No, virologists do not consider it inevitable that the H5N1 virus will aquire the capability for efficient, sustained transmissibility between humans. What they do consider inevitable is that at some point, some influenza virus will do that.
Many virologists and epidemiologists have expressed their concerns about this particular virus in terms somewhat uncharacteristically strong for nerdy labcoat-wearing types, and in passing these concerns on to a popular audience, many media sensationalists have (as is their wont) chosen a tone best described as “shrill”. Be that as it may, the virologists and epidemiologists are concerned for some very specific reasons, and any hope of realistically evaluating the validity of those concerns lies in gaining at least some rudimentary grasp of those reasons.
Influenza is a profoundly contagious disease. Not only is it capable of airborne droplet transmission, but it is also contagious before onset of symptoms. The significance of this two-pronged threat is invariably overlooked by those who, wishing to minimize the threat posed by H5N1, attempt to draw parallels to other diseases which either require insect vectors or direct contact, or which are only contagious during the symptomatic stage. The H5N1 influenza virus is most definitely NOT like any of these.
Another thing that sets influenza apart from the “thousands of other diseases” mentioned above as potential candidates as pandemic-producers is the fact that viral replication in avian influenza is especially error-prone (roughly 100,000 times that typical of DNA replication). Each fresh batch of virions therefore includes a high percentage which are genetic “experiments” (most of which, lucky for us, fail). In addition, its genome comes packaged in eight segments, offering unique opportunities for an event referred to as “reassortment”. In a host co-infected with multiple strains of influenza, segments from each can (and do) end up getting repackaged as new, hybrid virions. Ebola can’t do this trick. Neither can Marburg, or measles, or mumps, or yellow fever, or rubella, or rabies. This is the event, long dreaded by virologists, that could cause a pandemic strain to erupt suddenly. Anyone currently offering to assign numbers (like one in ten million) to the probability of such an event occurring is pulling those numbers right out of thin air – but one thing that IS certain is that whatever they are, they are increasing as the virus becomes endemic (actually, it’s enzootic) in populations of both wild and domestic birds. They are significantly higher where instances of infection in humans with seasonal flu are widespread.
The significance of sudden introduction into the human population of a new subtype of influenza is also not easily appreciated by non-epidemiologists. Familiarity with seasonal influenza leads many to view flu as a mere nuisance; life-threatening perhaps for the very young, the very old, or those with underlying conditions, but not a serious disease for those with strong immune systems. (To make matters worse, the term “flu” tends to get applied rather loosely to any illness accompanied by sneezing, coughing and fever).
One of the broad subtypes by which virologists classify viruses in the family Orthomyxoviridae is by the protein spikes which protrude through their viral envelopes: “H” for hemagglutinin, and “N” for neuraminidase. There are nine NA subtypes, and sixteen HA subtypes – of which only the H1, H2, and H3 subtypes have previously been known to produce infection in humans to any extent. What this means is that the only humans on earth who have any immunological memory of this virus are the fewer than one hundred people who have contracted the virus and survived.
Another commonly made claim is that the current case fatality rate of over fifty percent fails to take into account large numbers of asymptomatic or subclinical cases. If true, this could be verified by testing for antibodies to the virus, focusing on those with whom known patients had contact. Epidemiologists are crying for more such seroprevalence studies, and of those which have been performed, access has been difficult; but Michael Perdue, a World Health Organization scientist working on the global influenza program, had this to say:
“The evidence for widespread asymptomatic infections is just not there. The (more recent) studies that have been done, one of the reasons frankly that I think they haven’t been followed up on, is they haven’t found many positives. You don’t get too excited about all negative serology.”
Having said that, it’s worth noting that “the people being paid to work on these issues” aren’t making projections based on the case fatality rate currently seen in the avian form of the virus; in fact, not even close. The consensus is to assume a CFR in a pandemic strain similar to estimates from previous pandemics, the 1918 Spanish flu pandemic being close to the “worst case” at about 2.5 percent (with an “attack rate” of around 30 percent). Let’s do the math: if 30 percent of 6 billion people get the virus, that’s 1.8 billion; if 2.5 percent of them die, that’s 45 million dead. If you call that fearmongering, consider that what they aren’t saying is that there really isn’t any firm scientific basis for assuming that the CFR won’t stay closer to what it is now. And that doesn’t even take into account the social disruption cowgirl mentioned.
Another thing the “people being paid to work on these issues” aren’t doing is making optimistic statements about their ability to actually do very much of anything about an influenza pandemic should one erupt anytime soon. Culling may work with chickens, but culling humans always raises a stink. Quarantine won’t work either (in fact, the whole idea is a joke). The WHO’s response to the outbreaks in Turkey suggest that by the time the “antiviral blanket” is ready for deployment, infected people will have de-planed in airports across the globe. Hospitals operate very near their capacities now, and surge capacity just doesn’t exist. There won’t be a vaccine until at least 4-6 months into a pandemic (don’t even ask how long it would take to produce significant numbers of doses), and supplies of antivirals are not even adequate to cover caregivers, first responders, and other essential personnel. Before “bird flu” started getting press, Roche complained that it could hardly give Tamiflu away, and robust supplies are years in the future (plus, we aren’t even sure if the antivirals will even work). There never has been much of a margin on producing flu vaccines, which is why half the US supply is imported… on a “just in time” basis, like most everything else (when borders are open, that is). And there is the real crux of the problem. It doesn’t even have that much to do with H5N1; it has to do with so many millions of people being so dependent on supply chains that are so efficient, but oh, so brittle. Half of what I ate for breakfast this morning was grown in another hemisphere. In addition, a lot of us wouldn’t survive interruption of pharmaceutical supplies alone lasting more than a few weeks, even if we never got the bug.
Does this mean that “there is no way to prepare for the coming avian pandemic”? No. It just means that just like pre-Katrina residents of New Orleans, there are limits to what we can expect from governmental agencies, public healthcare systems, and pharmaceutical manufacturers. If the CFR stays below (say) ten percent, the lights will probably stay on, and the toilets will still flush, but a lot of people will be wanting to stick close to home for a while. If the WHO announces phase 4, it’s going to suddenly dawn on a lot of people just what a good idea that might be, and the first thing they’re all going to do is head for the grocery store.
Not me, though. I’m all stocked up.