even Macfarlane Burnet sometimes called the Q fever microbe a “virus” in casual usage, though by then he knew perfectly well it was a bacterium.
The effects of viruses were detected long before viruses themselves. Smallpox and rabies and measles were excruciatingly familiar at the clinical level for centuries, millennia, although their causal agents weren’t. Acute disease and epidemic outbreaks were understood in a variety of inventive ways—as caused by miasmal vapors and “effluvia,” by decaying matter and filth, by poverty, by the whim of God, by bad magic, by cold air or wet feet—but the recognition of infectious microbes came slowly. Around 1840, a German anatomist named Jakob Henle began to suspect the existence of noxious particles—creatures or things—that were too small to be seen with a light microscope and yet able to transmit specific diseases. Henle had no evidence, and the idea didn’t immediately take hold. In 1846, a Danish physician named Peter Panum witnessed a measles epidemic on the Faroe Islands, a remote archipelago north of Scotland, and drew some keen inferences about how the ailment seemed to pass from person to person, with a delay of about two weeks (what we’d now call an incubation period) between exposure and symptoms. Robert Koch, who had been a student of Jakob Henle’s at Göttingen, advanced beyond observation and supposition with his experimental work of the 1870s and 1880s, identifying the microbial causes of anthrax, tuberculosis, and cholera. Koch’s discoveries, along with those of Pasteur and Joseph Lister and William Roberts and John Burdon Sanderson and others, provided the empirical bases for a swirl of late-nineteenth-century ideas that commonly get lumped as “the germ theory” of disease, which marked a movement away from older notions of malign vapors, transmissible poisons, imbalanced humors, contagious putrefaction, and magic. But the germs with which Koch, Pasteur, and Lister mainly concerned themselves (apart from Pasteur’s brilliant guesswork on rabies) were bacteria.
And bacteria weren’t quite so ineffable. They could be seen with a normal microscope. They could be cultured in a Petri dish (the invention of Julius Petri, Koch’s assistant) containing a nutrient-rich medium of agar. They were bigger and easier to grasp than viruses.
The next crucial insight came from agronomy, not medicine. During the early 1890s, a Russian scientist named Dmitri Ivanofsky, in St. Petersburg, studied tobacco mosaic disease, a problem on plantations within the empire. The “mosaic” spots on the leaves led eventually to stunting and shriveling, which lowered productivity and cost growers money. Earlier work had shown that this disease was infectious—it could be transferred experimentally from one plant to another by applying sap drawn from infected leaves. Ivanofsky repeated the transmission experiment, with one added step. He put the juice through a Chamberland filter, a device made from unglazed porcelain, with tiny pores, for purifying water by screening out bacteria. Ivanofsky’s report, that “the sap of leaves infected with tobacco mosaic disease retains its infectious properties even after filtration,” constituted the first operational definition of viruses: infectious but “filterable,” meaning so small they would pass through where bacteria wouldn’t. Soon afterward, a Dutch researcher named Martinus Beijerinck arrived independently at the same result and then pushed one step farther. By diluting the filtered sap from an infected plant and using that tincture to infect another plant, Beijerinck found that the infectious stuff, whatever it was, regained its full strength even after dilution. That meant it was reproducing itself in the second plant’s living tissues, which meant in turn that it wasn’t a toxin, a poisonous excretion, of the sort that some bacteria produce. A toxin, diluted in volume, is reduced in effect—and it doesn’t spontaneously recover its strength. This stuff did. But in a container of filtered sap alone, it wouldn’t grow. It needed something else. It needed the plant.
So the cumulative work of Martinus Beijerinck, Dmitri Ivanofsky, and a few colleagues showed that tobacco mosaic disease is caused by an entity smaller than a bacterium, invisible by microscope, and capable of multiplication within—only within—living cells. That was the basic profile of a virus, though still nobody had seen one. Beijerinck guessed that the tobacco-mosaic agent was liquid and labeled it contagium vivum fluidum, a contagious living fluid. Later work, including the invention of the electron microscope in the 1930s, proved him wrong on that point. A virus is not liquid but solid: minute particles.
This was all about plants. The first animal virus discovered was the one causing foot-and-mouth disease, another sore problem to agriculture. Cattle and swine passed it to