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Stahler: Ebola

The Ebola virus - a colorized electron micrograph.
CDC/ Frederick A. Murphy |

A organism that is free-living can live on its own, but at a cost. Humans, wolves, bacteria — all must expend energy and resources to find something to eat.

Parasites are not free-living; they depend on their hosts to do the hunting. Thus, a tapeworm, firmly attached in the gut, absorbs pre-digested food. With no need for stomach, legs, or teeth, the worm devotes itself to making more tapeworms.

But even the tapeworm’s minimal requirements require some effort: the worm’s body cells must grow, divide, make repairs, and produce eggs.



A virus is the ultimate parasite. It has no body — not even a single cell; it does not eat, and does no work.

Genes are the blueprints for life; plants and animals typically have tens of thousands of different genes. A virus is comprised of little more than a dozen-or-so genes, plus a few helpful molecules, all packaged within a protective membrane. That’s it — a virus is basically a bundle of genes.




All things alive — people, plants, bacteria — have, within our cells, molecular machines to take us apart and put us back together; to manage wastes; to extract energy from food. Viruses have none of these, leading biologists to debate whether viruses are alive.

A virus is a pirate. By hook or by crook, the virus inserts its genes into a cell. Some viruses literally inject their genes into the cell; others trick the cell into importing its genes.

Once inside, the pirate genes hijack the cell’s machinery. Molecules that once assembled host cells are now forced to assemble viruses, using the dozen-or-so viral genes as blueprints.

The viral genes might also instruct the body’s immune system to wind down, to ignore the infection; Ebola does this.

With its cellular machinery no longer taking care of (the host’s) business, the host feel sick, low-energy.

Having assembled its quota of viruses, the enslaved cell bursts. Thousands of virus particles stream into the blood, which carries them around the body to infect yet more cells.

Viruses are specialists; each virus infects only certain organisms (dogs or cats, petunias or people). Within those organisms, the virus infects only certain cells. Ebola attacks the cell’s lining, (among other tissues) the blood vessels.

When its cells burst, the blood vessel weakens, and it, too, bursts. Ebola victims bleed profusely — at least half die.

A corpse is not an efficient vector — carrier — of disease. Much better, from the viewpoint of a virus, are victims who walk among — and infect — their fellows. That the Ebola virus kills roughly half its human hosts is a sign that it is new to humans … that it has not yet “learned” — evolved — to be gentle with its host.

The machinery that copies our genes includes a proofreading system, to find and repair mistakes in the copies. But this proofreading system only works on genes made of DNA. Ebola genes are made of a different nucleic acid: RNA. With no proofreading system, defective Ebola genes abound.

In complex organisms (humans, goldfish, mushrooms), defective genes are bad news. Bad blueprints lead to cellular machines that don’t work right. But the virus could not care less about defective — mutant — genes. Mutations are the raw material of evolution. Most mutant viruses fall by the wayside, but a lucky few find themselves with genes that give them new powers.

The West African outbreak of Ebola is infecting more people than any previous outbreak, producing more viruses … and thus, more mutants.

Should the outbreak continue, we might expect to see a less deadly strain emerge, one that doesn’t kill its victims — at least, not so quickly.

We might also expect to see other mutant talents evolve; just what those talents may be, remains to be seen.

Al Stahler’s science programs can be heard on alternate Tuesdays at noon on KVMR-FM (89.5 MHz). He teaches students of all ages, visits classrooms, and may be reached at stahler@kvmr.org


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