I will be keeping an eye on one thing, though…

This is what the flu season looks like so far in the US. The red line in this complex graph shows that we are at a very high point right at this moment:

It is a big bad year for the flu, so one-point-five gazillion people moving across the landscape and hanging out here and coughing on each other can be a problem. But, if we look just at Minnesota, there is a more nuanced picture. Similar data for just the North Star State graph out this way:

Notice that here, the flu season appears to be rapidly going away. That red line is still up high, which means lots of flu around, but we are in a downward swing.

But also notice that it is not uncommon for a flu season to have a second, smaller but meaningful, bump on the way down, and sometimes (like last year) that can be a big bump. So, my question is this: Will we have another bump starting next week, and will that bump be because one-point-five-gazillion people showed up to contribute to our flu?

Or, since people who are really sick may not travel, maybe having one-point-five-gazillion non-flu-ridden people sprinkled around in the population will provide some sort of epidemiological buffer, a contribution to local herd immunity of sorts, to hasten the decline of our flu numbers.

Maybe all the flu will jump on the Eagles fans and they’ll leave with it.

Anyway, I think there is a small but not insignificant possibility that we will have a Super Bowl Bump in our flu statistics.

Watch this space. If it happens, I’ll post on it and crow. (If it doesn’t, I’ll delete this post!)

If this is a thing, a Super Bowl Bump for the flu, we would have seen it before. Unfortunately, different states keep and present their data in different ways. I’m sure there is some database out there I can mine, but since I don’t now where it is, we’ll have to use less than ideal data.

Have a look at Texas:

This is a graph from Texas showing the flu season, using an OK but not ideal metric, percent of medical facility visits due to a flu like symptom. Notice that there is a bump at the time of the Super Bowl in 2017, when it was in Houston. But the bump starts to happen before the Super Bowl and is that year’s main influenza event in Texas. And Texas is huge, so a Houston event would not show up. Conclusion: Texas does not inform, nor does it falsify. More study needed.

(By the way, yes, I’m aware that a venue-by-venue look does not show what happens when newly infected fans from out of state go home, it only shows the effects of an influx of people on that area.)

The 2016 Super Bowl was in Santa Clara California. Again (not bothering with the graph), California’s flu season tends to peak around Super Bowl time and it died that year. Also, it was not a very big year. But, again, this is a large state with way too much data watering down any effect, unlike Minnesota, where half the people here live in the Twin Cities and the Twin Cities is where the Super Bowl is being held.

New Orleans in 2013? Yes,there is a tiny bump so minimal I won’t even show you, and it was a low level year for the flu. Again, not an ideal scenario.

Really, the best case I can find among all the Super Bowl Sites for a flu bump in a state, i.e., bad flu year, the state on the way down and not at peak, and a concentration of population, is 2018, though Minneapolis had the Super Bowl in 1992. There are no reliable data that I can find for 1992. So, if this is ever a thing, this is the year that may happen.

Do feel free to look at the visiting team’s home towns over the last dozen years or so and report back if you see anything!

By the way, Pink a) will be singing the national anthem and b) has the flu, it is said. So, that should be interesting. Maybe that will be the controversy.

A new wrinkle in the process for North Americans, possibly with parallels elsewhere, is the summer camp phenomenon. This is where we take children from multiple communities, only some of which have some dreaded disease, or perhaps just an annoying meme, and we ship them all to one location either every day for the whole day, or for weeks at a time overnight. In this way, the diseases or annoying memes can spread among them and all the children can bring them home!

There have been some summer camp closings.

Despite rumors to the contrary, the novel swine flu is roughly as deadly as the regular flu. I’m still seeing people, even experts, indicate that it is relatively mild. It is not. It is typical.

The novel swine flu seems to be affecting younger individuals in part because of an immunity found in older individuals, presumably from exposure to a similar flu in the past. This is interesting news if confirmed. This touches on another area of confusion. The 1918 pandemic flu was famous for being extra deadly for healthy individuals. This was for a very specific medical reason. The current flu seems to be affecting ‘healthy’ individuals more as well. This is for a totally different and utterly unrelated reason, probably.

This is subject to revision, but here’s the story:

The 1918 pandemic flu killed healthy people more because healthy = stronger immune system. These people were killed by the way their immune system reacted to the flu. A person with a strong immune system would be more strongly affected by the flu, possibly fatally.

The novel swine flu appears to be affecting healthy people more because healthy = younger than a certain age. That age cut off separates individuals (older) who have an immunity from prior exposure to a similar virus from younger individuals who don’t.

Again, this is subject to revision. This is subject to revision in two ways:

1) The assertion I make above about the 1918 flu is very likely true and well demonstrated, but the assertion I make about the novel swine flu is speculative at this time; and 2) the phenomenon seen in the 1918 pandemic flu, while apparently not happening with the current novel swine flu, could develop later on during the pandemic.

Why do I say that? Because that is what happened in 1918. The flu went around the world ‘off season’ (as the current flu is doing) and was typical in virtually every way but its timing. Then it went around the world again with this extra glitch of killing people with their own immune system.

The fact that the 1918 flu did this has flu experts worried, and they should be. However, I have yet to see a biological argument for why this flu should follow the same pattern in regards to this specific feature.

What is going to happen next? In late (?) September (+/-) there will be a flu vaccine available for the regular flu. Get one.

Later, maybe in October (?) there may be a vaccine available for the novel swine flu. This may be a two dose vaccine. Get it, get them both if there are two. There will be instructions as to who should get it and when. But since those instructions will be filtered through the usual sources, be careful what you pay attention to. The little people sitting at the colorful desk on the news show will not be giving you useful information. They never get this stuff right. You should rely on the blogosphere this time around, I think.

(People who have gotten the novel swine flu already seem to be immune but unless you know you had it from a clear test, I would not assume that.)

And speaking of people getting it all wrong … have you heard about any of the flu woo scams going around regarding the flu? There is a treatment in which photons are passed into your cells to kill the virus. There is an anti-flu vaccine. There is a ‘do it yourself’ flu vaccine kit, which involves you sending in your credit card number but then never hearing back from them.

Obviously, don’t fall for that.

CDC flu site; WHO

The new Swine Flu has now been verified in nineteen US states, with 141 cases. Technically there is 1 death, but since the young girl who died actually caught the flu in Mexico (and came to Texas for treatment) it is hard to say how that should be counted.

WHO characterizes the global spread of the flu as a “rapidly evolving” situation. As of an early morning update from WHO, the swine flu has been confirmed in Mexico (156 confirmed cases) as well as Austria, Canada, Germany, Israel, Netherlands, New Zealand, Spain, Switzerland and the UK. Each of these countries has between 1 and about a dozen cases, except Canada which has 34.

My comments:

1) I’m annoyed at the playing around with the name of the flu. The Israeli Government was wrong to insist on not calling this Swine because of the kosher-pork issue. Nothing about that makes sense. The Minnesota Government led by Republican “I’m not very smart but I won’t raise your taxes” Pawlenty is also wrong in insisting that it be called the H1N1 flu. Pawlenty has stated that we should not call it the “swine flu” because that is disparaging of the pork industry (which is reasonably important here in Minnesota).

That is utterly stupid because you can eat pork chops, ham,and bacon all day, from swine who have the flu, and never get it. There are times when it is appropriate to adjust the name of a disease for various social or political reasons, but it is wrong to do so in response to utter ignorance. Instead, deal with the ignorance. Pawlenty will not deal with the ignorance directly because he is a Republican and, quite honestly, Republicans prefer to foster, and when convenient use, ignorance for their own monetary and political gain.

2) There is no validity whatsoever to the idea that the swine flu is more deadly in Mexico than elsewhere, or that Mexicans are somehow more likely to die of it. Well, the latter may ultimately be true because of health care differences. It may turn out that people in Mexico and Panama will be more likely to die of this flu than people in Sweden and France, owing to disparities in health care across countries. It may also be the case that people in Louisiana will be more likely to die of this flu than people in Minnesota or Massachusetts for the same reason. However, it is also true that the data that are currently available are not sufficient to say anything other than this, and only in a very preliminary way: The current swine flu outbreak seems to have a mortality rate that is roughly similar to the seasonal flu, at present. (But see below.)

3) It s not true, as is reported again and again by reporters who should really stuff a sock in their mouth on waking and keep it there all day, that the swine flu is “mild” in the United States. This misconception and mis statement comes from an illogical extension of number 2 above. This is a serious flu. You get sick as a dog for a week or so, and it can kill you, just like the seasonal flu.

4) Regarding the spread of this flu: More and more people who know what they are talking about are saying that the spread of this flu is similar to that of seasonal flu. In the same way that we can characterize the mortality rate as similar to seasonal flu, we can probably say the same regarding the rate of spread. However, both characterizations are subject to change as data become more available.

There are two separate issues here. On one hand, we have the accumulation and verification of case by case data, and on the other hand, we have the spread of the flu. Over time, the quality of the data will become good enough to make longer term projections and to make assumptions about the missing or lower quality data areas of the world. So, right now, as we see reports of more states in the US or more countries across the world reporting cases for the first time, are we watching the actual spread of the flu, or the improvement of data? Answer: Both, and we can’t separate the two right now with any degree of reliability.

5) Regarding the flu’s virulence and mortality: Good news and bad news. I have one piece of good news and two pieces of bad news.

First the good news: It does seem (see above) that this flu is not extra deadly.

Now the first bit of bad news: The seasonal flu is deadly. This new flu … the swine flu … is like the seasonal flu. It is also deadly. It might be that the currently spreading strain of Swine H1N1 ends up being less deadly, it might end up being more deadly, but if it turns out to be about the same as the seasonal flu and goes though a similar cycle, you can expect several tens of thousands of Americans to die of it.

Maybe thats a good thing. Maybe killing 38,000 Americans twice in one year instead of once will result in a change in attitude towards both the flu and towards vaccination in general. Maybe I’m too cynical. Maybe I’m not.

Now the second piece of bad news, and this is the scary bit. This flu may be worse than a regular flu in that more people will get it … there is not vaccine available now, so it’s initial spread will be unchecked compared to a normal seasonal flu for which vaccines may have been distributed. There is probably not as much of an immunity to this flu as for the seasonal flu (this has yet to be determined but is likely true) so it may be that more people will end up getting this flu.

Fine. But that’s not the real bad news.

The real bad news is that since this is a new flu part of which (flu has different parts that may have different histories) only recently entered the human environment, there might be a slightly higher than we would like to have chance that this flu, while it swaggers around the human population making people sick, will recombine with one or more other flu viruses that are already out there with very nasty results.

This flu could spread around the world as a regular flu, making lots of people sick but not being overly deadly. Then, some time during its spread, or even after it has largely abated, it could mutate through recombination (of some of its parts) and come back as a much more severe flu, causing a truly deadly world wide pandemic.

How possible is this? We have no way of knowing, but that scenario has happened before. From a paper by Taubenberger and Morens:

Historical records since the 16th century suggest that new influenza pandemics may appear at any time of year, not necessarily in the familiar annual winter patterns of interpandemic years…. Thereafter, confronted by the selection pressures of population immunity, these pandemic viruses begin to drift genetically and eventually settle into a pattern of annual epidemic recurrences caused by the drifted virus variants.

In the 1918-1919 pandemic, a first or spring wave began in March 1918 and spread unevenly through the United States, Europe, and possibly Asia over the next 6 months … Illness rates were high, but death rates in most locales were not appreciably above normal. A second or fall wave spread globally from September to November 1918 and was highly fatal. In many nations, a third wave occurred in early 1919 … Clinical similarities led contemporary observers to conclude initially that they were observing the same disease in the successive waves. The milder forms of illness in all 3 waves were identical and typical of influenza seen in the 1889 pandemic and in prior interpandemic years. In retrospect, even the rapid progressions from uncomplicated influenza infections to fatal pneumonia, a hallmark of the 1918-1919 fall and winter waves, had been noted in the relatively few severe spring wave cases. The differences between the waves thus seemed to be primarily in the much higher frequency of complicated, severe, and fatal cases in the last 2 waves.

That paper characterized the pattern of the 1918 flu well, but was written before some key findings in the nature of flu evolution, so I won’t pass on the speculations those authors provide for why this pattern developed.

Taubenberger, Jeffery, & Morens, David (2006). 1918 Influenza: the Mother of All Pandemics Emerging Infectious Diseases, 12 (1)

Less traditional and less reliable sources have suggested that there are a large number of cases of type A flu (not necessarily the swine flue) in Queens New York, perhaps something like 100, and two cases in Kansas. If these are real, they will probably be reported by WHO and CDC over the next 24 hours.

In Mexico, there are three separate situations being reported. According to WHO:

In the Federal District of Mexico, surveillance began picking up cases of ILI starting 18 March. The number of cases has risen steadily through April and as of 23 April there are now more than 854 cases of pneumonia from the capital. Of those, 59 have died. In San Luis Potosi, in central Mexico, 24 cases of ILI, with three deaths, have been reported. And from Mexicali, near the border with the United States, four cases of ILI, with no deaths, have been reported.

Of the Mexican cases, 18 have been laboratory confirmed in Canada as Swine Influenza A/H1N1, while 12 of those are genetically identical to the Swine Influenza A/H1N1 viruses from California.

Swine flu us common, not surprisingly, in pigs and passes to humans fairly often. There is a low level background of swine farmers getting the swine flu … and getting sick enough to notice it (many more may get infected but don’t become ill or mistake it for a cold). Rarely, swine flu shows up in a form that can pass between humans.

Flu evolves (if that is the correct term) by exchanging large sections of genome back and forth during its life (if that is the correct term) cycle. A flue can be constructed of bits of avian, bits of swine, and bits of human flu, for instance. A combination of swine and human flu may have the property of transmission between humans and some added virulence (because the swine part is new to the immune system). This particular flu seems to be a combination of swine and human as well as avian components.

One alarming feature of this flu, if confirmed, is that it seems to be worse in healthy prime age individuals. Now, don’t get too worried about this yet, but this could be a problem. This was the case with the 1918 flu, which infected half of the human population and killed millions. The so called “Spanish Flu” was a combo of human and avian genetic components. It killed by causing an overreaction in the immune system. The healthier you are, the better your immune system. The better your immune system, the more likely that flu would kill you.

So you can see why health officials are worried about this flu. You don’t have to worry yet, though. This could still fizzle out. Just keep an eye on things.

Or, panic.

The World Health Organization (WHO) has a threat level system. The lowest threat level is 1, the highest is at 6. The good news is that we are currently only at level 3, which means you should not be worried. The bad news is that some experts think we should be at level 4 already, and as far as I can tell they are correct. Which may make us worry about WHO more than it does about the flu…

Level 3 means that there is no or limited human to human transmission of a flu virus. Since the vast majority of flu viruses are non-human, and the most dangerious ones to humans are those that primarily originate from non humans, or have genetic components that originated from non-humans and are able to spread form humans to humans, as the amount of human to human spread increases the threat level goes up.

So Level 4 is for “increased” human to human spread, and Level 5 is “significant” human to human transmission. We are probably at level 4 because there are apparently dozens of human cases of fatal results out of hundreds (a few hundred, perhaps) cases of a novel flu virus.

It is also notable that this flu affects those who are most likely to be immune or resistant to the more run of the mill flu viruses. This is the hallmark of a new genetic combination that humans are are highly susceptible to.

But even at level 4, you should probably not worry too much. Rather, you should be concerned about the possibility that you will have to start worrying soon, maybe. This could fizzle out over the next couple of weeks, or it could expand. If we go to Level 5, start to worry. If we get to Level 6, put on the mask.

I recommend subscribing to the RSS feeds of a couple of sites:

Effect Measure

H5N1

If you read the better done public-oriented literature of this period, you will learn that the nature, cause or origin, and pattern of the 1918 epidemic has been very mysterious. The same level of mystery (but with only a few victims) arose in connection with the Swine Flu threat of the 1970s (see expecially Garret’s book for how this event links to current attitudes as well as public policy regarding vaccines).

This brings us to some time last year or so, when key papers were published (and I presume presented at conferences) regarding what may ultimately be seen as the most important single step in the history of understanding the way the flu vaccine works, and thus, how to combat it. (See this to explore one of those key moments in research history.)

The new knowledge is essentially an improved evolutionarily and developmental understanding of how influenza virus strains change over time. To put it very simply, these viruses are made of chunks that come apart in the host and then recombine. If there are multiple ‘strains’ (think species, more or less) of influenza in an individual, these genetic chinks, each representing a huge percentage of the influenza genome, can and do re-combine to form entirely new strains.

That is in a sense macro-evolution of a pathogen in situ, in the host. What is an immune system to do!?!!?!?? Not much, really. This can be very fatal.

It is now understood that these epidemic or pandemic influenza outbreaks arise from these recombination events. If you now look back at the quirky data, the odd logic influenza seemed to be patterned by, the epidemiological dead ends that seemed to confound everyone through the lens of knowledge of these genetic chunks, called “reassortants,” things suddenly become much much clearer.

A paper has just come out in PNAS reporting research using a primate model to explore immune response and associated pathology under the influence of a recombinant influenza virus, and this research is a direct outcome of this new way of looking at the flu. I offer it here without comment largely because you can get the article yourself, since this one is an OpenAccess piece from the normally not OpenAccess PNAS. Here.

The Abstract from the paper:

The mechanisms responsible for the virulence of the highly pathogenic avian influenza (HPAI) and of the 1918 pandemic influenza virus in humans remain poorly understood. To identify crucial components of the early host response during these infections by using both conventional and functional genomics tools, we studied 34 cynomolgus macaques (Macaca fascicularis) to compare a 2004 human H5N1 Vietnam isolate with 2 reassortant viruses possessing the 1918 hemagglutinin (HA) and neuraminidase (NA) surface proteins, known conveyors of virulence. One of the reassortants also contained the 1918 nonstructural (NS1) protein, an inhibitor of the host interferon response. Among these viruses, HPAI H5N1 was the most virulent. Within 24 h, the H5N1 virus produced severe bronchiolar and alveolar lesions. Notably, the H5N1 virus targeted type II pneumocytes throughout the 7-day infection, and induced the most dramatic and sustained expression of type I interferons and inflammatory and innate immune genes, as measured by genomic and protein assays. The H5N1 infection also resulted in prolonged margination of circulating T lymphocytes and notable apoptosis of activated dendritic cells in the lungs and draining lymph nodes early during infection. While both 1918 reassortant viruses also were highly pathogenic, the H5N1 virus was exceptional for the extent of tissue damage, cytokinemia, and interference with immune regulatory mechanisms, which may help explain the extreme virulence of HPAI viruses in humans.

C. R. Baskin, H. Bielefeldt-Ohmann, T. M. Tumpey, P. J. Sabourin, J. P. Long, A. Garcia-Sastre, A.-E. Tolnay, R. Albrecht, J. A. Pyles, P. H. Olson, L. D. Aicher, E. R. Rosenzweig, K. Murali-Krishna, E. A. Clark, M. S. Kotur, J. L. Fornek, S. Proll, R. E. Palermo, Carol. L. Sabourin, M. G. Katze (2009). Early and sustained innate immune response defines pathology and death in nonhuman primates infected by highly pathogenic influenza virus Proceedings of the National Academy of Sciences DOI: 10.1073/pnas.0813234106