Fist-fighting with the wuflu

A rare intermission in which we cut to current events.

The situation seems, broadly considered, as follows. This not a vaccine but a ‘vaccine’—at best we can call it a leaky vaccine. This ‘vaccine’ is probably not some vast conspiracy but is more than likely shaped by the typical standards of corporate shills and pharmaceutical companies. Bayer knowingly sold HIV-infected blood products to shithole countries out of a purely financial interest simply because it knew that it could. Some folks were punished for this overseas, but nobody in the United States was. The same rules likely apply here. A fair amount of side effects will be deemed justifiable, not by some rational evil but simply because evidence is fuzzy and money warps the incentive structure. Basically the same goes for politicians, as few who seem to be associated with this will want to admit anything. Nobody wants a loss this big. They can tack back and forth on a bunch of things but this would be too far. Everybody is looking at this thing and nobody is going to just forget; it isn’t Epstein or WTC7.¹ This is, at best, a gambling alignment of perverted interests.

Side-effects, however, are not the only relevant aspect. We are forgetting the other player in this game: the virus itself. There were initial hopes that we could reach ‘herd immunity,’ which has always been a somewhat vague goal. The gist seemed to be that we could starve the virus out by walling it in with immunity. Currently there’s no such thing as immunity, with any resistance in terms of percentages—whether from the vaccine, natural antibodies, or even both combined. The goal here seems to have been a resistance sufficient to maintain viral loads below infection during ordinary exposure. While perhaps higher loads would be unavoidable in certain situations, it is enough to simply present it from moving about in public. Of course, major events seem like a problem also. We might compel the redesign of such locations to increase ventilation, for instance, which would help some; but ultimately it would still depend on the transmissibility of the virus.

Viruses want to live, but for most this means constant movement. Herpes is an outlier here, as it survives by hiding away within the body. If the virus does not hide, then the body will knock it back and to wipe it out eventually—or it will win and kill the person. Thus the individual virus just wants to reproduce itself; that’s what they do. They want to live, just like us. We often have a mutual interest in this aim, as the virus requires a host to survive. This is like the joke about cancer, that at best it can hope for a draw: mutually-assured destruction. Better for the virus as a species is that its host spread it, for which they probably want to survive a while at least. The ideal would seem to be a silent illness that spreads without harming the host. Toxoplasma gondii seems to have achieved basically this, which is variously measured as present in more or less a third of the population. This varies according to geographic locations and, as I understand, the presence of cats.

We know that viruses mutate rapidly, with some predictable variation: “RNA viruses mutate faster than DNA viruses, single-stranded viruses mutate faster than double-strand virus, and genome size appears to correlate negatively with mutation rate.” The coronavirus is an RNA virus; it is single-stranded; but in terms of relative genome size, it is at the higher end of RNA viruses. Nevertheless, we can expect that this will mutate at a rate which far exceeded what might be expected of any animal or plant species. The virus is a barebones evolutionary schema; it is repetition and mutation ad infinitum with minimal steps between. The virus infiltrates the body and finds a factory, then it provides counterfeit plans and thus hijacks its host’s own means of reproduction. This replication is the point of mutation, as each involves a process of printing susceptible to more or less random variation.

Mutation can thus be spoken of at two levels; at one the process resembles Brownian motion and blindly proceeds at a constant pace with mostly insignificant variations. The other requires we take a more abstract perspective and consider the qualitative dimensions of this variation over time. An obvious and important example here is the severity of illness caused by the virus. We might here take up leaky vaccines again to consider a concrete case. Marek’s disease is caused by the herpesvirus, and it’s an expensive annoyance primarily for the poultry industry. This has led to the developments of vaccines, but sadly these tend to be leaky. None has managed to ensure lasting immunity and instead seems to ameliorate the effects. This may mean that the virus is unable to take, at least sufficient to ensure any significant transmission; else it may simply reduce the severity of illness. Of particular interest to us here is the interaction of these leaky vaccines with the evolution of the herpesvirus that causes Marek’s disease.

We will here consider Read and colleagues (2015): Imperfect Vaccination Can Enhance the Transmission of Highly Virulent Pathogens.

Could some vaccines drive the evolution of more virulent pathogens? Conventional wisdom is that natural selection will remove highly lethal pathogens if host death greatly reduces transmission. Vaccines that keep hosts alive but still allow transmission could thus allow very virulent strains to circulate in a population. Here we show experimentally that immunization of chickens against Marek's disease virus enhances the fitness of more virulent strains, making it possible for hyperpathogenic strains to transmit. Immunity elicited by direct vaccination or by maternal vaccination prolongs host survival but does not prevent infection, viral replication or transmission, thus extending the infectious periods of strains otherwise too lethal to persist. Our data show that anti-disease vaccines that do not prevent transmission can create conditions that promote the emergence of pathogen strains that cause more severe disease in unvaccinated hosts.

The experiment entailed infecting eight-day old chicks with five strains of the Marek’s disease virus (MDV): “from the less virulent HPRS-B14, which killed 60% of unvaccinated birds over 2 months, to the highly lethal Md5 and 675A, which killed all unvaccinated birds in 10 days.” They found that, despite the imperfect vaccine, vaccinated individuals shed less of the MDV than those who were vaccinated. This seems reasonable, as even a leaky vaccine will likely hinder the virus in its effort to get production off the ground. Where the body is less well prepared, the virus may take more territory early on, hence shedding will be higher as the offensive gets on its feet. But they also found that the more virulent strains killed their unvaccinated hosts quickly, and during this period there was little shedding. The less virulent strains in which the hosts survived had far higher rates of shedding, as can be expected in the time differences: two months rather than ten days.

Thus, the least virulent strain shed several orders of magnitude more virus from unvaccinated birds than did the virulent strains. By preventing death, vaccination greatly increased the infectious period of the most virulent strains, increasing the total amount of virus shed by several orders of magnitude, and increasing it above that of the least virulent strain.

The main event in this study, however, is the subsequent part of this study which examined the further interaction of this effect with the transmission between individuals. This involved the same two groups, vaccinated and unvaccinated, which were split into three and infected with the three most virulent strains of the MDV from the first stage. The difference here is that these groups were each co-housed with sentinel birds that were unvaccinated and were not exposed to the virus. Here we’ll let the study speak for itself:

When unvaccinated birds were infected with the two most lethal strains (Md5 and 675A), they were all dead within 10 days, before substantial viral shedding had begun. Consequently, no sentinel birds in those isolators became infected and none died. In contrast, when HVT-vaccinated birds were infected with either of those hyperpathogenic strains, they survived for 30 days or more, allowing substantial viral shedding. All co-housed sentinels consequently became infected and went on to die as a result of MDV infection.

Of course, the upside is that the coronavirus currently isn’t all that lethal; at least for the majority the population who aren’t otherwise compromised—as by a specific disorder or age, some such vulnerability. There is no selective pressure which will specifically compel greater lethality in the virus, but there is no way of knowing whether an evolutionary drive towards breaking through these defenses will not entail a more general increase in virulence. Symptom severity seems to be correlated with viral load, for instance, and so an increase in transmissibility may mean that lesser loads are necessary for reproduction and transmission. This could mean that the genomes may have a greater density, so to speak, and thus more readily cause worse symptoms when the viral load is sufficient. The overall point here is no doomsaying but simply to note that a possible line of development may lead the unvaccinated to be at risk primarily from the vaccinated.

1. Whatever happens here will likely not even be as obvious as the outbreaks of polio caused by the vaccine itself; and even then, see how many know about that. This seems unlikely to be a threat here, given the m RNA vaccine only replicates the spike protein.