Return of swine-origin H1N1 influenza to the US

Of the many questions that I receive about influenza, one of the most common is “when will swine flu return to the US?”. In other words, when will the 2009 pandemic H1N1 strain, first recognized in humans in April 2009, emerge for the 2009-2010 influenza season?

“Return” is probably not the correct word to use, because the 2009 swine-origin H1N1 virus has never left the US. The latest statistics published by CDC show that for week 34, 1,109 of 6,410 specimens tested for influenza were positive for the pandemic H1N1 strain. As shown in the graph below, the number of isolations of swine-origin H1N1 virus peaked at week 24 and declined thereafter. Since week 32, the number of isolations of that virus has remained constant.


The decline in the number of virus isolations is probably are a consequence of population immunity and other factors like temperature and humidity that may regulate transmission.

There have likely been many more infections with the 2009 pandemic H1N1 strain than have been reported by the CDC. Together with the relatively constant isolation of the virus since week 32, this suggests that the onset of school in the US – which brings individuals together in large numbers across the country for the first time since June – will trigger the next wave of infections. It has already been reported that influenza activity is rising in the southeastern region of the US, where school began earlier than in the rest of the country.

Seasonal influenza typically does not increase until later in the fall in the northern hemisphere. This timing allows immunization of a good portion of the population with a vaccine that is released at the end of August. A vaccine against the 2009 pandemic H1N1 strain will not be available until October. Until then, there will be many infections with the new strain. The best way to prevent influenza is by immunization, but common sense and good hygiene should be part of everyone’s preventative plan.

41 thoughts on “Return of swine-origin H1N1 influenza to the US”

  1. I will be grateful if someone answer the following questions:
    i) Why h1n1 is considered an emergency if it killed approx. 2800 worldwide while seasonal flu kills approx half a million?. Being pandemic is only a measure of its geographical extension not its severity.
    ii) How can a vaccine be safe if it has been developed in less than a year? What about side effects which may take years to appear?
    iii) In the worst case scenario and the virus mutates to become a severe killer will these vaccines be effective?
    iv) Is there an explanation why this disease affects the ages 25-45 and not the standard young or old ages??

  2. i) You are correct, pandemic refers to extent of spread, not severity. There is little immunity to the pandemic h1n1 strain, hence it has the potential to infect 20-40% of the population in the coming year, with significant mortality.
    ii) The inactivated influenza vaccine produced in eggs has been produced for over 40 years in essentially the same way. Therefore it has been thoroughly tested and the side effects are known. The 'new' vaccine differs only in that it contains a different strain.
    iii) Mutating to become a 'killer' does not mean that immunity will be ineffective. These are two separate properties.
    iv) H1N1 viruses circulated from 1918-1957; therefore those who lived during that time were infected with similar strains, perhaps more than once, are less likely to be infected with the 2009 H1N1 strain.

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  4. I would note that the epidemiology from New Zealand and Australia around 11% as the wave falls off shows a much lower estimated infection rate in the population than the expected 30% +/- 10%. Modeling and historical data show that large populations that have no initial immunity should have total morbidity rate of roughly 40%. The southern hemisphere data is, however, not based on serology yet.

    That the southern hemisphere developed world is showing such low morbidity rate when weather is conducive is strong evidence that roughly 20% – 30% of the population has enough cross immunity from something else to achieve the approximate 40% level and block H1N1. This could occur in a spectrum. On one end is cross-immunity effectively provides sterilizing immunity. On the other end of the spectrum cross-immunity generates a subclinical or mild disease with a shorter, low level of virus shedding.

    In studies where cross-immunity has been shown, these are older people who lived through previous influenza infection, which is somewhat tautalogical. Note also that in the developed world the baby boom generation provides a lopsided age demographic since the boom happened in all the developed nations simultaneously after WWII.

  5. If the government has any confidence in the efficacy of the pandemic strain vaccine, then it makes no sense from a public health point of view why the general US policy is to keep schools open at all costs… I understand arguments that closing schools may not decrease the end total number of infections, but it will clearly slow the rate of spread, and if a vaccine will save us in October it seems that slowing infections now could theoretically save many lives in the end. I know, the true goal of the government here is to minimize social and economic disruption. I also realize that the injected flu vaccine may not actually be very effective for many people, and I realize how much disruption school closure would cause, but it seems that someone should call the CDC on this.

  6. Great points, Brian. We should remind everyone that H1N1 viruses
    circulated from 1918 to 1957 and those who lived though that time are
    the ones who are least susceptible to the 2009 H1N1 virus. The H1N1
    virus that circulated from 1997 – 2009 is sufficiently different from
    the pandemic strain such that there is no protection against

  7. I believe there is confidence in the vaccine, it's just that many
    people will not take it. Hence there will be many nonimmune
    individuals to help spread such that school closings will have little

  8. That the 1997-2009 strain is sufficiently different that there is no cross-reactivity does fit the epidemiology demographics. But, based on my modeling experience with influenza, I tend to doubt that nothing since 1957 could be cross-reacting. I don't put much credence in the idea that hand washing is doing enough to cut the expected percentage morbidity by a factor of 2 or 3. And with the peak at 24 years or so, if it was 1957 cross-reacting, then one would expect high morbidity up through 52 years of age. It's true that middle aged people don't mix as much with their peers, and they are more hygenic, but they do mix. Generally they are hit pretty good.

    But, it is possible that New Zealand and Australian society is less stratified by age demographics than the USA is. That could plausibly explain blocking of transmission within the network of relationships in those societies. And people in Australia and New Zealand may ride long distance buses less often and use heat less these days. The former would remove a significant transmission vehicle, and the latter could keep humidity in the 50% region.

    But this low morbidity report as the pandemic wanes down there is distinctly odd; it doesn't fit the rest of the reported immunology, nor does it fit the age demographics well. Quite curious.

  9. but the 1977ff virus was the same as the <1957 one so I don't see
    why people older than 52 should be particularly more protected

  10. Seems that those 65 years and older are showing more protection; this
    would equate to having experience with an H1N1 from earlier than 1944.

  11. 1947 was a severe epidemic in USA and reassortments (which u.a. gave
    the reduced PB1-F2). But it's still 94+29=123 years away going back
    to ~1915 and forth to 1944. While 2009-1976=33 years from
    the 1976-vax looks much better

  12. The second wave is rolling at full speed already in the US, as can be seen here:

    Flu surveillance shows explosion of ILI cases in the past weeks.

    Pandemic waves usually hit much sooner in autumn than the seasonal flu.

    Unfortunately its exactly the opposite when it comes to vaccine availablility: seasonal vaccine ready by august but no pandemic vaccination before october/november 🙁

  13. Very good questions !

    I've been asking myself the same ever since the first wave in Mexico ended suddenly after what could not have been more than 1-5% infection rate of the total mexican population.

    What stopped the virus from infecting the remaining 29% of the population to reach the 30% attack rate to be expected from the models for a fully adapted human-to-human transmissible flu virus without any herd immunity to stop it ? was it only the weather ?

    another speculation besides the “residual-immunity”-theory:
    maybe this anmial-origin virus is still notquite as *perfectly* adapted to the human host as other common flu viruses (as suggested by one ferret study and by the still missing E627K mutation)
    But then how was the novel H1N1 capable of “crowding out” any other seasonal strain in the southern hemisphere ?

    So many questions …. We will have some more answers not before the end of the coming northern hemisphere winter, I'm afraid…

  14. Weather is most probable reason for early termination of the mexican outbreak. Epidemics require aerosol transmission conditions and superspreaders. (See: Lloyd-Smith et al, Superspreading and the effect of individual variation on disease emergence. Nature 2005) Contact transmission is just not good enough at superspreading. And above 30 C, aerosol transmission is near zero.

    I was more surprised that a serious outbreak of influenza happened at all in Mexico more than I was surprised it died out quickly. I was surprised because in that part of Mexico buildings have good air exchange, there is lots of UV to deactivate virus, people spend a lot of time outdoors, and it tends to get hot enough for part of the day to block aerosol transmission.

  15. ok. so high temp. , high humidity conditions probably helped terminate many of the northern “summer waves” early.
    (The question remains why the winter waves of the south too seemed to fell short of the full infection potential too by a factor of 2-3)

    BTW very interstingly, the deadly 1918 pandmic's main wave (i.e. in northern fall) swept the southern hemisphere (New Zealand, Australia) only two months later in the middle of southern *summer*(!) … Apparently that virus did not have to wait until the southern winter to reach its maximum transmissibility conditions …

    It still seems that we do not fully understand the seasonality of flu transmission …

    @Vincent: do you have a list of papers showing the “state of the art” with respect to flu virus seasonality ?

  16. I'll add my two cents to this terrific discussion. I don't know why the infection rate falls short of predictions. But it seems likely that there are differences in the virus that impact transmission. In ferrets it has already been shown that the 2009 H1N1 strain transmits more efficiently by aerosol than seasonal strains. If this is also true in people, it could explain the atypical emergence in Mexico, as pointed out; the same properties of the virus could also impact the infection rate. I await transmission studies by Palese et al to determine how heat and humidity impacts this strain. It's clearly a different beast from what we are accustomed to.

  17. I'd lay good money heat and humidity is identical. The physics of enveloped viruses is regulated by the membrane of the cell they bud from and the proteins they insert into the membrane, and how those bind to proteins in the capsid. Different cell types vary in the strength of the membrane under osmotic pressure. Kidney cells are about 3x as strong as tracheal cells. (One wonders if tracheal cells might have evolved lower membrane tensile strengths to disable enveloped viruses, or if kidney cells are just selected to be able to withstand osmotic gradients? Clearly, the latter has to be true, but I wonder if the former is also.)

    There is variance in literature from cell type for cultured viruses. There is no reason to think though, that H1N1 has changed the ability of an enveloped virus of this size to survive. That should vary by size of the virus against cell rupture studies according to the formula: F = Pr/2 where F = tensile force on the membrane, P = internal pressure, r = radius. (It's a spherical pressure vessel, essentially. )

    It is much more reasonable to suggest that this virus has variance in binding sites that might favor people of a lower age. And even more reasonable to think that when it all comes out, that some degree of cross-protection occurred in older people from a previous infection's antibodies.

  18. It is known that the interaction of the viral M1, HA, and NA proteins
    with the membrane influences the stability of the envelope. Thus,
    changes in these proteins can regulate stability. I'm not sure why
    receptor binding needs to be invoked to explain any of this; the
    age-dependency I agree is likely a function of having immune memory.

  19. Cites? To significantly change physical stability of the virion from one strain to another would require large changes in structure. I am wondering what exactly you are referring to as I just finished reading on virus stability experiments.

    The recent item I read showed a difference in infectivity, but the effect was the same for aerosol and non-aerosol virus, which points to binding, affinity, and perhaps efficiency of packaging.

  20. That is simply not true, that 'to change physical stability of the
    virion…would require large changes in structure'. A single amino
    acid change is sufficient and has been shown to be so in many cases.
    I'm talking about stability of the virion as measured in cell culture.
    That is the only way you can dissect effects on stability, packaging,
    receptor binding, etc.

  21. I think we are talking about somewhat different things. Not meaning to tweak here. I was referring to making a significant change in the norm of the stability of the enveloped virus in aerosol. I believe that the norm for influenza is near the upper limit of what can be achieved by an enveloped virus. As I understand it, the stability of the virus in cell culture is based on time course titration of infectious dose.

    I would still appreciate a couple of cites if you have them so I tell what page we are both on. Cheers.

  22. it can't be the weather. We do see the typical waves with a sharp decline after
    the peak and this does not concide with weather conditions but rather
    with the typical flu-wave timing.
    Why are only 5-10% infected ? Why also only 5-10% in a seasonal “wave” ?
    Maye just only the superspreaders must gain immunity.
    School children with close talking habits and many friends ?

  23. Aha! This makes sense!
    The 1976 flu vaccine cross-reacts with this current H1N1.
    If there are approximated 43 million people age 50 and older in the USA practically immune to H1N1, that's approximately 15%. If those demographics hold for Australia/New Zealand (no idea if they are higher or lower) that would give a total immunity level there of 26%. That leaves approximately 15% more unaccounted for.

    In the USA, approximately 12% of the population is over 65. That's a reasonable facsimile of the people exposed to influenza. Since influenza tends to infect a larger percentage of the toddler through teen group, we could safely assume that half of the 65+ age group had cross-immunity. So that adds another 6% or so. (The age group should be a little larger by a few years, but some of those immune from 1947 will also be members of the 1976 vaccine group.)

    So that brings our network blocking immunity total prior to a major H1N1 epidemic in the USA to around 20%. Thinking this through further, the fact that there is such a large pool blocking transmission at the outset means that progress should be slower. That should skew the total required to reach sufficient herd immunity to block transmission to the lower side of the 30%-40% range.

  24. In other words, we should expect a shorter epidemic cycle that hits the end at something slightly north of 10% of total population. There should be a long tail on it of periodic small outbreaks from time to time. That tail should max out at another 5% of total population of the nation.

  25. I found a couple of blog type articles that indicated that Australia produced a “Victoria strain” vaccine and deployed it first, before the USA did. One of these was by a claimed physician who clsaid aimed it caused 6 aborigines in Australia to suddenly die within days when he administered it as a young man. Deploying first in Australia would fit the weather influenced pattern such as we are seeing now. Also 1976 was around the time that Australia had become quite a player in immunology, (see Zinkernagel, Doherty. Ex: so producing their own vaccines fits.

    I found an article evaluating the Australian 1976 vaccine (abstract only online). This suggests strongly that it was used there. It is unclear if it was exactly the same vaccine, and I didn't confirm the virus strain was correct. But assuming it is the same '76 flu virus, a different vaccine would be expected to show similar cross-reactivity.

    Someone in Victoria public health service in Autralia should know for sure. Or, more lit search. I haven't had time to concentrate on it.

    Short answer is my guess is yes, but I am not absolutely certain. I'd place my bets that way though.

  26. A/Victoria/3/1976 is H3N2, not H1N1
    I once read somewhere(AFAIR), that only the Dutch joined in 1976,
    but can't find it confirmed online now.
    Canada had tried to get vaccine from USA but they
    couldn't (wouldn't) deliver or such.

  27. Hi,

    On the note of stability, just wondering if any of you can comment on why this enveloped virus is able to sustain the acidic environment of the GI tract while most enveloped viruses are not.


  28. Very good question. Some avian influenza strains can survive passage
    in the intestine, even in humans, and of course there are other
    enveloped viruses that can pass unharmed through the gut (e.g. enteric
    coronavirus). We have no idea why these viruses can survive the harsh
    conditions; nor why some influenza viruses can and others cannot. The
    old adage that an enveloped virus can't survive the GI tract is
    clearly wrong.

  29. (speculating)
    they clumb together and the inner ones are protected by the “dead” outer ones
    doesn't seem to work for disinfectants, though

  30. Speculation and thinking aloud alert here but …

    Influenza viruses are on the order of 100 nanometers in size, composed of cell membrane envelopes with HA an NA groups poking through + whatever proteins happen to be present in the section of membrane when it buds. Based on literature, cells have variable resistance to osmotic rupture (which may be neither here nor there, but may be an indicator of membrane tensile strength). Literature shows that influenza viruses of the same strain vary in viability time somewhat based on cell type they were produced from in culture.

    Maybe the external portions of H and N groups vary in acidity or hydrophobicity between strains?

    Maybe the density of H and/or N groups varies in density by strain?

    Maybe different strains vary in diameter somewhat? The tensile force on the membrane should vary by F = (Pr)/2 where F = tensile force, P = internal pressure and r = radius. A smaller virus would be stronger and present less surface to chemistry, bacteria and mechanical forces in the gut to work on.

    Maybe a combination such that critical regions were protected by a combination of salts and water molecules? Structural chemistry of large proteins is very tweaky.

  31. don't forget that the (genetically)same virus can be spherical and filamentous.
    I always wondered, why …

  32. Yes, I had forgotten that. And human infective forms usually contain some filamentous forms. Both show infectivity in plaque assay.
    Relative to why, that could be answered different ways.… – HA, M and NP genes.… Discussion of filament structures.
    doi:10.1006/viro.1997.8916 – M1 and M2 as phenotype determinants.
    doi:10.1016/j.virol.2003.12.009 – M1 as phenotype determinant.

    But probably your real question was what benefit the virus receives because of it? Good question.

  33. Realized that whether the virus is filamentous or not doesn't matter for the calculation above because regardless what matters is the radius. So the tensile force, F, on the envelope is the same for a filament as it is for a sphere for a given internal pressure for a given radius.

  34. Realized that whether the virus is filamentous or not doesn't matter for the calculation above because regardless what matters is the radius. So the tensile force, F, on the envelope is the same for a filament as it is for a sphere for a given internal pressure for a given radius.

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