Virologists have long thought of baculoviruses, a group of viruses that can liquefy their insect hosts in a matter of days but don't induce so much as a sneeze in mammals, as potential pesticides. But the viruses would require tweaking to be effective since they kill insects more slowly than chemical insecticides. Studying baculoviruses also yields insights into general viral behavior. The current study examined how baculoviruses took the evolutionary leap needed to become the nasty bugs they are today.
In the study, reported in the July 1 issue of the Journal of Virology, BTI researchers Gary Blissard and Oliver Lung investigated whether a fruit fly gene, called an f gene, had originally moved from an insect to a virus or the other way around. (Retroviruses, such as HIV, insert their own genes into their hosts' DNA in order to replicate, and remnants of these invaders can be passed to descendants.) In viruses, an f gene codes for a fusion (F) protein, which enables the virus to penetrate the host cell's membrane and infect it. Scientists had shown that some other viral genes were probably copied from host cells, but the origin of so-called fusion proteins, like F, has remained a mystery.
"The gigantic step was when the Drosophila melanogaster [fruit fly] genome was published," Blissard says. "The first thing was to ask whether the gene was turned on or not, to validate whether it's a bona fide gene."
Blissard and Lung found messenger RNA (mRNA) copies of the gene in fruit fly cells, as well as F proteins--both products unlikely to arise if f were a piece of "junk DNA" left over from a long-departed retrovirus. The researchers then looked for evidence that the fruit fly regulates the f gene, switching it on and off as needed. Indeed, they found
Source:Cornell University News Service