IT IS a solemn custom in science to mark the names of collaborators who pass away during the course of an article's publication with a superscript no different than that indicating their academic affiliation. Very rare indeed is the case that five names on a single report should share that mark. Such a report was published in Science this week. It demonstrates the astonishing speed at which genetic sequencing can now be carried out. At the same time, the fact that Ebola claimed five of its authors is testament to the deadliness of the paper's subject. On June 4th, Stephen Gire, a public health researcher at the Broad Institute in Cambridge, Massachusetts, took delivery of a polystyrene box from Kenema, Sierra Leone. Inside were vials of deactivated biological samples from 78 patients suspected to have Ebola. Mr Gire and a colleague began to tease out the letters of each virus sample's genetic code with some of the most advanced technology yet devised for the task; before long, half of Mr Gire's 30-strong laboratory had volunteered to help.

Then, those sequences of genetic letters were fed into a computer model that looks for hints of mutations where the letters differ. The particular mutations that separate each sample gave hints as to how closely related each was and, because mutations happen naturally at a predictable rate, how long ago they diverged from a common ancestor virus. The networks of transmission from one person to another were laid bare in a laboratory half a world away.

The data suggest that the virus that has now killed more than 1,400 and infected more than 3,000 arose as a distinct strain in 2004. It descended from the 1976 Zaire variant, which usually emerges in central Africa. It may have been lurking in Guinea in the interim, in the "natural reservoir"—presumed to be an animal such as a fruitbat, which can carry the virus without harm. The outbreaks in Guinea and Sierra Leone, as was suspected, appear to have emerged from a single point of contact with the reservoir, and it seems all of the known cases in Sierra Leone stem from one group of women who attended the funeral of a traditional healer in Guinea in May.

All this insight was gleaned in record time. In all, the genetic sequencing—a quadrupling of the world's genetic knowledge of Ebola—took five days. The computational analysis took four more. Even compared to just a few years ago, that is an extraordinary pace. Mr Gire is now working to accomplish the same wizardry in the places where the outbreaks occur. He runs a programme sponsored by the World Bank to provide the technological tools and the training to scientists in Nigeria and Sierra Leone within the next two years.

Such near-real-time feedback to front-line researchers could head off the transition to a pandemic, helping to spot mutations that change its virulence or its transmission characteristics. It could also help epidemiologists pick up where field studies fall off, honing the understanding of human factors in the spread of disease. But none of this gives immediate cause for hope on the ground. That is instead provided by a study published in Nature on Friday that examined a potential treatment for Ebola infection. Gary Kobinger, a veteran vaccine researcher at the Public Health Agency of Canada, and colleagues tested the experimental drug ZMapp, a blend of three monoclonal antibodies, which give the body's immune system a way to recognise and destroy the virus. The treatment made headlines in August when Kent Brantly and Nancy Writebol, two aid workers working in Liberia, recovered from infection after taking ZMapp. Yet it remains unknown whether or how the drug saved them. In the new work the mix, developed in part by Dr Kobinger, was administered to rhesus monkeys infected with a lethal dose of Ebola. Three groups of six monkeys were given the drug at different intervals after infection, up to its latest stages 11 days later. All 18 survived, and three weeks later all had undetectable levels of the virus in their blood. That 100% success rate on a small sample is surely encouraging. But the experiment was performed using an earlier variant of the virus preserved from the 1995 Kikwit, Congo outbreak, rather than the current strain. Nevertheless, the drug appears to slow the newer virus replicating in a dish, and the Broad Institute’s work shows that the two strains are genetically close. But human clinical trials are needed.

Mr Gire said that other ZMapp researchers were looking at his genetic sequences "as they came off the machines" in June. Real-time sequencing can inform treatment design and response in an outbreak, but a pipeline between the two remains distant; for now, it is a hoped-for tool in the field-work kit.

Mr Gire knew Mohamed Fullah, one of the authors who died in Sierra Leone. He was a teacher at the Eastern Polytechnic College and a haematologist with his own lab, where he had worked most often with another haemorrhagic fever, Lassa. There are only a handful of talented epidemiologists in Sierra Leone; losing just one deals a blow both to the scientific community and to the local one. As profiles in Science bear out, Mr Fullah, as well as Mbalu Fonnie, Sheik Humarr Khan, Alice Kovoma and Alex Moigboi were working at science's most dangerous frontier. Their colleagues have a long road ahead.