Alien vs. Predator
Dallas: [looks at a pen being dissolved by alien’s body fluid] I haven’t seen anything like that except, uh, molecular acid.
Brett: It must be using it for blood.
Parker: It’s got a wonderful defense mechanism. You don’t dare kill it.
NASA announced earlier this month one of its research teams discovered an ‘alien’ bacterium at the bottom of California’s Mono Lake. Call off the men in black, it’s strictly still a matter for the nerds in white.
The bacterium isn’t really from another planet, even as we all are a kind of astronaut wherever and whenever we find ourselves spinning through space and time. Rather, this earthly bug showed under the kinds of stringent conditions found on other planets it could assimilate arsenic into its very cellular fabric in place of what was until now thought mission-critical phosphorous.
Arsenic and phosphorous share a similar electric charge and atomic radius. Arsenate–arsenic bound with four oxygen molecules–is for the most part poisonous to most Earthling species because it mimics phosphorate, the biologically useful form of phosphorous.
The team, led by Felisa Wolfe-Simon, inoculated in vitro colonies of the Halomonadaceae family of Gammaproteobacteria with a series of highly alkaline sediments from Mono Lake differentiated only in their ratios of arsenate-to-phosphorate. In effect, Wolfe-Simon and her colleagues increasingly starved sequential generations of the bacterium of phosphorous, in the meantime offering arsenic hors d’oeuvres in phosphorate’s stead.
The team found the free-floating arsenate it radio-labeled became associated with the proteins, metabolites, lipids and nucleic acids of the GFAJ-1 strain of the bacterium, consistent with the arsenate’s incorporation into the newly evolved strain’s proteins and DNA.
Despite its publication in Science, one of the world’s most respected peer-reviewed journals, the work has been subjected to scurrilous attack. Critics, burned by NASA’s 1996 announcement of bacterial tracings in a Martian meteorite, objected (here, here and here) to among other things,
- the failure of the Wolfe-Simon group to wash GFAJ-1’s DNA of contaminants and loose arsenic before testing for the latter’s biological presence, basic microbiology 101.
- the small concentrations of arsenic found, consistent with contamination rather than incorporation.
- the failure to rule out the possibility the alleged arsenate-based bacteria survived the high arsenate-low phosphorate environment by scavenging phosphorate off dead comrades.
- the premise arsenic bonds in a DNA backbone would be stable enough.
- the premise a transition phenotype with both arsenate and phosphorate could survive, as multiple enzymes must interact with DNA with great precision, or that it would emerge in such short order.
Some of the criticisms appear on their face pointed, others seem founded on the self-referential presumption that surely evolution can’t do that because our models tell us otherwise.
Whatever its ultimate fate, NASA’s announcement has as much to do with life on Earth as with extraterrestrial biological entities. If not phosphorus-starved bacteria switching to an arsenic-based life form, then those thriving in the deepest layer of the oceanic crust in the face of caustic heat and crushing pressure, eating methane and benzene, show the extent to which our planet’s microbes can adapt.
For agriculture that should mean kaputs for a propagandistic reification. Contrary to the term’s connotations of Level 4 protection, there is no such thing as total ‘biosecurity,’ blocking any and all pathogens from inside a confined animal feedlot or other intensive operation. If bacteria can survive in the face of arsenic or benzene, what can livestock operations possibly do in their own defence?
Even ignoring the routine violations in biosecurity and biocontainment built into the industrial livestock model, we must now assimilate the impediment that eliminating the conditions under which many a microbe, influenza included, thrives only establishes niches for new and at times strange strains. If fastidiously sterile First World hospitals are routinely assaulted by drug-resistant pathogens, then feedlots turfed in shit, run by predatory agribusinesses minimizing margins in offshore hovels, stand no chance.
Indeed, the problem of livestock pathogens was already locked into a Nietzschean syllogism from the get-go. What kills many pathogens makes those left over stronger. The few with the weirdo mutation that lets the virus or bacterium survive a new threat now emerge to thrive. Even the very notion of causality appears threatened, with cause and effect effectively reversed: how do we protect ourselves against influenzas and other pathogens which have already evolved a counterresponse several times even only in the past week to any prophylaxis we could ever imagine?
Influenza’s phenotypic variation, generated at mind-boggling mutation rates (2.0 x 10–6 mutations per site per infectious cycle), embodies the choices with which the virus–if you’ll excuse the anthropomorphism–can naturally select a solution to the problems it faces, including those it has yet to even encounter. Along with producing new viral functions, including molecular exaptations, the mutations permit escape from learned immune T- and B-cell responses fixated on previous epitopes.
By reassortment that variation is multiplied at the broader genome level: influenza can trade whole genomic segments like card players on a Friday night. Both H5N1 and last year’s H1N1 emerged as multiple reassortants from across many serotypes.
- Transformations beyond point and double-point mutations, including partial, complete and flanking deletions, can induce changes in viral protein conformation.
- A polybasic site in the glycoprotein hemagglutinin expands the range of host proteases able to cleave the hemagglutinin precursor, increasing the range of host tissue that supports infection and diversifying modes of transmission. Poultry infected with the worst H5N1, their insides liquidating, suffered both bloody coughs and diarrhea.
- Amino acid replacement E627K in polymerase protein PB2 increases the efficiency of viral replication in mammalian cases, as does the SR polymorphism in poultry. Other polymerase markers for mammalian adaptation include PB1 P13 and PA R615.
- Several influenza proteins block or down-regulate the immune response. The alternate reading frame PB1-F2 protein, found in several pandemic strains, induces apoptosis in macrophages. H5N1 NS1 protein with glutamic acid at position 92 acts as an antagonist to host interferon. NS1 with carboxyl terminus motif EPEV can also disrupt human regulatory pathways.
- H5N1 proved viable across hosts of a diversity of animal orders traditionally thought each other’s epizootic barriers.
- Several years ago Robert Webster reported H5N1 samples were becoming increasingly viable at warm temperatures, at which they are expected to degrade. If the result still holds the implications are fundamental to the virus’s persistence in equatorial estuaries and perhaps even sewage systems.
The outlandishness may transcend individual virions, infections and strains. By virtue of infecting multiple-million hosts, in which a multitude of molecular and epizootic problems are simultaneously addressed, the virus engages in an emergent unconscious cognition the discoveries from which are traded among strains by reassortment. We find ourselves confronted with a distributed intelligence arrayed across whole continents. The truly unworldly here on Earth.
And yet this is no counsel of despair, no lost regret to be discovered by the outraged survivors of an oncoming apocalypse. We should be able to better corral pathogens once we reimagine control–and agriculture more generally–across levels of biocultural organization.
An integrated pathogen management might depress capitalist surplus value over the short term—frankly no bad thing—but it should multiply the dimensions of the problems our world’s little green men must solve in the course of stalking poultry, pigs and people alike. And what could be more important, even for monomaniacal economists concerned with little else than macroeconomic indicators? A bad pandemic would along with much of humanity destroy its economies.
At the cost of next quarter’s shortsighted returns a fully applied IPM would put us in a better position to save a billion people from a deadly pandemic. In contrast, the present agricultural model is, alongside meat monocultures, farming tomorrow’s deadliest pathogens.
That is, despite their apparent antagonism, today’s influenzas increasingly feed on agribusiness to little punishment. Indeed, Big Ag has gone so far as to use the new diseases to its own advantage, rubbing out smaller competitors that can’t afford biosecurity upgrades.
The new spate of virulent strains and of those of a variety of other pathogens, to reference Ridley Scott’s cult flick, are bursting out of the Livestock Revolution’s belly, bloody-mawed and shrieking. And in perhaps their greatest trick, in the most sadistic of ironies, they are being allowed free range.
To control the alien we must kill the predator.