With the recent outbreak of swine flu, interest in how these little buggers change to thwart mankind's hard won resistance and modern treatment has understandably increased. So far it's too early to say if the new strain is particularly contagious or unusually virulent; there's conflicting evidence for cautious optimism and genuine concern on both counts. The raw science can sound a bit mysterious:
[It takes] only a few days to sequence, clean up the data, and submit to NCBI. Seven H1N1 swine flu sequences are up. I've not had a chance to crack anything open ... However, one bummer is that they don't have any from the [fatal] Mexico cases available ...
But one thing is certain, hidden deep inside every tiny cell infected with flu is a fascinating act in one of nature's greatest stories, well worth knowing, and easy to follow with just a few basics.
Viruses are submicroscopic pirates, parasites of a sort, that need to board and commandeer a host cell many, many times their size to survive and multiply. In simple schematic the influenza virus is composed of eight strands of RNA acting as mini-chromosomes, coated in a roughly spherical container covered with knobby and spiky protrusions. The tiny virus uses these knobs and spikes to latch onto to receptor sites embedded in the outer membrane of a much larger animal cell, usually one lining the throat or respiratory tract in a bird or a mammal. After binding, it cleverly opens the portal controlled by those receptors and sneaks into the cell in a process called receptor mediated endocytosis -- a fancy word that means, in analogy, using a fake ID to get inside a high security area.
After slipping through the membrane, the RNA strands worm their way deeper and deeper, until they reach the cell's nucleus where they break into the cell’s chromosomes, get all frisky, and start making copies of themselves. If everything goes OK, from the virus's point of view anyway, hordes of newly minted RNA strands then work their way back out to the cell's membrane where they group into octets, don a glossy new coat, and exit the cell (Exocytosis), free to infect new cells and repeat the process.
Not so fast! In humans there are layers of interlocking systems that act as security -- preventing access inside the cell or inside the nucleus -- and that search and destroy any scrap of virus they sniff out. The over all immune response, especially the efficacy of those interlocking immune systems in warding off infection from a specific microbe, are what determine the susceptibility or resistance in a particular individual.
Some of the immune particulars are innate, you're either born with them or you're not, a worthy subject for enough books to fill a library. But some are learned, the components in the vast immune arsenal can 'remember' a particular virus after having once faced it, and the next time it rears its ugly head -- or spiky, knobby coat since it has no head – those trained components swing into action like well oiled micro-molecular machines. Among other measures, they deploy prefabricated antibodies that lock onto and clog up the particular arrangement of knobs and spikes in a particular strain of flu, thus wrapping the virus and leaving unable it to latch onto a cell's surface in the first place. Vaccines utilize learned resistance by introducing similar, weakened, or dead viruses that 'teach' the immune system what to prepare for if and when the hostile, live fire version shows up. Kind of like a flu drill teaches emergency responders how to deal with a real pandemic.
But say a person infected with a common strain of human flu we'll call "H" is working in close proximity to other animals, like chickens or pigs, infected with their own strain adapted to them, let's call that one "N". Sooner or later both strains, H and N, might be in one probably soon-to-be-deathly-ill critter, meaning that sooner or later two strains of flu virus infect a single host cell. When that happens, the newly replicated strands of RNA from each respective strain can get mixed up in the stampede to form up in groups of eight and exit the unlucky cell.
Suppose for example strand 5 from H finds itself grouped together with strand 1 from N. We could call that combo H5N1 for short and the sorting process that produced it could be referred to as recombination! Likewise, this re-sorting of RNA strands can result in different arrangements and kinds of knobs and spikes on the coat -- much like different genes in humans can affect an individual’s eye or skin color -- referred to as antigenic shift. Yes, this is simplified and not entirely accurate, but it gets us there.
When many combos of RNA strands and viral coat are tried out in this manner, sooner or later by sheer dumb luck, one permutation might arise better equipped to latch onto and take over human cells than others. And because the combo is new, depending on the details, learned resistance and prior vaccination are weak and ineffective, or over the top and counterproductive. If one such HN hybrid arises that's both highly contagious and terribly virulent in people, whammo! A deadly flu pandemic is born.
Which takes us to a much larger picture: Reshuffling the genetic deck is so damn useful in producing new adaptations that it's not limited to viruses in infected cells! Long ago, the remote ancestors of vast collections of living microbes, plants, and animals perfected the gene shuffle and rode it for a billion years to astonishing new heights of biological complexity: we're talking 'bout sex, baby! But the overall process for incremental changes in generations of man and microbe remains the same: variation in genetic combos, acted on by natural selection, producing cumulative change in form and function in a population of organisms over time.
That simple outline of how populations change through time at the genetic level goes far, far beyond swine flu. Fleshed out, it explains and unifies every organism, tissue, and cell, past and present, along with every sub-discipline in modern biology, in dazzling detail. It explains why our world is so richly draped in breathtaking, living diversity. Take it away and nothing in biology makes much sense. It furthers fits like a finely tailored glove with every other great field of modern science, from geology to astronomy. It has earned a place beside Quantum Physics or the Periodic Table of Elements as one of the most powerful, successful, well tested, elegant, and useful explanations ever devised. It's been called a fact and theory, some misinformed people think it's false, biologists might call it a 'change in the frequency of alleles in a population over time,' but most people know it simply as EVOLUTION.
