The collaboration between Alick Isaacs and myself started in the summer of 1956. Our initial project was to show, by electron microscopy, that interference between inactivated influenza virus and live virus involved the transfer of material from the interfering virus to the host cell. This approach failed for technical reasons. However, in the course of this work it appeared that more interfering activity remained in the system than we were entitled to expect. One possible explanation was that a substance, not identical with the initial interfering virus, was being generated. Subsequent experiments, aimed at checking this hypothesis, led to the description of interferon.

In 1956, when we started our collaboration, both Alick Isaacs and myself had done previous work on interference between inactive and active influenza viruses. We were aware of the state interference research had reached and of the two alternative explanations that had been envisaged.

Several women scientists have contributed to typhus research, which carried an exceptionally high risk of laboratory infection. The work of five of them, Ida Bengtson (1881-1952), Muriel Robertson (1883-1973), Hilda Sikora (1889-1974), Hélène Sparrow (1891-1970) and Clara Nigg (1897-1986), is reviewed and the names of several others are mentioned. The lives of these women seem typical of rickettsiologists and reflect the disasters that befell the world during the first half of the twentieth century.

After the louse transmission of epidemic typhus had been established (1909), a small microorganism (thought to belong to a new genus, Rickettsia) was shown in enormous numbers in the guts of lice that had fed on human typhus victims. Attempts at cultivating this organism on inert media failed; transfer from louse to louse without loss of virulence for the vertebrate host was successful. Some scientists were not convinced of the etiologic role of Rickettsiae, because the presence of this microbe in blood and organs of victims or of experimentally infected animals was difficult to demonstrate. This uncertainty was dispelled in 1928, when in guinea pigs infected with material from the closely related disease Tabardillo (murine typhus) abundant Rickettsiae were revealed in the tunica vaginalis. Live vaccines, derived from strains of murine typhus and deployed in French North Africa, were considered by outside observers as unsafe. Killed vaccines were derived from the masses of Rickettsiae present in louse guts, in chick embryo yolk sacs or in vertebrate lungs. These developments were not spurned by any 'upswing of virology' but by the threat of typhus in endemic areas and, after 1938, in a war-torn world. Their basis was firmly anchored in bacteriological thought styles and techniques.

Hermann Mooser (1891-1971), a Swiss rickettsiologist, sent his friend Peyton Rous (1879-1970) of the Rockefeller Institute (New York) a telegram on November 3,1941, asking for financial help for the manufacture of typhus vaccine in Zurich for the Warsaw Ghetto. His explanatory letter from November 4 reached Rous too late to have any influence on the negative decision (by the Rockefeller Foundation and the American Red Cross) in this matter. Contrary to Weindling's affirmation Mooser was neither in Warsaw in 1941, nor was he a member of the Swiss Sanitary Missions to the eastern front.

In 1905 two different etiologic agents for syphilis were proposed in Berlin, one, the Cytorrhyctes luis, by John Siegel, the other, Spirochaete pallida, by Fritz Schaudinn. Both scientists were pupils of Franz Eilhard Schulze, and were outsiders to the Berlin medical establishment. Both belonged to the same thought collective, used the same thought style, and started from the same supposition that the etiologic agent of syphilis must be a protist. Both used the same morphological approach, the same microscopes and the same stains. Both presented their findings in the same societies, used the same rhetoric, published in the same journals, used the same arguments to criticise each other's shortcomings. Both were backed by powerful institutions and enlisted the support of prestigious patrons. Within half a year, the scientific community at large had in its overwhelming majority accepted Schaudinn's results and rejected those of Siegel. Social forces thus cannot be shown to have played any role in deciding the issue. Ludwik Fleck's suggestion that ‘appropriate influence’ and a ‘proper measure of publicity throughout the thought collective’ would have been sufficient for Siegel's ideas to win the day is untenable.

I have recently read a book by Jan Golinski who is a historian of science trying to explain to his graduate students what modern history of science should be. In his introduction he writes: “The history of science has had a long struggle to free itself from science’s own view of its past.” This may explain to you why there can be a discrepancy between what eye-witnesses or participants in certain developments believe to have lived through and what an outsider who looks at things from a much more general perspective may perceive.

un terme, mais de nous apprendre quand le terme est ap- paru, comment et pourquoi il acomme c'est souvent le cas -passé d'un emploi de la langue courante à un emploi médical.Prenons un exemple.L'article «(fu/Tz/mw nous