Editorial for Infectious Diseases - Drug Targets (in silico issue)

International audienceComing from Crimea, the Black Death spread to Western Europe and North Africa during the 1340s. From 1346 to 1352, the plague killed an estimated 25-40% of Europeans of all age-groups [1] , i.e., 30 to 60% of Europe population. One of the earliest and most widely accepted explanations was that God was punishing humanity for their sins. One remedy for the curse was to do penitence. Thus in 1348 there rapidly arose a mass movement of flagellation [2]. In fact flagellation could not really help against such threat. The Black Death or Bubonic plague is caused by Yersinia pestis, a Eubacteria discovered in 1894 by Alexandre Yersin. It is transmitted by the bite of the flea Xenopsylla cheopsis. This flea lives by feeding the blood of many species besides man but its most preferred relationship is with the black rat (Rattus rattus). Fossilized remains of the plague flea have been found in large numbers in Amarna, Egypt [3, 4] about 1350 BC, and thus could be directly linked to the events described in the Book of Samuel [5, 6]. During the epidemic of Bubonic plague in London in 1665-1666, the known treatments were made use of, e.g. the so-famous Theriac or Venice Treacle which is used from the time of ancient Rome as a remedy against poison [7]. Since then, more specialized and novel treatments have been developed. However, since the characterization of Yersinia pestis, numerous drugs have been developed against it, e.g. gentamicin or doxycycline [8]. These researches had been carried out using more elaborated biochemical, biophysical and biological approaches