No human is more indestructible than an 18-year old especially when it comes to infectious disease. An 18-year old has a matured and educated immune system backed up by a body in the peak of health. Therefore when we encounter a disease that strikes teenagers, it raises a serious warning flag.
This is why this report [h/t Instapundit] that the current Swine flu attacks teenagers should cause concern. (If true. There is so much noise in the epidemiology and reporting on Swine flu that everything needs to be taken with a grain of salt.)
The Great Influenza of 1918 also showed this pattern. Normal influenza kills infants and the elderly while being no more than an annoyance for everyone else. The 1918 influenza first tore through the military camps of WWI and people initially thought it was just one more of the many diseases that had traditionally ravaged armies. (Prior to WWII, roughly 60% of American wartime in-service deaths resulted from communicable diseases.) When it struck the general population, however, it soon became clear that it targeted teenagers and young adults.
One hypothesis explains this pattern by postulating that the influenza provoked an auto-immune reaction that turned the strong immune systems of young adults against their own bodies. In that case, the stronger a person’s immune system, the more damage the disease did. The current Swine flu might provoke a similar immune response.
Unfortunately, there’s not much we can do about the Swine flu except work faster to create a vaccine and inoculate as many people as possible before the true flu season strikes late next fall. Flu usually kills around 30,000 people in the U.S. every year, mostly the very old. It would be a horrific tragedy to lose 30,000 young people to disease in this day and age.
The more rational and accepted theory of the virulence of the Spanish Flu epidemic is that the older people who seemed to be able to deal with the virus had been exposed to a similar but less aggressive variant of the virus. This gave at least partial immunity, unlike the young who had not been exposed to anything like it.
Why are you making a distinction between Swine Flu and our garden-variety flu that kills hundreds of thousands of people each year? Swine flu is no more dangerous, is clinically identical, and can be dealt with in the same way. Hysteria is dangerous — let’s look at the data before we spend scarce medical capital on a disease that may not warrant the expenditure. For example, NYC is closing many schools based on flu symptoms, but not on testing. There have been documented cases of Swine Flu, but they are calling every case of the flu a possible Swine Flu outbreak. That’s just silly. How much does it cost to close NYC schools? What are the unintended consequences?
DHL,
Well, we need to take all the Swine-flu reporting with a grain a salt, hence the title of the post. However, if the age ratio pans out it is cause for concern because it would indicate an unusual disease process.
If the previous infection protects idea is true, then we should see higher rates of infection among the young but no particular clustering of severe cases. In other words, kids would get the flu at higher rates but wouldn’t suffer from it anymore than any other strain.
I kind of doubt the previous infection hypothesis in the case of flu because (1) flu mutates so readily that we have to create a new vaccine every year. How likely is it that a strain of flu that went around 20 years ago confers immunity to a current strain? (2) We haven’t really established any kind of pattern that would suggest that this effect occurs.
Cytokine storms are what are suspected of causing the untoward number of deaths of the ostensibly ‘healthy’ young people. The young are so healthy that their immune systems jump right into the attack on the virus, but overshoot the mark leading to autoimmune reactions.
While it’s true that viruses mutate quickly, they do not have an infinite toy box from which to pull new parts. Many parts are recycled. Some are put away, only to be picked up at a later date. Memory T-Cells do a good job of matching antigens to invasions that have been seen before. They can be quite specific, but don’t always need to be. ‘Close enough’ works with antibodies as well as horseshoes, grenades, and government services. A flu that came around 20 years ago can carry surface proteins that are swapped and shifted with this year’s new flavor. Existing antigens, however, can recognize them and attack. It’s all a matter of ID-ing the virus as non-self. A totally novel surface protein won’t cause a quick reaction–in fact, the reaction can come too late.
Media is certainly hyping swine flu at the moment. But CDC is expressing concern as well. Most international health bodies are getting very freaked out over a rebound of this flu come the cooler months. I don’t think it particularly wise to simply blow them off.
John Burges,
The idea that previous infections of related viruses provides immunity is plausible and probably occurs in some cases. It’s obviously true in the case of viral infections that confer life long immunity. It’s just that we don’t have any clear proof that it’s a significant effect in diseases that don’t confer long term immunity. I don’t think we see the age distribution that the hypothesis would predict.
We would expect to find odd age groupings staggered randomly between the first flu and the subsequent flu that followed it. For example, if 40 years separated the two flu then we would expect to see more people under 40 effected. If ten years separated the two flu, then we would see a flu that hit children under 10. In my reading, no one has established such a pattern in the case of influenza.
Also, the pattern is not that people under a certain age are hit harder but that people between ages are hit harder. The 1918 pandemic did not disproportionately affect children 14 and under. IIRC, it affected people between the ages of roughly 14 to 26. Conferred immunity from a previous infection could not produce that pattern.
Many viruses contain genes for proteins that down regulate the innate immune response. The lethality of the bird flu is linked to such a gene. Given the vagaries of the feedback loop control system of the immune system it is quite possible that a virus’s attempt to down regulate the innate immune system could cause runaway up regulation in individuals with strong immune systems.
This is entirely consistent with cytokine storms. The immune systems of the young are not fully armed; those of the elderly are fading. Only the notionally vital and fit have immune systems so potent that they can over-react with deadly force.
I don’t think we need to look for one, single (and simple) answer here. I think it likely that several processes are operating simultaneously. Some vaccines do, indeed, give life-long immunity, as do prior infections. In many people. But not all enjoy the same degree of immunity: it’s not binary. Many enjoy some level of protection, less than total but more than none.
I ran across this when being re-vaccinated for smallpox in the run-up to the latest war in Iraq. Some of my colleagues in the Embassy in Riyadh had no residual immunity from vaccinations they had had 40 or 50 years earlier; others had full immunity–or at least the health people could get no reaction from the vaccine, even after multiple attempts to produce it.
Nor, I think, should we think that all influenza viruses necessarily act or react in exactly the same manner. Some proteins may very well be shut down on meeting the proper antigen. Others might be only partially disabled. Who knows? Maybe some viruses actually get juiced from something that was supposed to have the opposite effect!
Shannon,
“If the previous infection protects idea is true, then we should see higher rates of infection among the young but no particular clustering of severe cases. In other words, kids would get the flu at higher rates but wouldn’t suffer from it anymore than any other strain.”
Why wouldn’t we see clustering of severe cases? An aggressive strain can be local. And, as John Burgess explained, the antibodies do not have to match perfectly, so partial immunity can come from many variants of flu. However, the data that show increased death among the young does not exist. People are suggesting many things, much of which is just that; supposition. Until each case is identified as the Swine Flu variant, all of this is just guessing (very little of it intelligent). And all of those cases in New York that have caused the hysterical shutting of dozens of schools? There has been one death, in a middle-aged, overweight man with cardiac problems.
John Burgess,
This is entirely consistent with cytokine storms.
Yes, that is the most likely mechanism in the immune system that would cause death in response to a viral infection. Most of the symptoms of flu are actually the effects of cytokines. That is why so many viral illnesses feel the same even when the viruses attack different cells in the body.
I don’t think we need to look for one, single (and simple) answer here.
I don’t disagree I just think the previous infection hypothesis is rather weak because the age patterns don’t really support it.
Nor, I think, should we think that all influenza viruses necessarily act or react in exactly the same manner.
Immunity persistence appears related to the physical complexity of the virus. Paradoxically, simpler viruses provoke less of an immune response. This is probably because each persons individual immune system reacts to one or more specific proteins. If the virus presents fewer proteins, the immune system may only react to one protein. If that protein mutates, the immunity fails. Simpler viruses can also mutate faster because they’re more robust in design.
Flu viruses are small and simple compared to smallpox and measles viruses. This makes it hard to develop immunity to them as a class because they vary so much. That is another reason I doubt the previous infection hypothesis. We don’t really have any proof that immunity against the a particular flu last more than a few years.
DHL,
Why wouldn’t we see clustering of severe cases? An aggressive strain can be local.
I meant age clustering of severe cases. I was talking about a pattern in which infections are symmetrically spread out over the age groups i.e every age group has the same rate of infection but only certain age groups have high fatalities. This was seen in the 1918 epidemic in which there was a spike in deaths in the 14 to 25 age range.
And, as John Burgess explained, the antibodies do not have to match perfectly, so partial immunity can come from many variants of flu.
If this was true we should expect to see infection or fatality rates that increase smoothly with a decrease in age because the older a person was the more experience their immune system would have with flu virus. Instead with normal flu we see symmetrical rates of infection with fatalities clustered in the infant (undeveloped immune systems) and the very old (failing immune systems).
However, the data that show increased death among the young does not exist.
Not for this round of flu but it did exist for the 1918 influenza and has shown up in other types of disease outbreaks as well.
I’m not saying we should run for the bunker I’m just pointing out that such a patten, if it was confirmed, would be cause for concern. Hence the title.
Shannon,
We won’t see smooth graphs correlated to age because exposure to variants wasn’t universal. And fatalities are clustered around high-risk groups, which include those with COPD, cardiac problems, obesity, etc.
I think that the ultimate measure should be death rate, and the current Swine Flu does not seem to be any more virulent than the typical flu. Focusing on death rates among sub-groups may make good press, and create hysteria, but it doesn’t make the disease any more dangerous.
I agree that it should be monitored, and it is being watched very well — perhaps too well.