There’s a moment in the history of medicine that’s so cinematic it’s a wonder no one has put it in a movie. The scene is a London laboratory. The year is 1928. Alexander Fleming, a British microbiologist, is back from a vacation and is cleaning up his workspace. He notices that a speck of mold has invaded one of his cultures of Staphylococcus bacteria. It isn’t just spreading through the culture, though. It is killing the bacteria surrounding it.
Fleming rescued the culture and carefully isolated the mold. He ran a series of experiments that confirmed it made a Staphylococcus-killing molecule. And Fleming then discovered it could kill many other species of infectious bacteria as well. "I had a clue that here was something good, but I could not possibly know how good it was," he later said.
No one at the time could have known how good it was. In 1928, something as minor as a scraped knee could be a death sentence, because doctors were mostly helpless to stop bacteria infections. Fleming was the first scientist to recognize an antibiotic--a discovery for which he’d later win the Nobel Prize. Penicillin saved countless lives, killing off a wide range of pathogens while causing few side effects. Fleming’s work also led other scientists to discover more antibiotics, which collectively changed the rules of medicine. Now doctors could prescribe drugs that effectively wiped out most bacteria, without even knowing what kind of bacteria was making their patients sick.
Of course, even if all the bacteria in the world were eradicated, we would still get sick. Viruses--which cause their own panoply of diseases from colds and the flu to AIDS and Ebola--are profoundly different from bacteria, and so they don’t present the same targets for a drug to hit. Penicillin interferes with the growth of bacteria cell walls, for example, but viruses don’t have cell walls, because they aren’t even cells; they’re just genes packed into protein shells. Other antibiotics, such as streptomycin, attack the factories inside bacteria that make new proteins, known as ribosomes. A virus doesn’t have ribosomes, but instead uses the ribosome inside its host cell to make new copies of itself.
We do currently have "antiviral" drugs, but they’re a pale shadow of their counterparts that fight bacteria. Typically, antivirals will drive down the number of virus particles in the body, but they can’t wipe the virus out completely. People infected with HIV (for example) can avoid developing AIDS by taking a cocktail of antiviral drugs. But if they stop taking antivirals, the virus will rebound to its former levels in a matter of weeks. They have to keep taking the drugs for the rest of their lives to prevent the viruses from wiping out their immune system.
And antivirals have a limited scope of attack. You can treat your flu with Tamiflu, but it won’t cure you of dengue fever or Japanese encephalitis. Scientists have to develop antivirals one disease at a time--a labor that can take many years. As a result, we still have no antivirals for many of the world’s nastiest viruses, like Lassa fever and Ebola. We can expect new viruses to leap from animals to our own species in the future, and when those new viruses begin to spread, there’s a good chance we won’t have any antivirals to help stop them.
Virologists, in other words, are still waiting for their Penicillin Moment. But they might not have to wait forever. Buoyed by advances in molecular biology, a handful of researchers in labs around the US and Canada are trying to engineer a new and unprecedented type of antiviral: a broad-spectrum virus-killer, one that could wipe out viral infections with the same ruthless efficiency that penicillin and Cipro bring to the fight against bacteria. If they succeed, future generations may struggle to imagine a time when we were at the mercy of viruses, just as we struggle to imagine life before Fleming’s moldy dish.
[read full article at Wired