It’s a common misconception that evolution is a matter of faith, because it happens too slowly to observe. Here’s the way one reader sees it: “I don’t see any fish walking around, nor do I see any other creature in mid-evolving mode. . . . Simply stated, both creationism and evolution should be taught as competing theories; both are not provable, and both cannot be duplicated in a lab.”
But evolution does happen in the lab, in real time, and it’s bad news for us because such rapid evolution allows organisms that can kill us by evading drugs, vaccines, and our own immune systems.
Viral evolution is in the news because scientists reportedly created a new strain of bird flu (H5N1) that’s highly contagious, prompting a government advisory board to request that scientific journals not publish the details.
As I quizzed Penn bioterrorism expert Harvey Rubin about the situation, he continued to talk about evolution and “fitness” of flu viruses. Indeed, he said, the whole point of creating a newer, scarier H5N1 was to help anticipate the virus’ future evolution.
It’s not easily transmissible now. But thanks to evolution, that might change.
This conversation led me to biologist Eddie Holmes of Penn State’s Center for Infectious Disease Dynamics. “Viruses give us the best, most precisely defined examples of evolution you could possibly think of,” he said.
Flu viruses evolve particularly fast because they’re based on RNA – the single-stranded relative of DNA. RNA doesn’t have any mechanism by which to repair copying errors, the way DNA does, so these viruses mutate much faster than DNA viruses.
Working with viruses, Holmes said, “is like watching human evolution on fast-forward.” In 10 years, a virus can undergo as much evolution as a human could in 10 million.
The fact that these viruses undergo mutations is just part of the story. Their mutated progeny are subject to the sorting effect of natural selection. Those that are best at surviving and reproducing themselves predominate.
Viruses have hit upon a number of survival strategies, said Holmes. Measles infects children, thus ensuring a constant crop of new potential hosts. Herpes viruses can lie low, going undetected by the immune system much of the time, so it can survive in a host and spread for decades.
For flu viruses, the strategy is to evade the host’s immune system. People are immune to whatever flu viruses have made them sick in the past, but evolution leads to slightly different versions coming back each season.
Some mutations change the proteins, called antigens, that are the targets of the immune system. By natural selection, the viruses that acquire new antigens can infect a lot more people and will be much more successful than those that have the same old antigens.
Holmes said evolutionary ideas were guiding the quest for a universal flu vaccine – one that would protect us not only from evolving seasonal viruses, but also from new ones, such as H5N1, that jump from other species.
To get such universal protection, scientists need to attack something that’s common to all flu viruses. They are using genetic sequencing to find stretches of common genetic code, hoping to find a common Achilles’ heel. If viruses didn’t evolve from a common ancestor, this wouldn’t work.
Meanwhile, at Penn, biologist/computer scientist Joshua Plotkin is learning about evolution by studying both flu and HIV.
Viruses disprove the common misconception that random mutations can’t lead to improvements in an organism, he said. Unfortunately for us, random mutations lead to flu viruses that can escape our immune systems and vaccines.
“That’s proof positive that some mutations are of adaptive utility,” Plotkin said. “I can’t think of a more straightforward example than that.”
Understanding evolution helps scientists stay a step ahead of flu.
There are patterns, he said, that can be discerned from the last 30 years of flu evolution. Sometimes, two mutations act in concert, for example, so if scientists see one, they can anticipate the other and base a vaccine on an educated guess about its future course.
In his work, Plotkin also studies the way natural selection acts along with the laws of physics to lend some order and predictability to evolution.
The physics comes in because some mutations lead to new proteins whose physical structure may or may not be stable.
Success breeds more success for flu. The more virus gets out there, the more possible new mutants. “Flu is the most successful organism on the planet,” said Plotkin. The better it does, the more opportunities it gets to do even better.
Another type of evolution leads to pandemic strains such as the H5N1, which jumped from birds in the late 1990s. Such a jump was also responsible for the 1918 pandemic, and the more recent swine flu outbreak.
In this kind of evolution, viruses of different types exchange pieces of genetic code to produce something new. H5N1 has pieces of a virus that infects waterfowl and pieces of a human seasonal flu.
Penn State’s Holmes said the evolutionary relationships among hosts could help us understand these rare events. Viruses have an easier time jumping between closely related species, such as humans and chimps. That’s because the virus uses a lock-and-key-type system to infiltrate cells, and chimp cells are similar to our own. Luckily for us so far, bird flu has a hard time getting into human cells.
But now we know that it could mutate to gain access, thanks to those researchers who’ve created the new lab-altered, super-infective version that started this tale.
Some readers have said they accepted microbial or viral evolution, but felt that scientists still hadn’t shown enough evidence it could happen in more complex organisms – especially us. Complex species like us evolve slowly. But we know microbes evolve through the same mechanism. They share with us the same types of molecules – RNA and DNA – that transmit the genetic code.
“The same laws of physics that operate on microbes also operate on large organisms,” said Plotkin. “We have no reason to believe protein evolution will be substantially different.”