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Influenza viruses were found to have horns or spikes. On some of these is an enzyme that can dissolve part of a cell's outer coating. Presumably, this is what the flu virus uses to open a hole in the cell-factory wall for its nucleic-acid core to slip through. A virus known as T2 bacteriophage (it attacks bacteria) was found to have a tadpole shape; the "tail" is like a coiled spring around a tiny hypodermic needle that stabs the cell wall, and through this the nucleic-acid core is injected. Micrographs show whether viruses are basically cubic or helical in structure. They also reveal that viruses may have an exquisitely complex symmetry around as many as five axes, and contain hundreds of submolecules, each of which may have a hollow hexagonal structure. Chemical tests show whether viruses have cores of ribonucleic acid (RNA) or deoxyribonucleic acid (DNA), and whether they have enzymes or fats in their coats.
The Vaccination Mechanism. The most practical results so far of virological research are vaccines, and vaccines depend on the basic concept of viral structure as a nucleic-acid core with a protein overcoat. The coat is a foreign substance to the body it invades, and in the higher animals, including man, the system fights back by making antibodies that gang up on a virus particle, surround it and neutralize it. Unhappily, it takes days or weeks for the body to mobilize its antibody police, so the first viral invasion is likely to succeed and make the invaded victim sick, or may even kill him. But if the body survives such an invasion, it learns to remobilize its defenses quickly, like emergency police, whenever it recognizes an old viral enemy or one wearing a similar protein overcoat.
Vaccination imitates the natural process for creating antibodies, using similar but less harmful viruses (cowpox instead of smallpox, for example) or weakened viruses, or even killed viruses. But in some individuals, and against some viruses more than others, the antibody memory is short —hence revaccination. If a virus mutates, as often happens with flu, a new vaccine containing the mutant must be prepared.
When John Enders got interested in measles in the 1930s, it was not clear even to him that he was sliding over from bacteriology to virology. "There was still conjecture as to whether measles was caused by a virus.'' he recalls. "Measles intrigued me as a problem that had been elusive for so long." Dr. Enders, working with Dr. William McD. Hammon, promptly ran into frustration of his own. The only animals that would catch measles were monkeys, and only a few of these. The researchers thought that they had got measles virus to infect a cat, only to discover that the animal had a different virus disease: cat distemper. This led to the production of a valuable veterinary vaccine, but not what Enders was looking for.
Enders tried again. Drs. Alice Woodruff and Ernest Goodpasture of Vanderbilt University had recently given virology (and vaccination) a big boost with the discovery that some viruses grow well in incubating eggs. Enders put fluid from a measles patient into eggs, but had no luck. Searching for a better medium, he turned his attention to embryonic tissue culture, sensing that growing viruses in live cells—the technique that Harrison pioneered—held unrealized possibilities.