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A few months ago, I blogged on the appearance of a mysterious new fever that behaved much like Ebola.In that blog, titled (and linked here) called Do we have another species jump in Africa?, I speculated (as did the rest of the world) that we had ourselves another new, species-jumping virus.

DINGDINGDING! Yes, it's new. It's name is the Lujo virus. Yes, as suspected, it is an arenavirus, which is normally carried and spread by rodents.

Now here's the problem: It is an aggressive little sucker, and has an incubation period equivalent to influenza. From my blog of October, 2008:

The index case -- Patient Zero of this new and so-far unknown variant -- is a Zambian who was hospitalized in Johannesburg, South Africa. Two persons who were in the hospital for treatment unassociated with the index patient's disease(nosocomial) also develped symptoms and died. A fourth patient -- a nurse treating the second, NOT the index patient -- is in isolation and is being treated with ribavirin, which helps against lassa fever but is experimental when dealing with this new virus.

Here's a chilling paragraph from the proMED report:

"Arenaviruses cause chronic infection in wild rodents (multimammate mice) with excretion of virus in urine, which can contaminate human food or house dust. Arenaviruses have been found in southern African rodents in the past, but there has been no previous association with human disease. The virus associated with the present outbreak may prove to be a new member of the group." (bold mine)

So we have a new and previously undiagnosed form of arenavirus which has apparently jumped the species barrier from animals (rodents) to humans. Isn't that just lovely? And the virus is highly contagious to boot, as evidenced by the rapid spread to other patients in the hospital -- and the infection of the nurse who was attending one of the follow-on cases.

Now here's the press account, from the AP and found at MSNBC.com:

New killer virus found in Africa

Scientists discover disease that causes Ebola-like bleeding The Associated Press updated 8:17 p.m. ET, Thurs., May 28, 2009

ATLANTA - Scientists have identified a lethal new virus in Africa that causes bleeding like the dreaded Ebola virus.

The so-called "Lujo" virus infected five people in Zambia and South Africa last fall. Four of them died, but a fifth survived, perhaps helped by a medicine recommended by the scientists.

It's not clear how the first person became infected, but the bug comes from a family of viruses found in rodents, said Dr. Ian Lipkin, a Columbia University epidemiologist involved in the discovery.

"This one is really, really aggressive," he said of the virus.

A paper on the virus by Lipkin and his collaborators was published online Thursday on in PLoS Pathogens.

The outbreak started in September, when a female travel agent who lives on the outskirts of Lusaka, Zambia, became ill with a fever-like illness that quickly grew much worse.

She was airlifted to Johannesburg, South Africa, where she died.

A paramedic in Lusaka who treated her also became sick, was transported to Johannesburg and died. The three others infected were health care workers in Johannesburg.

Investigators believe the virus spread from person to person through contact with infected body fluids.

"It's not a kind of virus like the flu that can spread widely," said Dr. Anthony Fauci, director of the National Institute of Allergy and Infectious Diseases, which helped fund the research.

The name given to the virus — "Lujo" — stems from Lusaka and Johannesburg, the cities where it was first identified.

Investigators in Africa thought the illness might be Ebola, because some of the patients had bleeding in the gums and around needle injection sites, said Stuart Nichol, chief of the molecular biology lab in the CDC's Special Pathogens Branch. Other symptoms include include fever, shock, coma and organ failure.

Samples of blood and liver from the victims were sent to the United States, where they were tested at Columbia University in New York and at CDC in Atlanta. Tests determined it belonged to the arenavirus family, and that it is distantly related to Lassa fever, another disease found in Africa.

The drug ribavirin, which is given to Lassa victims, was given to the fifth Lujo virus patient — a Johannesburg nurse. It's not clear if the medicine made a difference or if she just had a milder case of the disease, but she fully recovered, Nichol said.

The research is a startling example of how quickly scientists can now identify new viruses, Fauci said. Using genetic sequencing techniques, the virus was identified in a matter of a few days — a process that used to take weeks or longer.

Along with Fauci's institute, the National Heart, Lung, and Blood Institute and Google also helped fund the research.

© 2009 The Associated Press. All rights reserved. This material may not be published, broadcast, rewritten or redistributed.

URL: http://www.msnbc.msn.com/id/30989694/

The link to the study, published in the journal Public Library of Science Pathogens, is at:

http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1000455

But wait, there's more! In my December post, I make reference to a woman who died on a Virgin flight from Johannesburg, South Africa, to London in May of 2006.  The initial speculation was that she died of Ebola, but we never had a follow-up news story.  I strongly urge health authorities to retest her samples to determine if she died of Lujo.  that would give us a glimpse of how old this "new" virus really might be. 

Now this virus does not travel as influenza does -- it is not "airborne," as they say.  It can currently only be transmitted via contact with bodily fluids.  The good news within the bad news is that the virus does seem to be sensitive to the antiviral ribavirin, which is used to treat Lujo's distant viral cousin, Lassa Fever.  And it is still a rare virus. 

So my question of last October -- Do we have another species jump in Africa? -- is answered.  The answer is Yes.  And it could be a doozy. 

Earlier today, I pointed out with some thumping of the ol' chest that the CDC has indirectly confirmed my theory of late April regarding swine flu; namely, that we could compare this event with the 1946-47 pandemic/epidemic of H1N1 and the 1951 H1N1 severe epidemic to see if there was a correlation.

The New York Times article was the first confirmation of that.  Now, the AP has also written on the topic.  But their story is more precise in the age group (persons ages 60 and above) that seem to have natural antibodies against 2009's swine H1N1. 

A simple subtraction of the number 60 from the number 2009 (or 2008 if you prefer, since the virus apparently first manifested itself in September 2008 in Mexico) yields the number 1948.  This is so close to the 1946-47 severe epidemic that it cannot be considered coincidence.

As I have mentioned many times previously, the 1946-47 epidemic may have, in fact, been a pandemic of influenza.  It was certainly an epidemic, and was by accounts as severe, illness-wise, as the 1957 H2N2 "Asian flu" pandemic, with roughly the same mortality, which was serious but not apocalyptic. 

Textbook research shows that flu seasons had been relatively mild from 1930 until 1946, when all viral Hell broke loose.  A serious antigenic event -- a huge drift, or perhaps a more likely antigenic shift due to reassortment of human flus -- took place.  It rendered vaccines useless (sound familiar?) and started a new chain of H1N1 flu that culminated in yet another antigenic seismic event in 1951.  That virus caused more epidemics until it was deposed by H2N2 in 1957.

It is highly unlikely that antibodies to pre-1946 influenza are helping seniors today.  In my own opinion, it must have been the 1946-47 strain of H1N1.  And that would seem to indicate a swine background for that mutation, but I will leave that for the researchers. 

At any rate, the roadmap is opened up and flattened out for viral researchers.  Good luck to them.

I just read a Tweet from my buddy Mike Coston, aka FLA_MEDIC, blogger of great repute at Avian Flu Diary. He mentioned an article in Nature by Dr. Peter Sandman, one of the world's leading risk communication experts. I encourage you to follow the link and read it now. I'll wait.

OK, welcome back. Didn't that all sound familiar? Having deja vu? that is because it sounds similar to my blog of April 28th, titled Mixed messages, cafeteria-style preparedness won't cut it in swine flu fight. In that blog, I cover many of the same themes. But Dr. Sandman puts things much more succinctly and with much greater gravitas than I ever could.

I met Dr. Sandman in February 2007 in orlando at the CIDRAP pandemic conference. The man and his work are both highly valued and woefully underutilized, I am afraid.

The thing I most remember about then-HHS Secretary Mike Leavitt, a former governor of Utah, is his suggestion -- painfully repeated over and over and over again -- that the easiest way to stock up for a pandemic was "When you go to the store to buy tuna, for every three cans you buy, get a fourth and put it under the bed." Overall, the entire Bush Administration message on pandemic preparedness was (uncharacteristically) clear, sensible, and sage. It was borne of Bush's own reading of John Barry's seminal work The Great Influenza," THE history of the 1918 pandemic.

President Obama's administration seems to have completely disregarded the role that concise risk communication must play in effective management of a flu pandemic. The role of individual responsibility needs to be played up, not downplayed in favor of "nothing to see here, move along." the American people can take it: Tell them exactly what they need to hear. Especially the part they never want you to hear: government can do very little to ensure your personal safety or health during a flu pandemic. That itself may be anathema to their way of thinking, but the truth is the truth.

From Dr. Sandman's article:

Richard Besser, the acting director of the CDC, isn't understating the risk. He says he is "very concerned", but expresses his concern with a soothing bedside manner. He doesn't have that rumpled, exhausted emergency-manager look that the Nuclear Regulatory Commission's Harold Denton perfected in the 1979 Three Mile Island crisis. Denton left people feeling that the risk was serious and that they were in good hands. Besser says it is serious but leaves us feeling that he doesn't want us to worry much.

Still, I don't fault Besser for looking and sounding reassuring. Good crisis communication means saying alarming things in a calm tone, and he is doing exactly that.

The problem is that he isn't giving us anything to do except being hygienic. He keeps telling us, accurately, that the CDC is being aggressive in its response to the outbreak. But he is not asking the public to take further action. He needs to urge citizens, schools, hospitals and local governments to follow Leavitt's advice.

Instead, we have a surreal situation in which the federal government has released one-quarter of the Strategic National Stockpile of antiviral drugs, so there will be enough oseltamivir (Tamiflu) to deploy to millions of sick Americans. But it hasn't yet asked those Americans to stock up on tinned fruit and peanut butter.

It's time to talk peanut butter, tuna and bottled water. But not for swine H1; for any calamity. As I said in my late April blog:

So what should we be telling people? We should be telling them to prepare and to learn more about influenza. I am not talking about the Romero-esque TV commercials that the Ford Administration ordered up during the 1976 swine flu scare. I am talking about telling people to get their "hurricane kits" or "earthquake kits" restocked and brought up to speed. It is time to re-educate the American people on previous pandemics and previous near-misses, such as 1946 and 1951, with viruses that were also H1N1 but were much more virulent and, some thing, either swine-like or were actual swine influenzas that jumped the species barrier back in the day.

Telling people to buy one to two weeks' worth of food, water and medicines to prepare for hurricane season -- an annual hit-or-miss proposition with a clear historical precedent of occurrences -- is not considered folly; it is considered prudent.

Great minds think alike.  Thank you for a great article, Dr. Sandman.

Well, well, well. It is always nice and gratifying to have a theory confirmed by the mainstream media and the flu experts.

Let me explain: A few weeks ago (April 26th), I blogged that our current swine H1 might be a relative of the same virus that appeared in 1946-47 and 1951. I also proferred that theory to one of the world's top influenza experts via email. Trust me on that: It is literally a matter of public record.

Now comes an article written by the New York Times' Donald McNeil Jr., who is to the U.S. what Helen Branswell is to Canada when it comes to infectious disease newspaper journalism. In it, Mr. McNeil quotes Dr. Daniel Jernigan of the CDC, who states very clearly that informed opinion is coalescing around a theory that pre-1957 H1 successfully conferred immunity to now-older Americans.

The Times article is somewhat incomplete. It insinuates that all H1 was pretty much the same following 1918, just getting more and more diluted. If you look at influenza textbooks of the past twenty years or so, however, what actually happened is that an event of great significance produced much more severe epidemics of H1N1 in 1946-47 and 1951. It has been postulated that swine H1 might have crossed the species barrier in those epidemics, or a random mutation/mutations changed the gene segments just enough to cause some above-average morbidity.

Among influenza circles, debate still rages (that is a relative term, as "rages" for them might be a "harrumph" or a discreet rolling of the eyes) about whether or not 1946-47's epidemic was in actuality a real pandemic. There are considerable arguments on both sides, and I have seen the words "1946-47 pandemic" in print on more than one occasion, in more than one text. What is known is that some seminal event occurred that rendfered the seasonal vaccine for that year completely useless. The link atthe previous sentencewill take you to a study conducted by the living influenza legend Dr. Edwin Kilbourne on that very vaccine failure.

While quite possibly a pandemic, the 1946-47 epidemic produced huge spikes in morbidity, or illness. What it did not do, however, is kill a lot more people statistically. That was reserved for the 1951 epidemic of so-called "Liverpool flu."

The 1951 Liverpool flu epidemic was a terrible killer of people, strangely enough, in the English-speaking world. In the scientific paper 1951 Influenza Epidemic, England and Wales, Canada, and the United States, researcher Ceclie Viboud and others describe the impact that strain of H1 placed on Britain and North America. In some sections of Britain and the US Northeast, the case fatailty rate for 1951's H1 was worse than 1918-19!

We are used to uttering two words when discussing influenza antigenic mutations: Drift and shift. Drift is what happens when a virus makes copies of itself (badly). Shift is what happens when a major reshuffling of influenza genes takes place. Shift is what makes pandemics, or so we have always thought. Antigenic shift occurs when reassortment takes place between dissimilar flu strains. For previous descriptions of drift and shift, reassortment and recombination, just search this blogsite and Google the terms as well.

But what if antigenic shift occurs within the H1N1 subtype itself? Is the resultant virus truly a pandemic candidate? Is this what occurred in 1946-47? Is this what occurred in 1951? Scientists think so. From Science Daily of March 7, 2008:

ScienceDaily (Mar. 7, 2008) — The exchange of genetic material between two closely related strains of the influenza A virus may have caused the 1947 and 1951 human flu epidemics, according to biologists. The findings could help explain why some strains cause major pandemics and others lead to seasonal epidemics.

Until now, it was believed that while reassortment -- when human influenza viruses swap genes with influenza viruses that infect birds -- causes severe pandemics, such as the 'Spanish' flu of 1918, the 'Asian' flu of 1957, and the 'Hong Kong' flu of 1968, while viral mutation leads to regular influenza epidemics. But it has been a mystery why there are sometimes very severe epidemics -- like the ones in 1947 and 1951 -- that look and act like pandemics, even though no human-bird viral reassortment event occurred.

"There was a total vaccine failure in 1947. Researchers initially thought there was a problem in manufacturing the vaccine, but they later realized that the virus had undergone a tremendous evolutionary change," said Martha Nelson, lead author and a graduate student in Penn State's Department of Biology. "We now think that the 1947 virus did not just mutate a lot, but that this unusual virus was made through a reassortment event involving two human viruses.

"So we have found that the bipolar way of looking at influenza evolution is incorrect, and that reassortment can be an important driver of epidemic influenza as well as pandemic influenza," said Nelson, whose team's findings appear in the current issue of PLoS Pathogens. "We have discovered that you can also have reassortment between viruses that are much more similar, that human viruses can reassort with each other and not just with bird viruses. " (bold mine)

Nelson and her colleagues analyzed the evolutionary patterns in the H1N1 strain of the influenza A viruses by looking at 71 whole-genome sequences sampled between 1918 and 2006 and representing 17 different countries on five continents.

Big differences in the shapes of these eight trees signified that reassortment events had occurred.

The swapping of genes between two closely related strains of the influenza A virus through reassortment may also have caused the 1951 epidemic, which looked and acted in many ways like a pandemic as well. Deaths in the United Kingdom and Canada from this epidemic exceeded those from the 1957 and 1968 pandemics.

Currently, there are many types of influenza virus that circulate only in birds, which are natural viral reservoirs. Though the viruses do not seem to cause severe disease symptoms in birds, so far three of these viral types have infected humans -- H1N1, H2N2, and H3N2.

Understanding how each strain evolves over time is crucial. H3N2 is the dominant strain and evolves much more rapidly than H1N1. So the H1N1 component of each year's flu vaccine has to be updated less often. In comparison, the H3N2 component of the vaccine has been changed four times over the past seven years.

The H1N1 virus is particularly unusual because it disappeared completely in 1957, only to mysteriously re-emerge in humans in 1977 in exactly the same form in which it had left. It is still not certain what happened to the virus during its disappearance. But since it did not evolve at all over these twenty years, "the only plausible explanation is that it was some kind of a lab escape," says Nelson, who is also affiliated with Penn State's Center for Infectious Disease Dynamics (CIDD). (bold mine)

The Penn State researcher says the study shows that the evolution of a virus is not limited to the mutation of single lineage, and that there are multiple strains co-circulating and exchanging genetic material. The H1N1 and H3N2 strains, for instance, are occasionally generating hybrid H1N2 viruses.

"If we really want effective vaccines each year, our surveillance has to be much broader than simply looking at one lineage and its evolution, and trying to figure out how it is going to evolve by mutation," said Nelson. "You have to look at a much bigger picture."

OK. So here's what this says:

We got so wrapped around the axle of looking for Bird Flu under every duck's behind, and we got so lax at a) swabbing suspected flu patients and b) sending "untyped A" samples to the CDC/WHO, that we completely got snookered (a Southern technical term) by swine H1N1. It seems reassortment between similar subtypes happens all the time (I have seen several reports confirming that H1N2 combination) that this new hybrid swine/avian/human H1N1 could very well be following a path already traveled by the H1N1 viruses of 1946-47 and 1951. 

Now let me go a bit further: The Science Daily article also says that H1N1 does not change its genetic makeup easily, nor suffer fools gladly. But its resilience cannot be underestimated. Whether it takes its place in the pantheon of pandemic viruses is yet to be known. And indeed if there is immunity to this virus from baby boomers and older prople, we are having the same argument about "pandemic or not to be a pandemic" that people had in 1947 and 1951 -- arguments still underway today. This also explains why the WHO may be very unwilling to declare a Phase 6 pandemic when this may not actually be a pandemic. Recall that a pandemic by definition includes, at its core, a virus with little to no immunity in the general population.

If billions of people are over age 52, then the criteria for a pandemic virus has not been met -- yet. I say "yet" because I want to also talk about another statistic. And that is that it only took a few years from the 1951 epidemic to the total disappearance of H1N1 in 1957. Recall that influenza plays King of the Mountain. The year 1951 began H1N1's Farewell Tour, although now in retrospect it was one of those Cher/Streisand faux farewell tours, meaning "Farewell until the next big tour's big fat paycheck."

So which influenza strain will knock H1N1 back off the mountain? Will it be H5N1? A return of H2N2? You know, there is a developing consensus that pandemic viruses recycle themselves every three to four generations. When there are no more immune people to get in the way of a massive infection wave ( categorized as a lack of "herd immunity"), then an older virus energizes itself and springs forward.

Nobody knows what will happen with swine H1N1. But once again, if history is to tell us anything, it is that influenza is wildly unpredictable and we need to be prepared for anything. And we need to look closely at 1951 and 1946-47 for more immediate answers. Fortunately, many of those who researched those epidemics/pandemics are still with us. Let's use their talents and mine their recollections and get busy.

Avid readers,

This is as much for my own benefit as it is yours. I have been "out of pocket" with family medical matters for the past two weeks, and as you can tell, my blogging and Tweeting volumes have suffered. It is important for new readers to know (and especially to my followers on Twitter) that I do not blog or Tweet unless I have something to say that I think will help the cause or further debate.

OK, here's what we know. Swine H1 has exploded across the globe, which we all suspected would take place. It is everywhere, and the cases are too numerous to count, despite attempts to actually count them (more on that later).

It is also kind of futile to simply track the number of cases actually testing positive. As Ian Holm said in The Day After Tomorrow, "That time has come and gone, my friend." In the Internet Age, and with all the powerful real-time surveillance tools at our disposal, we still have no earthly idea how many positive swine H1 cases we have in our own municipalities, let alone the world. So counting is best left to the historians.

Is it any wonder then that we constantly mark up the number of dead from the 1918 pandemic? What started with some 20+ million dead from authors Beveridge and Crosby has grown to 50-100 million with Barry and Kolata. Personally, considering the later historical reports from China and India, I lean toward the latter numbers. I also say this because I know John Barry (The Great Influenza) and his research methods are beyond question.

So how many people have swine H1? According to the CDC, we should not be surprised if upwards of 100,000 are currently infected. I estimated just about that number a couple of weeks ago. It is an algorithm that one can work quickly in one's head -- or gut, more appropriately. It is a gut feeling that if we had, say, 4,000 positive results, many times that are actually infected. And considering how far behind all the public health agencies are in testing, we are actually constantly looking backward, rather than looking forward with these estimates. It's like steering by one's own wake, or driving via the rear-view mirror. We need to stop looking behind us and start looking forward again.

Los Alamos in New Mexico specializes in such algorithms and estimates. The CDC has probably been on the horn with them many, many times since the first outbreaks in Mexico, asking what the Big Board would look like in a few weeks.

What is equally clear is that we are now seeing what we did not see three weeks ago:sustained chain human transmission in this country and abroad. Japanese teenagers are dropping like flies from this malady. So are American teenagers. A recent Washington Post article showed where the virus is hitting hardest: young people ages 5 to 24. According to the article,

Compared with seasonal outbreaks, all flu pandemics cause a higher percentage of severe cases and deaths in younger groups. Although the overall mortality rate from the current swine flu is low, this trend is already apparent.

Last Thursday, when Fukuda announced that the global death total was 65, he noted that "half of them are healthy people who have no predisposing conditions. This is a pattern different from what we see with normal influenza."

There have been too few deaths in the United States to draw any conclusions. But of the 173 people who have been sick enough to be hospitalized, more than half are in the 5-to-24 age group.

Also, of great interest to this blogger, is the reference to the "mini-pandemic" of 1977. I have referred to this many, many times over the past three years, and it is gratifying to read confirmation of same in a newspaper as respected as the Post:

A variety of H1N1 strains circulated from 1918 to 1957, then disappeared for two decades. In 1977, however, an H1N1 strain surfaced that was nearly identical to the previous one, so much so that scientists suspect it was an accidental release from a lab freezer. It caused a pandemic -- Russian flu -- that was largely limited to people younger than 25, whose immune systems had never experienced H1N1.

The lab accident theory behind the 1977 epidemic is not universal, but anything is possible.  If you search this blogsite for the ongoing series "When labs attack," you will become convinced such things are indeed possible.  I believe it was Dr. Edwin D. Kilbourne, the Pope of Influenza before Webster inherited the vestments, who offered a contrary opinion that the virus was ID'ed in China prior to its typing in the Soviet Union.  Kilbourne is still with us and still offering counsel, as evidenced by the Post article.  that is excellent:  We need All Hands on deck for this almost-certain pandemic.

In fact, a dust-up of a sort occurred when veteran retired (I mean a veteran who is now retired, not a veteran of being retired) influenza researcher postulated openly that swine H1 was another accidental lab release into the wild.  Or a release that quickly reassorted with another strain.  Both the WHO and CDC are unconvinced, and have denied its plausibility.  Considering who the man was (Dr. Adrian Gibbs) and who the man worked with (Drs. Robert Webster and the late, great Graeme Laver), he was absolutely qualified to venture his hypothesis.  Gibbs had worked on the research that ultimately led to the development of Tamiflu itself.  Gibbs, Laver and Webster all swabbed birds' buttholes on an Australian beach, collecting influenza samples that they used to write the research that led to the breakthrough.

Gibbs' point was not that some costumed supervillain was conjuring up rogue flu viruses in a lab; believe me, no one is that good.  Only nature/God is capable of such randomness that could lead to a new flu virus.  Gibbs' point is that influenza for vaccines is still grown in eggs, like they did sixty years ago.  And these influenza strains can "drift" during the manufacturing process.  Think how hard it is to mix paint at your local hardware store if even a single extra drop of color seeps in.  Well, as flu grows, its RNA makes bad copies of itself, and the virus can mutate -- or "drift" -- beyond the target specified by the WHO.  Many, many batches of flu vaccine may be, and have been, destroyed each flu season as the virus drifts beyond the specs listed for that seasonal strain by the WHO. This also happened in 1976 during the development of the first swine flu vaccine. 

Gibbs also postulated that influenza grown for research purposes might have done the same thing.  the key here is biosecurity.  How much or how little is the question.  Again, refer to my "When labs attack" series for background.

So back to the issue at hand: We must not be focused on the minutae of positive test results. We need to start looking at, and tabulating,absenteeism in schools and the workplace. That is the indicator of where the virus has gone and the extent of its penetration into our communities.

That is also the logic behind the Google project to track pandemic developments by the number of targeted "hits" on Websites dealing with the treatment of influenza. Of course, you need to develop a baseline, and have a way to eliminate "chatter" that might come from people who read this blog, for example. But the possibilities are there, and any method of surveillance is helpful if it can be proven to be helpful. I guess Google will get back to us on that one.

There has been a lot of hand-wringing over the issue of closing schools and borders and such, both in the US and abroad. Everyone needs to remember that these steps, in the aggregate, are nothing more than delaying actions -- like a rear guard action in combat, which this surely is. We are trying to slow the advance of the virus, not stop it in its tracks. It is flat-out impossible to stop influenza in its tracks. The virus is just too good at what it does.  Only influenza can stop influenza.

There is a group of persons who were calling upon the world health community to allow this new virus to burn its way around the globe quickly, hypothetically allowing it to confer immunity while it was still relatively mild. This theory is interesting but ultimately does not hold water. Here's why not:

First, delaying the spread allows us precious time to study the virus, to try and understand its genetic makeup, and to prepare a vaccine candidate.

Second, because seasonal H1N1 holds the dreaded Tamiflu resistance gene, (and you should know from reading my recent and past blogs exactly what that is), the faster swine H1 does its Magellan impression, the more likely it is to pick up that gene more quickly. that would render the world's entire stockpile of Tamiflu useless against a new pandemic.

Already, CDC and WHO are recommending the use of Tamiflu only to treat those in high-risk groups: The immuno-compromised (chemotherapy patients, HIV/AIDS patients, COPD, pregnant women, etc.). And maybe or maybe not the elderly. This is being done in an effort not to over-prescribe Tamiflu, which scientists fear could lead to Tamiflu resistance. But as we know today, the acquisition of the Tamiflu resistance gene has absolutely nothing to do with the overprescription of Tamiflu itself. If it did, Japan would be completely lost, because doctors there (who profit from prescriptions they write) prescribe Tamiflu like American doctors prescribe Motrin. Why do you think the Japanese discovered the possibility that youthful sufferers of influenza, dosed with Tamiflu, might jump off buildings? because they had such a large statistical sample to work with.

Third and finally, hastening the circumnavigation of the world by a new pandemic virus ruins any chance we might have to re-educate the masses on pandemic preparedness. Slowing the spread allows precious time to plan, to educate, to train and to prepare. Of course we should have been doing those things already. But people and organizations procrastinate.

I wanted to return to the topic of Tamiflu-related suicides among Japanese teenagers (Google it if you are unfamiliar). This is why Roche created Childrens Tamiflu, which is available in a smaller dosage than adult Tamiflu. If you have a young child who is diagnosed with swine H1N1, you should ask your doctor about Childrens Tamiflu as an alternative to regular Tamiflu. I am not aware of any Childrens Tamiflu in the Strategic National Stockpile, because the Stockpile began before Roche began the manufacture of the kids' dosage. Again, check with your doctor if you have a child under the age of 16 who is swine H1-positive.

OK, I think I/we are all caught up now.