. And death.

There are myriad reports available now, all of which detail the (thankfully) infrequent deep lung infections experienced by victims of H1N1/2009.

But first, my speculation: I think that currently, and in the lion’s share of cases, H1N1v is a mild, relatively harmless virus. But once in a great while, it “runs home to Momma.” Momma, in this case, comprises the real origins of the virus: The 1918 pandemic strain, plus bird flu. In both cases, the flu virus penetrated/s deep into the lungs and did/does its damage there. Without Tamiflu administered quickly and decisively, this virus can cause ARDS, or Acute Respiratory Distress Syndrome. We have seen this phenomenon time and again in Vietnam, Indonesia, Egypt, China, and everywhere else that H5N1 has gained any foothold in the human population.

It is precisely these exceptions that make me nervous. As more and more people catch this disease, we will see more and more cases of ARDS in victims. The more we see ARDS-related flu cases, the more that particular phenomenon could turn into a much more frequent occurrence.

Now let me shift gears and talk about the three confirmed species jumps this virus has made. In Canada and Australia, the H1N1v virus has returned to its swine roots, infecting pigs on farms in those nations. A small number of hogs became sick, but enough to provoke concern among hog farmers everywhere.

And in Chile, turkeys have been sickened by H1N1v. In all these cases, the virus retained enough of its original genetic material and proclivities to infect multiple species. This tells me, as a layman (but a well-informed layman, to be sure) that this virus is fully capable of vacuuming up whatever genetic material it wants from whatever source, without sacrificing its ability to infect humans.

This is one big reason why I listened carefully to the words of virology professor John Oxford of Britain’s St Bartholomew’s and the Royal London Hospital. Dr. Oxford is one of the biggies in flu research; a man who bridges the span between Kilbourne and Webster and Kawaoka, who knows pretty much every researcher on the planet, and whose opinions deserve respect. Dr. Oxford made headlines recently when he prognosticated that the spring, and not the fall, will mark a decided turn for the worse with H1N1v.

A link to that story is at:

http://www.straitstimes.com/Breaking%2BNews/World/Story/STIStory_422344.html

Here is a snippet from that story:

‘For the moment, the virus is running around the world finding lots of young people and infecting them. It is doing very nicely, thank you, why should it change?’, he said by phone.

‘But once the virus has infected about a third of the world’s population – which is what we expect – it will find less ‘susceptibles’. That is when mutants will have a selective advantage.’ It would be a serious mistake to think that once the impending flu season is over, the danger will have passed, he added.

Prof Oxford said he had just returned from Australia, where he met front-line doctors who were concerned about an emerging pattern in swine flu patients.

Whether they are people in high risk groups – the obese, pregnant women, asthmatics – or young adults with no underlying conditions, an alarming number of patients wind up in intensive care units. ‘One minute they are okay in a hospital bed, the next minute they are in intensive care,’ he said.

There have been more than 100 confirmed deaths from the pandemic H1N1 strain in Australia, which is just emerging from the southern hemisphere winter. Epidemiologists sifting through data from other countries have also found similar – and disquieting – patterns.

French epidemiologist Antoine Flahault reported a 100-fold increase, compared to seasonal flu, in the number of swine flu deaths in Mauritius and New Caledonia attributed directly to the virus itself rather than secondary bacterial infections or underlying conditions.

Many of those deaths were caused by acute respiratory disease syndrome (ARDS), which requires intensive-care treatment for an average of three weeks.

Only 50 per cent of ARDS patients survive. — AFP

I intend to cover Dr. Oxford’s theory more fully in a separate blog regarding pandemic waves. But I do want to forward a theory of mine, which nests nicely with Professor Oxford’s.

This virus has seen a dramatically accelerated pattern of movement in the industrialized world. Dr. Chan of the WHO has said this is the fastest-moving pandemic in recorded history, which should surprise no one. We are moving faster than at any other time in recorded history.

However, when H1N1v hit Asia, it took on a more familiar pandemic timeframe. This, in my opinion, has left the world watching what I would call two pandemic waves. One is the accelerated and elongated wave which never, ever really subsided and which may or may not now be considered the second wave of the virus; and one is the traditional, plodding, months-long Asian/Indian/African/Middle Eastern wave.

The following corrorborative data is from the WHO, and is current as of 6 September 2009.

Region

Cumulative total

as of 6 September 2009

Cases*

WHO Regional Office for Africa (AFRO)

6336

WHO Regional Office for the Americas (AMRO)

120653

WHO Regional Office for the Eastern Mediterranean (EMRO)

9844

WHO Regional Office for Europe (EURO)

Over 49000

WHO Regional Office for South-East Asia (SEARO)

22387

WHO Regional Office for the Western Pacific (WPRO)

69387

Total

Over 277607

Note that the total of the two Asian reporting regions is about half the cases from the Americas and Europe combined.

Look at recent news reports to see how long it has taken this virus to seed India alone. Admittedly, information is difficult to come by within Asia, especially China, on a good day, let alone during a pandemic. But it feels like the virus is plodding along in the interior of those remote countries. What the virus is doing in there, and what other flu virus it is coming into contact with, are anyone’s guess. But I am not optimistic about what may emerge from the other side.

Anyway, I see the intersection of these waves — the Core’s first wave (to use the definition of the industrialized world according to Thomas P.M. Barnett), and the developing world’s second wave — sometime in the spring of 2010. It is at that juncture that the virus may change, having exhausted a significant source of carriers to the milder form of the virus.

Well, as Forrest Gump would say, that’s all I have to say about that. To say any more would deprive me of the opportunity to write that other blog.

Another news story, this time from India, would tend to support my speculation. Public health officials are claiming a viral mutation has been discovered in a district there. There are other reports, awaiting confirmation, that a mutation in the PB2 gene segment has begun to appear that would make transmission even easier than it is today. H1N1v still retains avian proclivities to infect at higher temperatures (birds have higher core temperatures than we humans do). One reason why H5N1 has not “caught on” yet is that it refuses to shed that avian gene segment, known to researchers as E627K, on the PB2 strand.

Some speculate that E627K may explain why H1N1v never went away in the summer. It actually liked the warmer temperatures! And sensing, somehow, that colder temps are on the way, its Darwinian mechanisms would logically prompt it to seek out a more reasonable thermometer — a change in that genetic position, which it would probably seek to acquire from seasonal influenza.

If there is a shift in E627K toward human respiratory temperatures instead of a duck’s intestinal temps, this virus could become quite perilous.

So let me sum all this up. I believe H1N1v, for reasons yet unknown, occasionally decides to return to its infectious origins and cause severe and occasionally lethal infections. The virus retains enough of its original genetic material to have spawned species jumps to pigs and birds in the spring and summer, and there is no reason to believe it has not continued to do so. And we have not seen abatement of the virus’ first wave in the Asian and Indian regions, and so we should assume the virus’ first wave continues to traverse those regions.

For these reasons, it is absolutely imperative that we remain vigilant and watch carefully for any sign that this virus has become more virulent and more severe.

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