Viruses quickly evolve new ways of making people sick: Study
Washington: Scientists have discovered that viruses regularly evolve new ways of attacking the bacteria that host them in the human body, a finding they say throws
insight into one of the mysteries of evolution -- where do new traits come from?
In a series of experiments, a team at the Michigan State University found that viruses repeatedly acquired the ability to attack their host bacteria through a different "doorway" or receptor on the bacteria`s cellular membrane.
According to evolutionary theory, natural selection can favour certain members of a population because of traits they possess, such as camouflage or an ability to get at food
others can`t reach, LiveScience reported.
While it`s clear how natural selection causes a population to change, or adapt, explaining how new traits arise has been trickier, said Justin Meyer who led the study.
For their research, published in the journal Science, the Michigan team studied a virus known as lambda. It is harmless to humans, infecting only the gut bacterium Escherichia coli.
The standard way for lambda to get into a cell is to latch onto its outer membrane, attaching to a particular kind of molecule on the surface of E. coli. It can then inject its
genes and proteins into the microbe.
Meyer set up an experiment in which E. coli made almost none of the molecules that the virus grabs onto. But, within 15 days the viruses acquired the ability to infect bacteria
through another receptor, the researchers found.
Meyer was surprised not just by how fast the change happened, but that it happened at all. "I thought it would be a wild goose chase," he said.
In 102 trials, the researchers combined E.coli cells with the virus, called lambda. Lambda normally infects the bacteria by targeting a receptor, LamB, on the bacterium`s outer
The virus does this using a so-called J protein at the end of its tail; this protein unlocks the door into the bacterial cell, Meyer said.
When cultured under certain conditions, most E.coli cells developed resistance to the virus by no longer producing LamB receptors. To infect the bacterial cells, then, the virus had to find another doorway into the cell.
Once inside, the virus hijacks the bacteria`s cellular machinery to copy its own genetic code and reproduce. In 25 of the 102 trials, the virus acquired the ability to infect bacteria through another receptor, called OmpF. The viruses were genetically identical at the beginning of the experiment, so the researchers looked to see what genetic
changes had occurred.
They found that all the strains that could infect the bacteria shared at least four changes, all of which were in the genetic code for the J protein, and which worked together,
according to Meyer.
"When you have three of the four mutations, the virus is still unable to infect," Meyer said. "When you have four of four, they all interact with each other. In this case, the sum
is much more than its component parts."